June 2018

ADVANCING THERAPEUTIC

Hypertension Managing hypertensive patients in your practice Sleep apnoea OSA and its relationship to the eyes

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Editor JEFF MEGAHAN 02 20

Clinical Editor Cardiovascular Q and A CXO featured article Associate Professor Mark Roth Associate Professor Sheela E Kumaran, Jyoti BSc(Pharmacology) Mark Roth and Associate Khadka, Rod Baker and BAppSc(Optom) PGCertOcTher NEWENCO FAAO OAM Professor Leo Hartley Konrad Pesudovs

Publications Manager JESSICA DONALD 04 21 Obstructive sleep apnoea’s Outer retinal tubulations Cover design effect on the eyes Lachlan Hessing Abhishek Sharma Associate Professor Optometry Australia Leo Hartley ABN 17 004 622 431 25

Level 1, 201 Clarendon Street 10 Looking into the future: South Melbourne VIC 3205 the biological contact Ph 03 9668 8500 Brain injury assessments bandage Fax 03 9663 7478 Steven Leslie Dr Emily Glover and [email protected] Dr J James Thimons www.optometry.org.au 13 Copyright © 2018 The ocular effects of 27 Comments made in Pharma are of A new treatment a general nature and intended for Paula Katalinic and Professor Leo Semes guidance only. Optometry Australia and Gonzalo Jacome the individual contributors expressly disclaim all liability and responsibility 23 to any person in respect of, and for the consequences of, anything done or 14 Therapeutic News of note omitted to be done in reliance wholly or FEATURE Associate Professor partly on anything in this publication. Mark Roth Pharma is distributed in Australia Chair-side Reference: and New Zealand. All references to Hypertension pharmaceutical preparations in Pharma are applicable within Australia. Michael Yapp / Centre for Eye Health 2 JUNE 2018

Cardiovascular Q and A

mounting evidence that, at the very for face-to-face visits when you’re trying least, OSA contributes to faster rates to establish yourself in an area. Visiting of progressive field loss and retinal pharmacists is also very valuable, as ganglion cell loss. Obviously, larger they can refer patients to you and also studies will need to be conducted to feel comfortable calling you when they reveal the mechanism of damage that need advice. may be exacerbating (or even causing) primary open-angle glaucoma (POAG) Phoning the local ophthalmologist and normal tension glaucoma (NTG). when you first refer a patient will help We know that dysfunction establish a good rapport. results from hypoxia, acidosis, Associate Professor hypercarbia and airway obstruction, Roth: Hypertension is also a focus of frequently observed in patients with this edition of Pharma, which includes Mark Roth OSA. The mechanism I’ve reported on another excellent chair-side reference in is reperfusion injury as a result of these a series from the Centre for Eye Health. BSc(Pharmacology) factors. As the introductory article from Paula BAppSc(Optom) PGCertOcTher Katalinic and Gonzalo Jacome states: NEWENCO FAAO OAM Roth: I certainly will be including signs ‘hypertension significantly increases and symptoms of OSA in my history the risk of cardiovascular disease.’ What taking. This condition is yet another is the front line General Practitioner example of how optometry can work perspective and main challenges of more closely with medicine. Do you hypertension and cardiovascular health? Associate Professor Mark Roth OAM, think optometrists are under-recognised clinical editor of Pharma interviews with their clinical skills and expertise Hartley: Risk factors for cardio-vascular Associate Professor Leo Hartley, and the part they can play in the health health should be determined. These can one of Australia’s most prominent system? be modifiable and non-modifiable. Risk optometrists who has also completed a calculators have been developed for this medical degree. His dual qualifications Hartley: The increased use of the purpose. and clinical experience provides a ‘doctor’ title by optometrists (in rare insight into the commonality of my opinion, rightly) reflects the The first challenge GPs often have medicine and optometry. increased role that optometrists is getting patients to take care of play as true primary care health themselves (and that means taking Roth: Firstly, congratulations on your professionals. Optometrists have responsibility for their diet, exercise, obstructive sleep apnoea (OSA) article, excellent undergraduate (and in some alcohol intake and of course, smoking). published in this issue of Pharma. It’s cases, postgraduate) training in basic a massive work and it covers the topic sciences, medicinal systemic and eye Brief interventions and referrals to comprehensively. Why do you believe health which form the important STEM allied health professionals (exercise it’s an important topic for optometrists? knowledge needed to stay updated in physiologists, nutritionists) with GP this rapidly-expanding profession. follow-up, can really help to get patients Hartley: It’s my opinion that to change. A healthy diet (with minimal optometrists, as primary care health Roth: What would you suggest to early salt and an emphasis on unprocessed professionals, should be aware of what career optometrists who are interested foods, particularly vegetables and ophthalmic conditions can signal in taking greater responsibilities in some lower-fructose fruits) can go a systemic conditions in our patients. managing their patients? How can they long way to decrease body fat and OSA has emerged as an important risk build bridges with medical practitioners minimise reliance on antihypertensive factor for many systemic associations. and specialists? drugs. Cutting down on established drinking and smoking habits (which Roth: I was surprised to read of the Hartley: Communication is the key. are, effectively, self-medications) takes broad range of ophthalmic associations A routine eye examination report to considerable commitment from patients. of sleep apnoea, such as non-arteritic GPs builds confidence that you know ischaemic and what you’re talking about. Recognition As you know, depression is a significant central serous chorio-. Is by the government that optometrists risk factor for heart disease, so a healthy there sufficient evidence to include can diagnose and expedite referrals diet leading to a healthy gut biome has glaucoma? for has given been shown to decrease reliance on optometry greater credibility in the eyes medication for depression. Hartley: The literature provides of GPs. Of course, there is no substitute JUNE 2018 3

Pharma clinical editor Associate Professor Mark Roth and Associate Professor Leo Hartley discuss the role of optometrists and general practitioners in the management of the cardiovascular system

It can be frustrating (albeit essential, Roth: Hypertension is not like a dial in many cases) having to rely on where you can turn pressure up and medications to control patients’ blood down accurately. What drugs are mainly pressure. Also, of course, several studies used and are there new advances in have shown (as with glaucoma) quite medical therapy? poor medication adherence 12 months after initiation. Hartley: Firstly, just as in glaucoma, we want to assess the risk of morbidity Roth: On the positive side, there before commencing treatment. See Table is strong evidence that controlling 1 below for a list of hypertension drugs. hypertension leads to reduced cardiovascular disease-related morbidity Roth: All drugs come with potential Associate Professor and mortality. Is it as simple as that? side-effects. This is why an initial Leo Hartley case history of ALL the drugs a patient Hartley: Obesity, and dietary salt is taking is so vital. Several vascular MBBS DipAppScOptom FACBO intake of course, lead to hypertension, medications come with significant FACO GradCertHltProfEd cardiovascular disease and diabetes. ocular effects. For example: Digoxin for GradCertOcTh These conditions, if left untreated, lead atrial fibrillation can cause xanthopsia, to a cascade of events that include renal or yellowing vision. What are the main disease, stroke and heart attack. CV drugs for optometrists to look out University of Melbourne for? University of Sunshine Coast My emphasis is on the whole patient. That is: encouraging the patient to Hartley: Digoxin is fortunately not work with me to take charge of their used that often these days. Most of the health as a whole and to see me as beta-blockers will have an effect on their health coach (who has a wide IOP and may cause dry eye (so may armamentarium of advice, other health need tear lubricants concomitantly). I Hartley: I believe there is certainly professionals and medications to help usually don’t start a glaucoma patient no harm in checking in that process). Just as optometrists on a topical beta-blocker if they’re on a and doing a random blood sugar test. do when helping patients make systemic beta-blocker already. That’s not In some cases where the patient has appropriate lens choices, I try not to to say it won’t have an additive effect, never consulted a GP, it can be a game just prescribe treatments without the because it may. changer. For others, the more times a patient’s involvement in the decision- patient is reminded that they need to making. Although, sometimes in cases Roth: What are your views regarding look after themselves, the better. where patients refuse to be actively optometrists measuring their patients’ involved in their own care (‘just fix me blood pressure? Perhaps using a digital Before starting patients on doc’) that is necessary. sphygmomanometer? antihypertensive medication, I usually encourage them to buy a digital sphygmomanometer and measure their BP twice daily (just after waking and Medication Features before dinner) for at least five days. Relaxes blood vessels, lowers blood pressure and prevents ACE inhibitor That is far more accurate than doing it diabetes-related kidney damage in our rooms.

