O31 Giant cell arteritis - a rare ocular presentation

Case report - Introduction Giant cell arteritis (GCA) is a systemic vasculitis primarily affecting large- and medium-sized arteries. Classic symptoms include headache, scalp tenderness, jaw claudication and visual disturbances. Ophthalmic artery involvement commonly causes anterior ischaemic optic neuropathy. Uncommon ocular features include anterior segment ischaemia, hypotony, tonic pupil or rarely choroidal ischaemia. Heterogenicity of presentation can make diagnosis difficult leading irreversible visual loss. We report a case of bilateral macular choroidal ischaemia with atypical symptoms of GCA. It emphasises the need of complete evaluation in elderly patients with GCA and visual symptoms and the need to start aggressive treatment to prevent visual loss. Case report - Case description 73-year-old caucasian lady presented to the eye emergency department with diplopia. Medical history includes systemic hypertension, hypothyroidism and hyperlipidaemia, no past ocular history. Eye examination was normal except decompensated fourth nerve paresis. Thyroid function was normal. Diplopia resolved spontaneously. Patient re-presented with a floater in the right eye and left-sided atypical headache without jaw claudication. Investigations: normal FBC, CRP 126, ESR 100, PV 1.67. Following rheumatologist review she was commenced on oral prednisolone 60 mg with clinical suspicion of GCA. Temporal artery biopsy confirmed GCA. She had TIA subsequently. MRI revealed small area of acute infarct in left ganglio-capsular region. Clopidogrel was started for secondary prevention. In the ophthalmology clinic she saw a lacy pattern. Her Log MAR VA in right and left eye was 0.64 and 0.76, respectively. Fundoscopy revealed retinal pigment epithelial (RPE) mottling at the maculae, right more than left eye. Optical Coherence Tomography (OCT) macula revealed bilateral RPE elevations and serous pigment epithelial detachment bilaterally, patchy central RPE atrophy with external limiting membrane disruption, more pronounced in the right eye. Fundus fluorescein angiogram and indocyanine green angiography confirmed bilateral choroidal ischaemia (triangular shaped with the base at the equator) at the macula worse in right than left eye. Oral prednisolone was continued with gradual tapering. VA improved to Log MAR 0.5 and Log MAR 0.2 in right and left eye at six weeks. OCT showed signs of RPE re-modelling with resolution of sub retinal fluid (resolution of inflammation). At recent follow up Log MAR VA is 0.26 and 0.06 in right and left eye respectively. She is on oral prednisolone 20 mg once a day tapering 2.5 mg every 2 weeks. OCT shows further re-modelling of the ellipsoid zone in the left eye, but her right eye shows more RPE atrophy and thinning with RPE degeneration. Case report - Discussion We report an unusual case of GCA with atypical symptoms and bilateral choroidal ischaemia. Patients with GCA usually present with systemic symptoms and signs like headache, scalp tenderness, fever, and jaw claudication. Variable presentation can often lead to misdiagnosis and consequent irreversible loss of vision. Visual symptoms as the first and only sign of GCA was first reported in 1952. Posterior ciliary arteries in the eye can be affected leading to optic nerve infarction and subsequent anterior ischaemic optic neuropathy (AION). AION and visual field loss accounts for 80—90% of cases with ocular signs of GCA. Posterior ciliary artery occlusion can rarely cause patches of choroidal infarcts which appear as chorio-retinal degeneration in a couple of weeks. These patches are usually in the mid-peripheral fundus, usually triangular shaped with the base towards equator and apex toward posterior pole. In our case the presentation was very atypical in the sequence of symptoms. Her raised inflammatory markers raised the suspicion of GCA and prompt referral to rheumatology was done. Aggressive treatment with oral steroids was started with stomach and bone protection. Temporal artery biopsy confirmed the diagnosis. The bilateral triangular ischaemic areas found on FFA and ICG confirmed the macular choroidal ischemia. Her OCT also showed bilateral RPE mottling showing degenerative changes due to choroidal infarct from posterior ciliary artery occlusion. We managed to preserve the vision in our case by starting the timely aggressive steroid treatment. In summary, we report an unusual case of GCA with atypical symptoms and bilateral choroidal ischaemia where further visual loss was avoided due to timely intervention. GCA has variety of presentations; a combined team approach of ophthalmologists and rheumatologists can prevent irreversible visual loss in such cases. Case report - Key learning points GCA is a chronic idiopathic inflammation more commonly seen in the large- and medium-sized vessels. Posterior ciliary arteries in the eye can be affected in GCA leading to optic nerve infarction and subsequent anterior ischaemic optic neuropathy (AION). AION and visual field loss accounts for 80—90% of cases with ocular signs of GCA. Posterior ciliary artery occlusion can rarely cause patches of choroidal infarcts which appear as chorio-retinal degeneration in a couple of weeks. These patches are usually in the mid-peripheral fundus, usually triangular shaped with the base towards equator and apex toward posterior pole. Prompt diagnosis and aggressive treatment with corticosteroids can prevent visual loss in one or both eyes. Any patient over 50 years of age presenting with visual symptoms of amaurosis fugax, diplopia, or visual loss with ocular signs of anterior or posterior ischaemic optic neuropathy, central retinal artery occlusion or cilioretinal artery occlusion should create a high suspicion for GCA. This group of patients should have urgent ESR, CRP and PV evaluation. If suspected, high-dose corticosteroids must be started followed by temporal artery biopsy for confirmation. It is imperative to diagnose GCA early and start treatment urgently to prevent visual loss. A multidisciplinary team approach in patients with GCA can prevent sight loss and life too.