Diuretic Increases urine production to get rid of excess salt and water As I mentioned, having the patient really involved in their care increases Beta blocker Slows heart rate and decreases blood pressure the chance of adherence to the health measures we are trying to achieve Antihypertensive drug Lowers blood pressure (taking medication, better weight management, ceasing smoking or cutting down on alcohol). Calcium channel blocker Relaxes blood vessels Roth: Professor Hartley, thanks again Vasodilator Widens blood vessels for your great article and contribution to our discussion. Table 1. List of hypertension drugs 4 JUNE 2018

Obstructive sleep apnoea’s effect on the eyes

Associate Professor Leo Hartley

MBBS DipAppScOptom FACBO FACO GradCertHltProfEd GradCertOcTh

University of Melbourne University of Sunshine Coast

H2 Vision Centres, QLD

Obstructive sleep apnoea (OSA) is of sleep apnoea increases with age. seconds (associated with occlusion characterised by repetitive pharyngeal of the nasopharyngeal airway) and collapse during sleep, resulting in then sudden arousal (usually with a episodes of hypoxia leading to a typical gasping sound). Sleep is re- cascade of neurological, ophthalmic Typical signs of obstructive sleep established, followed by snoring and and systemic consequences. apnoea in an adult follow a pattern. the cycle repeats.4 Increasingly, it is recognised as a The patient initiates sleep followed significant cause of morbidity and by a shallowing of breathing and/ Symptoms of sleep apnoea include mortality.1 or snoring or loud breathing, then somnolence, insomnia, nocturia, cessation of breathing for several waking suddenly during the night, Pharyngeal patency is dependent on the competence of the dilator muscles and the bulk of the soft tissues of the throat. With the onset of sleep, the dilator muscles relax and, combined with the weight of the tongue, pharyngeal collapse occurs STOP-BANG questionnaire (Figure 1). This leads to cessation of breathing, resultant hypoxia and hypercapnia (build-up of CO2 in the STOP BANG blood) triggering the pons to arouse the sufferer. This temporarily restores Snoring BMI> 35 kg/m2 normal oxygen levels and allows sleep restoration. The cycle continuously Tired Age > 50 repeats, leading to neurological, ophthalmic and systemic sequelae.2 Observed apnoea Neck circumference > 40 cm

Epidemiology High blood Pressure Gender: male In most populations, about 50 per cent of middle-aged men and 23 per cent of High risk of OSA: answering yes to three or more items middle-aged women have moderate- Low risk of OSA: answering yes to fewer than three items to-severe sleep apnoea.3 As with , the incidence and prevalence Table 1. STOP-BANG screening test JUNE 2018 5

Associated ocular conditions resulting Obstructive sleep apnoea’s effect on the eyes from long-term OSA

Figure 1. Sleep apnoea. As the patient sinks into a deep sleep, the muscle tone of the surrounding throat tissues relax, allowing the patient’s throat to occlude. This is followed by a rapid decrease in saturated oxygen and a corresponding increase in carbon dioxide (and a concomitant increase in heart rate and blood pressure) which eventually stimulates the pons, causing arousal. Saturated oxygen increases and the patient again falls into a deep sleep. The cycle repeats several times a night.

neurological inflammation,5,6 Repetitive Increase in serum ↓ Tarsal ↑ Elasticity of tarsus and cerebrovascular disease,2 metabolic hypoxia MMP - 7 and 9 elastin ↑ papillae dysregulation, endothelial dysfunction,2 oxidative stress and 5,6 ↓ Stromal collagen hypercoagulation, neurohumoral changes,5,6 systemic hypertension,7 ischaemic heart disease,5–7 pulmonary Floppy 8–10 ↑ Demodex hypertension, congestive heart and lash failure,7 portal hypertension and liver disease,11 arrhythmias,5, 6, 12 metabolic syndrome and insulin resistance.4 ↓ Meibomian glands Ophthalmic associations of sleep apnoea ↑ Eye rubbing MGD dry eye Sleep apnoea has been implicated Figure 2. Keratoconus and floppy syndrome. Repetitive hypoxia may lead to an increase with several ophthalmic conditions in corneal and tarsal matrix metalloproteinases 7 and 9 (MMP) as well as a decrease in corneal including floppy eyelid syndrome and collagen and tarsal elastin. Floppy eyelids are often attributed to side sleeping. However this lash ptosis,13–28 non arteritic ischaemic doesn’t explain why everyone who side-sleeps doesn’t have floppy eyelid syndrome (FES). optic neuropathy (NAION),15,16, Floppy eyelids, lash ptosis, papillary and keratoconus result. Demodex infestation 29,30 idiopathic intracranial and meibomian gland dysfunction (MGD) often ensue. Resultant eye rubbing can contribute to hypertension (IIH),30–42 central serous floppy eyelids and keratoconus. chorioretinopathy (CSCR),15,16,43–57 retinal vein occlusion (RVO),16,50,58 keratoconus15,20,21 and glaucoma (POAG, NTG).15,16,59–69 However, some inability to get back to sleep, muscles and weight gain.4 studies have not found a correlation nightmares, mouth breathing, morning of glaucoma with OSA.61,67,70 , dry mouth, sore throat, Long term effects of sleep apnoea migraine exacerbation, irritability, Possible or proposed mechanisms of mood swings, so-called ‘brain fog’ Sleep apnoea causes intermittent cause of these conditions are outlined due to decreased mentation, daytime hypoxia, intermittent hypercapnia, sleepiness, increased risk of car sympathetic activation,2 intrathoracic crashes due to micro-sleeps, aching pressure changes,5,6 systemic and Continued page 6 6 JUNE 2018

Sleep apnoea Obstructed airway Repetitive hypoxia CO retention 2 From page 5 Peripheral Activation of vasoconstruction, astrocytes cerebral vasoldilation in Figures 2 to 7. (dysregulation) NOS-2 ↑ Unstable ONH HTP NTG↓↑ Screening tests for sleep apnoea perfusion Nitric oxide ↑ ↑ IOP perfusion There have been a number of screening tests for OSA. The Berlin Reperfusion damage Sleep questionnaire,71,72 the Epworth ONOO ↑ Sleepiness Scales73,74 and the STOP- BANG questionnaire59,73–75 are Oxygen species often used. While the Berlin Sleep Apoptosis questionnaire is often preferred by Tissue remodelling many Australian sleep physicians, the STOP-BANG test is very fast to Figure 3. Normal tension and high tension glaucoma. Repetitive hypoxia and reperfusion administer for the busy optometric damage at the level of the optic nerve head causes an increase in nitric oxide and peroxynitrite clinician. See Table 1 for an example leading to apoptosis. Reperfusion damage leads to tissue remodelling (increase in cupping). of the STOP BANG questionnaire. CO2 = carbon dioxide, NOS-2 = nitric oxide synthase 2, ONOO = peroxynitrite, HTG = high ten- Figure 8 shows suggested decision- sion glaucoma, NTG = normal tension glaucoma, ONH = optic nerve head. making regarding OSA for a busy optometrist.