Associating the biomarkers of ocular blood flow with lamina cribrosa parameters in normotensive glaucoma suspects. Comparison to glaucoma patients and healthy controls

Purpose To evaluate association between ocular blood flow biomarkers and lamina cribrosa parameters in normotensive glaucoma suspects compared to glaucoma patients and healthy controls. Methods A total of 211 subjects (72 normotensive glaucoma suspects, 70 with primary open-angle glaucoma and 69 controls) were included. Ocular blood flow biomarkers in ophthalmic artery, central retinal artery, as well as in nasal and temporal short posterior ciliary arteries were measured using colour Doppler imaging. Lamina cribrosa position was assessed by measuring its depth, deflection depth, lamina cribrosa shape index and its horizontal equivalent (LCSIH) on B-scan images obtained using optical coherence tomography. Results Ocular blood flow biomarkers in glaucoma patients were statistically significantly reduced when compared to healthy controls in peak systolic velocity (PSV) (P = 0.001 in ophthalmic artery and P<0.001 in central retinal artery) and mean flow velocity (Vm) (P = 0.008 in ophthalmic artery and P = 0.008 in central retinal artery), but not statistically significantly different to that of glaucoma suspects except for PSV in central retinal artery (P = 0.011). Statistically significant correlations corrected for age, central corneal thickness and intraocular pressure were found in glaucoma patients between LCSIH and end diastolic velocity of central retinal artery (P = 0.011), and of nasal short posterior ciliary artery (P = 0.028), and between LCSIH and Vm of central retinal artery (P = 0.011) and of nasal short posterior ciliary artery (P = 0.007). No significant correlations were observed between these parameters in glaucoma suspects and healthy controls. Conclusions Impaired ocular blood flow associated with the deformation of lamina cribrosa was found in glaucoma patients, whereas glaucoma suspects had similar lamina cribrosa shape to glaucoma patients but that deformation was not associated with ocular blood flow biomarkers.

Inflammation of a Posterior Ciliary Artery in a Naive Cynomolgus Macaque

This brief communication describes a previously unreported background lesion in the eye of a naive cynomolgus macaque. Inflammation of a posterior ciliary artery was, in this case, morphologically similar to vascular inflammation of other tissues described in naive cynomolgus macaques. However, the available literature does not describe this lesion at this anatomical site. The affected animal did not present with any abnormal clinical signs and ophthalmological examinations were within normal limits. Toxicologic pathologists should be aware of this finding in order to help differentiate it from a test item–related finding.

The effect of moderate treadmill exercise on the resistive index of the medial long posterior ciliary artery in dogs

The resistive index (RI) is an indirect measurement of arterial resistance by means of a ratio between the peak systolic and end diastolic velocities recorded with a spectral Doppler device, especially used to evaluate the vascular damage in ocular diseases such as glaucoma. Some ocular variables such as the intraocular pressure (IOP), the choroidal thickness, the axial length and the ocular blood flow may be influenced by physical exercise. The purpose of this study was to evaluate the influence of the exercise on the RI of the medial long posterior ciliary artery in dogs, and correlate the data obtained with the IOP values. Ten clinically healthy dogs were subjected to moderate physical exercise on a canine motorised treadmill at different speeds for 45 minutes. A colour Doppler examination was performed and the RI values were calculated for the medial long posterior ciliary artery at rest, immediately after the exercise, and after 60 minutes at the end of the exercise. At the same times, the IOP was recorded by applanation tonometry. The data were analysed by a two-way repeated ANOVA measurement in order to compare the RI and the IOP. Wilcoxon’s test was applied for the post hoc comparison. Spearman’s rank correlation for non-normal distribution was used to determine a relationship between the RI and the IOP. The at rest RI was 0.722 +/–0.022, IOP 12.38 +/3.21 mm Hg. A significant decrease in the RI was observed immediately after the exercise (0.697 +/–0.035) and during the passive recovery phase (0.682 +/–0.042). A significant decrease in the IOP (11+/3.39 mmHg) was recorded after 60 min of the passive recovery phase; at the end of the exercise, a slight decrease (12.29+/4.26 mm Hg) mm Hg was detected. During the test, a linear correlation between the RI and the IOP was observed. Our results suggest that exercise induces the modification of the ophthalmic blood flow in dogs, presumably related to the compensatory neuro-hormonal mechanisms.