Assessment of sleep apnoea Obstructed airway The gold standard in assessment CO retention & cerebral CO ↑ for obstructive sleep apnoea is 2 2 76–78 polysomnography. During this Repetitive hyoxia test, the patient has several functions monitored simultaneously. These ↑ Peripheral vasoconstriction, include oxygen saturation, heart rate leads to cerebral vasodilation and rhythm (ECG), breathing rate and depth as well as leg movements Acute surges in cerebral blood flow (EMG) and eye movements (EOG) NAION leads to increased ICP and systemic BP and electroencephalography (EEG). 1. Sudden onset of painless These functions are monitored while and/or visual field loss the patient sleeps. Snoring may be 2. Diffuse or sectoral oedema Ischaemia or hypoxia at measured with a sound probe. (exclude other causes) the optic nerve head

The tests can be administered in a Figure 4. Non-arteritic anterior ischaemic optic neuropathy (NAION). Repetitive hypoxia and sleep laboratory (overnight stay) or at cerebral hypercapnia lead to intracerebral surges in intracranial pressure resulting in ischae- home using an ambulatory unit which mia or hypoxia of the optic nerve head causing optic neuropathy. is fitted to the patient before he/ she goes home. The patient removes the sensors in the morning. A sleep physician reviews the recordings. Obstructed airway Treatment of sleep apnoea Treatment is recommended based Repetitive hyoxia CO retention on the severity of the OSA. Mild- 2 to-moderate OSA responds well to oral appliances which move the jaw forward, relieving the obstruction. Peripheral vasoconstriction, leads to cerebral vasodilation These have been found to be mostly well tolerated with a good compliance rate after 30 months of use.4,79–81 Increased cerebral blood flow Idiopathic intracranial leads to increased ICP and hypertension The mainstay of treatment is systemic BP continuous positive airway pressure 81,82 (CPAP) devices. These devices Figure 5. Idiopathic intracranial hypertension (benign intracranial hypertension). Sleep apnoea use continuous positive pressure to leads to raised intracranial pressure, most frequently seen in females between ages 20 and 30 keep the airways open. The patient with morbid obesity. Co2 = carbon dioxide, BP = blood pressure, BMI = body mass index. JUNE 2018 7

must exhale against this pressure. The OSA Type A personality Helicobacter pylori Steroids pressure can be set based on titration in an overnight test, or set using an automatic sensing CPAP machine Phosphodiesterase – 5 Caffeine Relative ↑ Cortisol which detects occlusions and inhibitors (> 600mg/day) increases pressure to overcome these occlusions. Automatic titration CPAP devices have been found to be non- ↑ Intraluminal pressure in ↓ Choroidal blood flow inferior to pre-set pressure devices. surrounding choriocapillaris Many CPAP devices feature humidifiers and warmed tubing to RPE decompensation improve comfort and decrease the and detachment likelihood of damage to susceptible airways.

CSCR CPAP has a disappointing compliance rate with up to 30 per cent of patients Figure 6. Central serous chorioretinopathy (CSCR). Sleep apnoea, Type A Personality, H. Pylori, refusing to continue past an initial systemic steroids, Phosphodiesterase-5 inhibitors, and caffeine have all been implicated in trial. Only 50 per cent of starting causing relative hypercortisolism which leads to a decrease in choroidal blood flow and in- patients comply after 12 months.82 creased intraluminal pressure in the surrounding choriocapillaris. This leads to retinal pigment However, a number of studies have epithelial decompensation and detachment and central serous chorioretinopathy. OSA = sleep shown a significant improvement apnoea, RPE = retinal pigment epithelium, CSCR = central serous chorioretinopathy. in compliance of greater than four hours a night to 70 per cent of Obstructed airway participants.83

Surgery has been largely unsuccessful, Peripheral probably because the actual Repetitive hypoxia CO2 retention vasoconstriction, leads mechanisms of occlusion are complex to cerebral vasodilation and multifactorial.84 Techniques to improve compliance include brief

Increased cerebral intervention, phone coaching, partner blood flow leads to coaching, upper airway assessment increased ICP and and alcohol consumption as well as a systemic BP smart phone application.85–90

Change in retinal Conclusion blood flow and local hyperviscosity Obstructive sleep apnoea has been linked to several ophthalmic Loss of vision noticed Occlusion of capillary Virchow’s Triad conditions including floppy eyelid on waking bed -> Retinal Vein 1. Increased viscosity syndrome, lash ptosis, non-arteritic Occlusions 2. Endothelial anterior ischaemic optic neuropathy, dysfunction 3. Stasis central serous chorioretinopathy, glaucoma, idiopathic intracranial Figure 7. Retinal vein occlusion. Obstructive sleep apnoea leads to hypercapnia and cerebral hypertension and keratoconus. vasodilation causing raised intracranial hypertension, hyperviscosity of retinal vasculature and ultimately venous occlusion. Sleep apnoea is a serious health condition that is mostly undiagnosed in Australia and the western world. Ophthlamic findings Observation of patient It is commonly seen in obese (lash ptosis, FES, IIH, NAION, POAG/NTG, RVO) (BMI > 35, > 50 years, male, appears fatigued) males who are over the age of 50 years. It has been associated with neurodegenerative and cardiovascular STOP-BANG disease (including hypertension and questionnaire heart failure), type 2 diabetes, obesity and, if left untreated, it can lead to multiple organ failure. STOP-BANG STOP-BANG Score ≥ 3 Score < 3

Refer to GP with Review 12/12 STOP-BANG Score

Figure 8. Suggested decision making in OSA in optometry practice Continued page 8 8 JUNE 2018

18. Dhillon PS, Lewis G. Floppy eyelid syn- hypertension. Rev Neurol Dis 2010; 7: drome. BMJ Case Rep 2015; 2015: pii: e56–68. Sleep apnoea bcr2015210168 38. Fraser JA, Bruce BB, Rucker J, et al. Risk 19. Karhanova M, Hobzova M, Maresova K. factors for idiopathic intracranial hyper- From page 7 [Floppy eyelid syndrome and obstruc- tension in men: a case-control study. J tive sleep apnoea]. Cesk Slov Oftalmol Neurol Sci 2010; 290: 86–89. 2012; 68: 22–26, 28. 39. Jindal M, Hiam L, Raman A, et al. 1. Yu J, Zhou Z, McEvoy RD, et al. Associ- 20. Fowler AM, Dutton JJ. Floppy eyelid Idiopathic intracranial hypertension in ation of Positive Airway Pressure With syndrome as a subset of lax eyelid otolaryngology. Eur Arch Otorhinolaryn- Cardiovascular Events and Death in conditions: relationships and clinical gol 2009; 266: 803–806. Adults With Sleep Apnea: A Systematic relevance (an ASOPRS thesis). Ophthal 40. Hanigan WC, Zallek SN. Headaches, Review and Meta-analysis. JAMA 2017; Plast Reconstr Surg 2010; 26: 195–204. shunts, and obstructive sleep apnea: 318: 156–166. 21. Ezra DG, Beaconsfield M, Sira M, et al. report of two cases. Neurosurgery 2004; 2. Javaheri S, Barbe F, Campos-Rodriguez The associations of floppy eyelid syn- 54: 764–768; discussion 8–9. F, et al. Sleep Apnea: Types, Mech- drome: a case control study. Ophthal- 41. Lee AG, Golnik K, Kardon R, et al. Sleep anisms, and Clinical Cardiovascular mology 2010; 117: 831–838. apnea and intracranial hypertension Consequences. J Am Coll Cardiol 2017; 22. Karger RA, White WA, Park WC, et al. in men. 2002; 109: 69: 841–858. Prevalence of floppy eyelid syndrome 482–485. 3. Crinion SJ, Ryan S, McNicholas WT. in obstructive sleep apnea-hypopnea 42. Marcus DM, Lynn J, Miller JJ, et al. Sleep Obstructive sleep apnoea as a cause of syndrome. Ophthalmology 2006; 113: disorders: a risk factor for pseudotumor nocturnal nondipping blood pressure: 1669–1674. cerebri? J Neuroophthalmol 2001; 21: recent evidence regarding clinical im- 23. McNab AA. Floppy eyelid syndrome 121–123. portance and underlying mechanisms. and obstructive sleep apnea. Ophthal 43. Chatziralli I, Kabanarou SA, Parikakis Eur Respir J 2017; 49: pii: 1601818 . Plast Reconstr Surg 1997; 13: 98–114. E, et al. Risk Factors for Central Serous 4. Ramar K, Dort LC, Katz SG, et al. Clini- 24. Netland PA, Sugrue SP, Albert DM, et al. Chorioretinopathy: Multivariate Ap- cal Practice Guideline for the Treatment Histopathologic features of the floppy proach in a Case-Control Study. Curr Eye of Obstructive Sleep Apnea and Snoring eyelid syndrome. Involvement of tarsal Res 2017; 42: 1069–1073. with Oral Appliance Therapy: An Up- elastin. Ophthalmology 1994; 101: 44. Brodie FL, Charlson ES, Aleman TS, et date for 2015. J Clin Sleep Med 2015; 11: 174–181. al. Obstructive sleep apnea and central 773–827. 25. Yuksel M, Kuzu-Okur H, Velioglu-Ogunc serous chorioretinopathy. 2015; 5. Xie J, Wei YX, Liu S, et al. Obstructive A, et al. Matrix Metalloproteinase-9 35: 238–243. Sleep Apnea Hypopnea Syndrome as Level and Gene Polymorphism in Sleep 45. Yavas GF, Kusbeci T, Kasikci M, et al. a Reason for Active Management of Disordered Breathing Patients with or Obstructive sleep apnea in patients with Pulmonary Embolism. Chin Med J (Engl) without Cardiovascular Disorders. Bal- central serous chorioretinopathy. Curr 2015; 128: 2147–2153. kan Med J 2013; 30: 8–12. Eye Res 2014; 39: 88–92. 6. Vijayan VK. Morbidities associated with 26. Ye J, Liu H, Li Y, et al. Increased serum 46. Kim JT, Eichling PS, Wang M. Central se- obstructive sleep apnea. Expert Rev levels of C-reactive protein and matrix rous chorioretinopathy associated with Respir Med 2012; 6: 557–566. metalloproteinase-9 in obstructive sleep narcolepsy. Retin Cases Brief Rep 2011; 7. Shamsuzzaman AS, Gersh BJ, Somers apnea syndrome. Chin Med J (Engl) 5: 302–305. VK. Obstructive sleep apnea: implica- 2007; 120: 1482–1486. 47. Ezra N, Taban M, Behroozan D. Central tions for cardiac and vascular disease. 27. Vuralkan E, Mutlu M, Firat IH, et al. serous chorioretinopathy associated JAMA 2003; 290: 1906–1914. Changes in serum levels of MDA and with topical corticosteroids in a patient 8. Wong HT, Chee KH, Chong AW. Pulmo- MMP-9 after UPF in patients with with psoriasis. J Drugs Dermatol 2011; nary hypertension and echocardiogram OSAS. Eur Arch Otorhinolaryngol 2014; 10: 918–921. parameters in obstructive sleep apnea. 271: 1329–1334. 48. Sancho-Chust JN, Chiner E, Lopez-Lizca- Eur Arch Otorhinolaryngol 2017; 274: 28. Tamaki S, Yamauchi M, Fukuoka A, et no R. [Central serous chorioretinopathy 2601–2606. al. Production of inflammatory media- as first sign of onset of sleep apnea-hy- 9. Suzuki A, Kondoh Y. The clinical im- tors by monocytes in patients with ob- popnea syndrome]. Arch Bronconeumol pact of major comorbidities on idiopath- structive sleep apnea syndrome. Intern 2010; 46: 449–50. ic pulmonary fibrosis.Respir Investig Med 2009; 48: 1255–1262. 49. Jain AK, Kaines A, Schwartz S. Bilateral 2017; 55: 94–103. 29. Ghaleh Bandi MF, Naserbakht M, central serous chorioretinopathy resolv- 10. Kohno T, Kataoka M, Kawakami T, et Tabasi A, et al. Obstructive sleep apnea ing rapidly with treatment for obstruc- al. Moderate-to-severe obstructive sleep syndrome and non-arteritic anterior is- tive sleep apnea. Graefes Arch Clin Exp apnea is associated with subclinical chemic optic neuropathy: a case control Ophthalmol 2010; 248: 1037–1039. myocardial injury and impaired hemo- study. Med J Islam Repub Iran 2015; 29: 50. Leroux les Jardins G, Glacet-Bernard A, dynamics in pulmonary hypertension 300. Lasry S, et al. [Retinal vein occlusion patients. Sleep Med 2017; 30: 121–127. 30. Fraser CL. Obstructive sleep apnea and and obstructive sleep apnea syndrome]. 11. Halank M, Langner S, Kolditz M, et al. optic neuropathy: is there a link? Curr J Fr Ophtalmol 2009; 32: 420–424. Nocturnal oxygen desaturation is a fre- Neurol Neurosci Rep 2014; 14: 465. 51. Kloos P, Laube I, Thoelen A. Obstructive quent complication in portopulmonary 31. Stevens SM, Rizk HG, Golnik K, et al. sleep apnea in patients with central hypertension. Z Gastroenterol 2008; 46: Idiopathic intracranial hypertension: serous chorioretinopathy. Graefes 1260–1265. Contemporary review and implications Arch Clin Exp Ophthalmol 2008; 246: 12. Goudis CA, Ketikoglou DG. Obstructive for the otolaryngologist. Laryngoscope 1225–1228. sleep and atrial fibrillation: Pathophys- 2018; 128: 248–256. 52. Leveque TK, Yu L, Musch DC, et al. Cen- iological mechanisms and therapeutic 32. Wardly DE. Intracranial hypertension as- tral serous chorioretinopathy and risk implications. Int J Cardiol 2017; 230: sociated with obstructive sleep apnea: a for obstructive sleep apnea. Sleep Breath 293–300. discussion of potential etiologic factors. 2007; 11: 253–257. 13. West SD, Turnbull C. Eye disorders as- Med Hypotheses 2014; 83: 792–797. 53. Giovansili I, Belange G, Affortit A. Cush- sociated with obstructive sleep apnoea. 33. Szewka AJ, Bruce BB, Newman NJ, et ing disease revealed by bilateral atypical Curr Opin Pulm Med 2016; 22: 595–601. al. Idiopathic intracranial hypertension: central serous chorioretinopathy: case 14. Wang P, Yu DJ, Feng G, et al. Is Floppy relation between obesity and visual report. Endocr Pract 2013; 19: e129–33. Eyelid Syndrome More Prevalent in outcomes. J Neuroophthalmol 2013; 33: 54. Caccavale A, Romanazzi F, Imparato M, Obstructive Sleep Apnea Syndrome 4–8. et al. Central serous chorioretinopathy: Patients? J Ophthalmol 2016; 2016: 34. Kalyoussef E, Brooks NO, Quraishi H, et a pathogenetic model. Clin Ophthalmol 6980281. al. Idiopathic intracranial hypertension 2011; 5: 239–243. 15. Skorin L, Jr., Knutson R. Ophthalmic in a child with obstructive sleep apnea 55. Haimovici R, Rumelt S, Melby J. Diseases in Patients With Obstructive cured by tonsillectomy/adenoidectomy. Endocrine abnormalities in patients Sleep Apnea. J Am Osteopath Assoc J Neuroophthalmol 2013; 33: 413–414. with central serous chorioretinopathy. 2016; 116: 522–529. 35. Stein JD, Kim DS, Mundy KM, et al. The Ophthalmology 2003; 110: 698–703. 16. Huon LK, Liu SY, Camacho M, et al. The association between glaucomatous and 56. Shang Q, Liu C, Wei S, et al. [Determi- association between ophthalmologic other causes of optic neuropathy and nation of cortisol in plasma and 24-hour diseases and obstructive sleep apnea: sleep apnea. Am J Ophthalmol 2011; urine of patients with central serous a systematic review and meta-analysis. 152: 989–998. chorioretinopathy]. Zhonghua Yan Ke Sleep Breath 2016; 20: 1145–1154. 36. Javaheri S, Qureshi Z, Golnik K. Reso- Za Zhi 1999; 35: 297–299. 17. Compton CJ, Melson AT, Clark JD, et lution of associated with 57. Garg SP, Dada T, Talwar D, et al. Endog- al. Combined medial canthopexy and OSA treatment. J Clin Sleep Med 2011; enous cortisol profile in patients with lateral tarsal strip for floppy eyelid 7: 399–400. central serous chorioretinopathy. Br J syndrome. Am J Otolaryngol 2016; 37: 37. Thurtell MJ, Bruce BB, Newman NJ, et Ophthalmol 1997; 81: 962–964. 240–244. al. An update on idiopathic intracranial 58. Turati M, Velez-Montoya R, Gonza- JUNE 2018 9

lez-Mijares CC, et al. Bilateral central 2014; 14: 27. 81. Carberry JC, Amatoury J, Eckert DJ. retina vein occlusion associated with 70. Gross NJ, Funk J, Pache M, et al. Personalized Management Approach for obesity-hypoventilation syndrome (pick- [Prevalence of glaucoma in obstructive OSA. Chest 2018; 153: 744–755. wickian syndrome). Retin Cases Brief sleep apnea]. Ophthalmologe 2015; 112: 82. Parsons C, Allen S, Parish J, et al. The Rep 2009; 3: 140–143. 580–584. efficacy of continuous positive airway 59. Rao DP, Senthil S, Choudhari N. Me- 71. Senaratna CV, Perret JL, Matheson MC, pressure therapy in reducing cardiovas- ta-Analysis of Association of Obstructive et al. Validity of the Berlin questionnaire cular events in obstructive sleep apnea: Sleep Apnea (OSA) With Glaucoma. J in detecting obstructive sleep apnea: A a systematic review. Future Cardiol Glaucoma 2017; 26: e130. systematic review and meta-analysis. 2017; 13: 397–412. 60. McMonnies CW. Glaucoma history and Sleep Med Rev 2017; 36: 116–124. 83. Ghosh D, Allgar V, Elliott MW. Iden- risk factors. J Optom 2017; 10: 71–78. 72. Verbraecken J, Hedner J, Penzel T. tifying poor compliance with CPAP 61. Keenan TD, Goldacre R, Goldacre MJ. Pre-operative screening for obstructive in obstructive sleep apnoea: a simple Associations between obstructive sleep sleep apnoea. Eur Respir Rev 2017; 26: prediction equation using data after a apnoea, primary open angle glaucoma pii: 160012 . two week trial. Respir Med 2013; 107: and age-related : 73. Soler X, Liao SY, Marin JM, et al. Age, 936–942. record linkage study. Br J Ophthalmol gender, neck circumference, and Ep- 84. Yamamoto T, Fujii N, Nishimura Y, et al. 2017; 101: 155–159. worth sleepiness scale do not predict ob- Mechanisms Underlying Improvement 62. Zhao XJ, Yang CC, Zhang JC, et al. Ob- structive sleep apnea (OSA) in moderate in Obstructive Sleep Apnea Syndrome structive Sleep Apnea and Retinal Nerve to severe chronic obstructive pulmonary by Uvulopalatopharyngoplasty. Case Fiber Layer Thickness: A Meta-analysis. disease (COPD): The challenge to predict Rep Otolaryngol 2017; 2017: 2120165. J Glaucoma 2016; 25: e413–8. OSA in advanced COPD. PLoS One 85. Sedkaoui K, Leseux L, Pontier S, et al. 63. Yuvaci I, Pangal E, Bayram N, et al. 2017; 12: e0177289. Efficiency of a phone coaching program Evaluation of posterior ocular changes 74. Mihaicuta S, Udrescu M, Topirceanu A, on adherence to continuous positive air- using enhanced depth imaging-optical et al. Network science meets respiratory way pressure in sleep apnea hypopnea coherence tomography in patients with medicine for OSAS phenotyping and se- syndrome: a randomized trial. BMC obstructive sleep apnea syndrome. Arq verity prediction. Peer J 2017; 5: e3289. Pulm Med 2015; 15: 102. Bras Oftalmol 2016; 79: 247–252. 75. Moseley BD. The STOP-BANG question- 86. Luyster FS, Dunbar-Jacob J, Aloia MS, 64. Wang JS, Xie HT, Jia Y, et al. Retinal naire improves the detection of epilepsy et al. Patient and Partner Experiences nerve fiber layer thickness changes in patients at risk for obstructive sleep With Obstructive Sleep Apnea and obstructive sleep apnea syndrome: a apnea. Epilepsy Res 2017; 134: 50–51. CPAP Treatment: A Qualitative Analysis. systematic review and Meta-analysis. Int 76. McGrath B, Lerman J. Pediatric Behav Sleep Med 2016; 14: 67–84. J Ophthalmol 2016; 9: 1651–1656. sleep-disordered breathing: an update 87. Lai AYK, Fong DYT, Lam JCM, et al. The 65. Chaitanya A, Pai VH, Mohapatra AK, Ve on diagnostic testing. Curr Opin Anaes- efficacy of a brief motivational enhance- RS. Glaucoma and its association with thesiol 2017; 30: 357–361. ment education program on CPAP adher- obstructive sleep apnea: A narrative 77. Griffiths AG, Patwari PP, Loghmanee ence in OSA: a randomized controlled review. Oman J Ophthalmol 2016; 9: DA, et al. Validation of Polyvinylidene trial. Chest 2014; 146: 600–610. 125–134. Fluoride Impedance Sensor for Res- 88. Jurado-Gamez B, Bardwell WA, Cordo- 66. Xin C, Zhang W, Wang L, et al. Changes piratory Event Classification during va-Pacheco LJ, et al. A basic intervention of visual field and optic nerve fiber layer Polysomnography in Children. J Clin improves CPAP adherence in sleep in patients with OSAS. Sleep Breath Sleep Med 2017; 13: 259–265. apnoea patients: a controlled trial. Sleep 2015; 19: 129–134. 78. Ugon A, Seroussi B, Philippe C, et al. Breath 2015; 19:509–514. 67. Wu X, Liu H. Obstructive sleep apnea/ Towards a Wireless Smart Polysom- 89. Jeong JI, Kim HY, Hong SD, et al. Upper hypopnea syndrome increases glaucoma nograph Using Symbolic Fusion. Stud Airway Variation and Frequent Alcohol risk: evidence from a meta-analysis. Int J Health Technol Inform 2016; 221: 23–27. Consumption Can Affect Compliance Clin Exp Med 2015; 8: 297–303. 79. Whitla L, Lennon P. Non-surgical man- With Continuous Positive Airway Pres- 68. Ulusoy S, Erden M, Dinc ME, et al. agement of obstructive sleep apnoea: a sure. Clin Exp Otorhinolaryngol 2016; 9: Effects of Use of a Continuous Positive review. Paediatr Int Child Health 2017; 346–351. Airway Pressure Device on Glaucoma. 37: 1–5. 90. Isetta V, Torres M, Gonzalez K, et al. A Med Sci Monit 2015; 21: 3415–3419. 80. Hamoda MM, Kohzuka Y, Almeida FR. New mHealth application to support 69. Bilgin G. Normal-tension glaucoma and Oral Appliances for the Management of treatment of sleep apnoea patients. J obstructive sleep apnea syndrome: a OSA -An Updated Review of the Litera- Telemed Telecare 2017; 23: 14–18. prospective study. BMC Ophthalmol ture. Chest 2018; 153: 544–553.

Self-monitoring leads to lower blood pressure A new study suggests that having patients monitor their pressure; usual care group). own blood pressure may help lower it. After 12 months, systolic blood pressure was lower in the The TASMINH4 trial aimed to assess the efficacy self-monitoring and telemonitoring groups compared with of self-monitored blood pressure, with or without the group in usual care (137.0, 136.0, and 140.4 mmHg, telemonitoring, for antihypertensive titration in primary respectively). care, compared with usual care. The study authors concluded that self-monitoring when The study was a parallel randomised controlled trial used by general practitioners to titrate antihypertensive done in 142 general practices in the UK, and included medication in individuals with poorly controlled blood hypertensive patients older than 35 years, with blood pressure, leads to significantly lower blood pressure than pressure higher than 140/90 mmHg, who were willing to titration guided by clinic readings. self-monitor their blood pressure. They suggested that, with most general practitioners and Patients were randomly assigned to self-monitoring many patients using self-monitoring, it could become the blood pressure (self-monitoring group), to self- cornerstone of hypertension management in primary care. monitoring blood pressure with telemonitoring (telemonitoring group), or to usual care (clinic blood Lancet. Mar 2018 doi: 10.1016/S0140-6736(18)30309-X 10 JUNE 2018

Brain injury assessments A systemic history and testing regime can elucidate symptoms and signs and lead to appropriate management

Steven Leslie

BOptom FACBO FCOVD GradCertOcTher

Eyes on Oxford, Perth, WA

It is not uncommon to have patients who report a history of a head injury, whiplash or concussion, stroke, or neurological conditions such as Parkinson’s disease or multiple sclerosis. Or you may have a patient whose symptoms or signs suggest the possibility of, or at least the need to reasonably rule out, neurological Figure 1. Right eye optic nerve temporal pallor issues.

You could refer the patient and wait a few months for an assessment, or you could make a probably-unnecessary online and sent back before the exam, Age is important. For instance, giant urgent referral; or you could work or done on arrival, alerting you to cell arteritis typically occurs in people through a measured process of symptoms and history, and suggesting older than 50; stroke in a younger assessment and testing to determine possible further questions and tests. woman can be due to a combination of the best options for professional care. Importantly, it can be saved to the smoking and contraceptive pills. patient’s record, providing evidence Rather than attempting to guess what of the questions asked and answered, Ask about the time course of the problem might be, or trying to which is sometimes helpful when presenting symptoms: when first remember a myriad of symptoms and there is pathology discovered by you noticed, any progression, any previous signs associated with neurological or someone else later. episodes, frequency, duration, issues, the best approach is: any triggering factors, previous If there is a suggestion of neurological investigations and treatment, any eye • Taking a careful history issues, I then move to an expanded pain (particularly if worse with eye • Conducting a systematic visual questionnaire. It saves having to movement) any transient loss of or and ocular assessment remember them. It is vitally important double vision, or ‘migraines’ (ask more that you record negative answers and questions about migraine features). Be wary of any previous diagnoses, test results, such as ‘no headaches/ as it is very easy to prejudice the double vision/pain/…’. Do not If there is a history of a brain injury outcome of your own assessment in make the dangerous mistake of only or stroke, ask about the details and the light of previous diagnoses.1,2 Start recording abnormal symptoms and effects at the time.Was there loss of afresh. results. A good history allows you to: consciousness and for how long?

• Define presenting complaints Were there effects on speech or History motor function, cognition, memory, • List pertinent health history and If you ask enough targeted questions, emotional behaviour (often suggests medications in many cases the patient will tell frontal lobe effects), depression or you their diagnosis. We routinely • List diagnosis or differentials epilepsy? Then explore the visual and use a two-page ‘Welcome to the ocular history regarding spectacles, • Plan further investigations Office Form,’ which can be filled out eye turn or surgery, diagnosis or JUNE 2018 11

palsy, or ; pursuit and saccadic eye movements, both horizontal and vertical; convergence A systemic history and testing regime can elucidate • Confrontation visual fields, perimetry symptoms and signs and lead to appropriate management • size in light and dark, direct response, near response, RAPD testing • External eye health from front to back: lids • Any ptosis or proptosis • and lens • IOP • Ophthalmoscopy of optic nerve, macula and retina

In my experience, many patients have significant ocular and neurological symptoms and yet:

• They have no diagnosis despite other assessments • They have a diagnosis which does not fit the signs and symptoms • They do not understand their Figure 2. Left eye healthy optic nerve diagnosis and effects • They do not connect their vision problems with neurological or other health issues

treatment of a ‘lazy’ eye such as symptoms of giant cell arteritis: new A systematic history and testing patching, eye drops, laser surgery or or severe headaches, scalp or temple regime frequently elucidates any history of eye disease. tenderness, difficulty or pain chewing, symptoms and signs which were ear pain, fevers, fatigue, weight loss, not obvious, and can lead to further Medical history can be reasonably or reduced appetite. testing, referral, discovery of unknown covered by asking about unusual and potentially-significant issues and fatigue, any history of cancer or auto- Comprehensive visual and ocular appropriate management. immune disease; any issues of heart, assessment diabetes, hypertension, cholesterol or head or neck trauma; or any history of If you systematically work through surgery. a comprehensive sequence of tests CASE REPORT of visual function and ocular health, Medications need to be questioned, you will record many normal results particularly steroids, heart, erectile (ruling out some issues), and gather dysfunction, oral contraceptives, all the abnormal results into a pattern ‘M’ is a 57 year-old male teacher cancer treatment (tamoxifen, radiation, which helps to guide further action. with good general health other than chemotherapy) and any medications Always assume results are abnormal slightly high cholesterol levels. He for depression, anxiety or psychosis. until proven otherwise. had unaided VA of R 6/12- L 6/7.5, improving to 6/5 each eye with Sometimes it is necessary to carefully Visual function tests should include: correction of moderate bilateral ask about smoking and alcohol use, or hyperopic . Pupil reaction ask: ‘Have you used any recreational • VA distance and near, BCVA, testing suggested a trace weaker drugs, such as marijuana, ice, speed, pinhole, VA refraction direct reaction of the right eye, and or coke?’—you may be surpised at the • Colour vision of each eye, red a trace right eye RAPD. Assessment answer. cap comparison of his function was unremarkable, with normal Anyone over 50 with a history of • Eye movements for normal transient or sustained visual loss movement, or signs of or , should be asked about or cranial nerve Continued page 12 12 JUNE 2018

Brain injury From page 11 convergence and a full range of eye movements.

His anterior eye health was normal, he had IOPs of R and L 16 mm Hg, no Figure 3. Right eye Medmont glaucoma visual field with inferior nasal step defect significant lens changes and normal maculas, but moderate sectoral temporal pallor of his right optic nerve, with the superior rim very pale, shelved and sloping towards the cup, with cup to disc ratios of R 0.4, L 0.3 produce bilateral visual field defects. optic atrophy. Medical review three (see Figures 1 and 2). It could be due to impaired optic nerve months later showed no change, with head perfusion, or a lesion or mass no specific aetiology identified, but it Medmont visual fields revealed an effect anterior to, or adjacent, to the is considered unlikely to progress. inferior arcuate (see Figure right anterior optic chiasm. 3). OCT showed significant temporal 1. Groopman J. How doctors think. Carlton (superior and inferior) retinal nerve North, Vic: Scribe Publications; 2010 The anterior chiasmal pathology over 2. Gawande A. Complications. New York, fibre layer thinning (Figure 4). He had time has probably caused either mild NY: Picador; 2002 central corneal thicknesses of 615 papilloedema which has resolved, or microns R and L with open angles. transneuronal degeneration along the right optic nerve, appearing as sectoral A recent CT scan was reported as unremarkable. Monocular colour vision Ishihara testing was equal and normal for both eyes.

He described slight memory changes over the last six months, but no specific neurological symptoms were elicited on comprehensive questioning. Specifically, he denied any recent acute and severe .

In view of the right eye optic nerve temporal pallor and associated inferior arcuate scotoma, without associated disc excavation or notching, he was referred for urgent ophthalmological assessment of other possible optic neuropathic aetiologies, including ischaemic optic neuropathy (unlikely due to age and good health) and multiple sclerosis or inflammatory vascular disease.

MRI showed thinning of the right side of the optic chiasm, and thinning of the pituitary gland, with the sella mainly filled with cerebrospinal fluid (empty sella syndrome).

The most likely explanations include a previous pituitary apoplexy (haemorrhage into, or reduced blood supply of the pituitary), or tumour. Pituitary function was normal.

The unilateral visual field defect argues against a post-chiasmal Figure 4. OCT of right eye shows significant temporal (superior and inferior) neurological insult, which would retinal nerve fibre layer thinning. JUNE 2018 13

DE GUI Hypertension chair-side reference guide PAGES 14–16

The ocular effects of hypertension

Paula Katalinic Managing hypertensive patients in BOptom (Hons) MOptom GradCertOcTher your practice

Gonzalo Jacome BOptom GradCertOcTher

Centre for Eye Health

is associated with the highest level of target organ damage (nephropathy or Australian health care expenditure of retinopathy).2 Oral anti-hypertensive any disease group, with a direct cost of treatment should be instigated within approximately $7.7 billion in 2008– 24–72 hours and hospitalisation may High blood pressure (HBP) or 2009.2 be required in some cases.2 A medical hypertension is a significant public emergency exists when blood pressure health burden. In Australia, nearly is very high (> 220/140 mmHg) Definitions of hypertension six million people are affected by and acute target organ damage or hypertension with potentially 68 The National Heart Foundation (NHF) dysfunction is present (papilloedema, per cent of hypertension remaining Guidelines for the diagnosis and haemorrhagic stroke or heart failure). undiagnosed.1,2 The condition affects management of hypertension in adults Hospitalisation is indicated in these more than a billion people worldwide, 2016 assists practitioners in making cases. increasing in prevalence with age. diagnosis and management decisions The complications of hypertension by categorising blood pressure into a Ocular effects of hypertension account for more than 9.4 million number of categories.2 Normal blood deaths worldwide every year.3 In pressure is defined as a systolic reading Elevated blood pressure can induce a 2014–15, approximately 34 per cent of of 120–129 mmHg and diastolic reading series of pathophysiological changes to Australians aged 18 years or older had of 80–84 mmHg and mild hypertension the retinal, choroidal and optic nerve high blood pressure. as 140–159 mmHg (systolic) or 90–99 circulations resulting in a constellation mmHg (diastolic). The decision about of clinical signs referred to as Most importantly, hypertension when to start anti-hypertensive hypertensive retinopathy, hypertensive significantly increases the risk of treatment depends on both the degree choroidopathy and hypertensive cardiovascular disease (specifically: of hypertension and the patient’s optic neuropathy.9 Hypertension also ischaemic and haemorrhagic stroke, cardiovascular risk profile. increases the risk of developing retinal myocardial infarction and heart failure), vein and artery occlusion, diabetic chronic kidney disease and premature Risk factors for CVD include diabetes, retinopathy, retinal macroaneurysm and death.2 Increased risk of cardiovascular elevated blood lipids, smoking, male ischaemic optic neuropathy, and may be disease (CVD) begins at 115/75 mmHg sex, ethnicity and age > 45 years, or associated with glaucoma and AMD.9-11 and doubles with each increment of > 35 years in Aboriginal and Torres 20/10 mmHg.4 Strait Islander peoples. For patients In early hypertension, local with a low cardiovascular disease risk, autoregulatory mechanisms lead There is strong evidence that controlling NHF and the Royal Australian College to vasospasm and increased retinal hypertension leads to reduced CVD- of General Practitioners recommend that arteriolar tone resulting in generalised related morbidity and mortality, anti-hypertensive therapy be instigated arteriolar narrowing. Subsequent including incident stroke (by 35 to 40 with persistent blood pressure thickening and degeneration of the per cent), myocardial infarction (by ≥ 160/100 mmHg to achieve a normal blood vessel wall leads to severe 15 to 25 per cent) and heart failure (by range.2,8 However, an optimal target generalised and focal areas of arteriolar up to 64 per cent).5-7 Furthermore, the blood pressure (< 120/80) may be more narrowing, arteriovenous nipping randomised, controlled SPRINT trial appropriate in patients with existing and copper wiring. As the condition showed that intensive blood pressure cardiovascular disease.8 progresses, disruption of the blood- control (systolic pressure of < 120 retina barrier manifests as retinal mmHg) reduces the risk of heart attacks, Urgent referral is required in cases stroke and death as compared to systolic of severe HBP (> 180/110 mmHg) 5 pressure > 130 mmHg. CVD disease associated with symptoms or moderate Continued page 17 Chair-side Reference: Hypertension

Hypertension is a chronic medicalChair condition-side in which arterialReference: blood pressure is elevated Hypertension. It affects over 1 billion people worldwide, increasing in prevalence with age. It is one of the most important preventable risk factors for premature death, as it increases the risk of ischaemic heart disease, stroke, peripheral vascular disease, other cardiovascular disease and nephropathy. Grading schemes available for hypertensive retinopathy Hypertension is a chronic(Mitchell medical condition-Wong Scheme in which usedarterial below blood: pressureWong & is Mitchell,elevated. ItNew affects England over 1 billionJournal people of Medicine, worldwide, 2004 increasing;351 (in22 prevalence):2310-7), with but age recent. It is evidenceone of the suggestsmost important only preventablea modest association risk between retinopathy and systemic organ damage. factors for premature death, as it increases the risk of ischaemic heart disease, stroke, peripheral vascular disease, other cardiovascular disease and nephropathy. Grading schemes available for hypertensive retinopathy (Mitchell-Wong Scheme used below: Wong & Mitchell, New England Journal of LESIONSMedicine, 2004;351 OF(22):2310 HYPERTENSIVE-7), but recent evidence suggests RETINOPATHY only a modest association between retinopathy and systemic organ damage. Category of Systolic, Diastolic, Chair-sideLESIONS Reference: OF HYPERTENSIVE Hypertension RETINOPATHY Category of Systolic, Diastolic, hypertension mmHg mmHg Vascular calibre changes (Mild retinopathy) Retinal haemorrhageshypertension (Moderate retinopathy)mmHg mmHg VascularChair calibre changesChair (Mild- retinopathy)side-side Reference: Reference:Retinal Hypertension haemorrhages Hypertension (Moderate retinopathy) Normal 90-119 60-79 Hypertension is a chronic medical condition in which arterial blood pressure is elevated. It affects over 1 billion people worldwide, increasing in prevalence with age. It is one of the most important preventable risk Normal 90-119 60-79 factors for premature death, as it increases the risk of ischaemic heart disease, stroke, peripheral vascular disease, other cardiovascular disease and nephropathy. Grading schemes available for hypertensive retinopathy and • Thickening and loss of •elasticityThickening of the arterial and loss wall of elasticity of the arterial wallFlame haemorrhage Flame haemorrhage and (Mitchell-Wong Scheme used below: Wong & Mitchell, New England Journal of Medicine, 2004;351(22):2310-7), butA recent evidence suggests only a modest associationA between retinopathy and systemic organ damage. Hypertension is aHypertension chronic medical is a chronic condition• Broadening medical in condition ofwhich light reflex arterialin• which Broadeningmasking bloodarterial the pressure bloodblood of light pressurevessel is reflex elevated is elevated masking. It. affectsIt theaffects blood overover vessel11 billion•billionOriginate people people from worldwide, worldwide,superficial increasing capillary increasing in bed prevalence or• radialinOriginate prevalence with age from. It with is superficialone age of .the It mostis capillary one important of thebed mostpreventable or radial important risk preventable risk factors for premature death,column, LESIONSas it represents increases OF the chronic HYPERTENSIVE risk of arterial ischaemic changes heart RETINOPATHY disease, stroke, peripheral vascular disease,parapapillary other cardiovascular capillariesCategory disease of and nephropathySystolic, . GradingDiastolic, schemes availableHigh for hypertensive normal retinopathy120 -139 80-89 High normal 120-139 80-89 factors for premature death, as it increases the risk of ischaemiccolumn, heart represents disease, stroke,chronic peripheral arterial changes vascular disease, other cardiovascularhypertension disease andmmHgparapapillary nephropathy mmHg capillaries. Grading schemes available for hypertensive retinopathy (Mitchell-Wong Scheme used below: Wong & Mitchell, New England Journal of Medicine, 2004;351(22):2310•-7),Appearance but recent evidencedue to RNFL suggests orientation only a modest association between retinopathy(prehypertension) and systemic organ damage. or (prehypertension) or (Mitchell-Wong Scheme usedVascular below calibreCopper :changes Wong vs.(Mild & silver Mitchell,retinopathy) wiring (A)New England Journal of Medicine,Retinal haemorrhages 2004; (Moderate351(22): retinopathy)2310-7), but recent evidence suggests only• Appearancea modest association due to RNFL between orientation retinopathy and systemic organ damage. Chair-side Reference Copper vs. silver wiring (A) • Resolves in aroundNormal 6 weeks 90-119 60Category-79 of Systolic, Diastolic, • Thickening and loss of elasticity •of theChanges arterial startwall off as “copperLESIONS wiring” OF (slightFlame HYPERTENSIVE broadening haemorrhage of RETINOPATHY • Resolvesand in around 6 weeks Stage 1 140-159 90-99 A• Changes start off as “copper wiring” (slight broadeningDot/blot haemorrhage of hypertensionCategory of mmHg mmHgSystolic , Diastolic, Stage 1 140-159 90-99 • Broadening of light reflex masking lightthe blood reflex) vesselLESIONS (top ) OF HYPERTENSIVE• Originate from superficial capillary RETINOPATHY bed or radial or Vascular calibre changes (Mild retinopathy) Retinal •haemorrhagesOriginate from (Moderate deep High capillary normal retinopathy) bed (INL, ONL,Dot/blot120- 139or OPL) haemorrhage 80-89 or column, represents chronic arterial• “Silver changes wiring” represents lightgreater reflex) broadening (topparapapillary) of reflex capillaries hypertension mmHg mmHg • Appearance due to RNFL orientation • Displaces retinal structures,(prehypertension) takes longer •to resolveOriginateor Normalfrom deep capillaryStage bed 902 (INL,-119 ONL, or60 OPL)-79160 -179 100-109 Copper vs. •silverVascularThickening wiring (A) calibre and loss changes (moreof elasticity “silver” (Mild of withinthe retinopathy) arterial the• vessel)“Silver wall (bottom wiring”) represents greaterFlame broadening haemorrhageRetinal of haemorrhagesreflex (Moderate retinopathy) and Hypertension • Resolves in around 6 weeks Stage 1 140-159 90-99 Stage 2 160-179 100-109 • Changes start off as “copper wiring” (slight broadening of • Displaces retinal structures, takes longer to resolve • May be more useful to quantify broadeningDot/blotA haemorrhage Normal 90-119 60-79 light reflex)• Broadening (top) of light reflex masking the blood vessel(more “silver” within the vessel)B• Originate(bottom from) superficial capillary bed or radial or • Thickening and loss of elasticity of the arterial wall • Originate from deep capillaryFlame bed haemorrhage (INL, ONL, or OPL) (Moderate retinopathy)High normal Stage 1203 (hypertensive-139 80-89≥180 and ≥110 • Can be focal or generalised • “Silver wiring”column, represents represents greater broadening chronic arterial of reflex changes May be more useful to quantify broadeningparapapillary capillaries • A • Displaces retinal structures, takes longer to resolve Stage 2 160-179 100-(prehypertension)109 • Broadening(more of “silver” light withinreflex the masking vessel) (bottom the) blood vessel • Originate• Appearance from due superficial to RNFL orientation capillaryB bed or radial emergency) or or Copper vs. silver wiringA/V (A)“nicking” (US) or “nipping” (UK) (B) Cotton wool spots (Moderate retinopathy) Stage 3 (hypertensive ≥180 ≥110 Chair-side Reference: Hypertension• May be more useful to quantify broadening • HypertensionCan be focal is one or of generalised the most important preventable risk factors• Due for to premature ischaemia death, of the as RNFL it increases the risk of ischaemic High normal 120-139 80-89 B • Resolves in around 6 weeks Hypertension is a chronic medicalcolumn, condition represents• Changes chronic start arterial off• asThickened “copper changes wiring” arteriole (slight can broadening impinge upon of the retinal veins,Cotton wool parapapillaryspots (Moderate retinopathy) capillaries Stage 3 (hypertensive ≥180 ≥110Stage 1 Isolated140 systolic-159 90-99≥140 <90 • Can be focal or generalised heart disease, stroke, peripheral vascular disease, other cardiovascular• Disruption of disease axoplasmic and nephropathy.flow manifests The as apresence grey- of emergency) or Dot/blot haemorrhage (prehypertension) or or in which arterial blood pressure is elevated.light reflex) (top) leading to potential veinA/V occlusions “nicking” (below) (US) or “nipping”• (UK)Appearance (B) due to RNFLwhite lesionorientation along emergency)the RNFL bundles • Due orto ischaemia of the RNFLhypertension (may be Copper vs.A/V silver “nicking” wiring (US) or(A) “nipping” (UK) (B) moderate hypertensive retinopathy correlates strongly with acute hypertension. The Mitchell-Wong classification scheme • Due to ischaemia of the RNFL• Originate from deep capillary bed (INL, ONL, or OPL) Chair-side Reference: Hypertension• Thickened• arteriole“Silver wiring”can impinge represents• uponSalus’s the retinalgreater sign: veins,Vein broadening deflected• Thickenedof by reflex arteriole arteriole (yellow) can impinge• Resolves upon the in around retinal• 6Usuallyveins, weeks appears within 3 disc diameters of the ONH normal in elderly) or Hypertension is a chronic medical condition in which arterial blood pressure is elevatedIt affects. It affectsover 1 billion over people 1 billion worldwide, people increasing worldwide, in prevalence increasing with inage. prevalence with age. It is onefor ofhypertensive the most• retinopathyDisruption important of isaxoplasmic detailed preventable flow •belowDisplaces manifests (Wong asretinalrisk &a greyMitchell, -structures, New England takes longer JournalIsolated to resolve of systolic Medicine, 2004;•≥140 351Disruption (22): 2310-7.Stage<90 of axoplasmic 2 Stage flow 1 manifests160-179 as a100 grey-140109- -159 90-99 Isolated systolic ≥140 <90 • Changes startleading off to potential (moreas “copper “silver” vein occlusions wiring”within• Bonnet (below) the (slight vessel) sign: broadening (Veinbottom banked) (courseof changed) (blue) leading to potentialwhite lesion vein along occlusions the Dot/blotRNFL bundles (below)haemorrhage • Typically resolves inhypertension 5-7 weeks (may be white lesion along the RNFL bundles or hypertension (may be factors for premature death, as it increases the risk of ischaemic heart disease, stroke, peripheral vascularChair disease,- otherside cardiovascular Reference:light reflex) disease• Salus’s (top sign:• )and May Vein benephropathydeflected more byusefulHypertension arteriole• Gunn to . quantify (yellow) Gradingsign: 90 broadening degree schemes vein banked available and tapered• Usuallyfor hypertensive (black)appears within 3 disc retinopathy diameters of the ONH • May have resultantnormal microvascular in elderly) infarcts with lossor • Bonnet sign: Vein banked (course changed) (blue) • Salus’s sign: VeinB deflected by• Originatearteriole (yellow)from deep capillary bed (INL, ONL, or OPL) Requires emergency referral to the patient’s Cotton wool spots (Moderate retinopathy) normal in elderly) (Mitchell-Wong SchemeHypertension used below is: aWong chronic & medicalMitchell, condition New England in which Journal arterial ofblood Medicine, pressure 2004is elevated;351(.22Chair It ):affects2310 -7over), but 1- billion siderecent people evidence •Reference: worldwide,“Silver suggests wiring” increasing only•representsCan a bein modest focalprevalence greater orHypertension generalised association• Note: broadening with arterial age . between Ittortuosity ofis reflexone ofis retinopathy notthe typically most important •expected Typicallyand systemic resolvesdue preventable to in 5- 7organ weeks risk damage . of retinal tissue and visual field changes • Usually appearsStage 3 (hypertensivewithin 3 disc diameters≥180 of the ONH≥110 or Chair-side Reference:• Gunn sign: 90 degree vein bankedHypertension and tapered (black) • Bonnet sign: • MayVein have banked resultant (coursemicrovascular• Displaces changed) infarcts retinal with (blue) loss structures, takes longer to resolve emergency) Stage 2 general practitioneror 160 and/or-179 local hospital,100- 109 factors for premature death, as it increases the risk of ischaemic heart disease, stroke, peripheral vascular disease, other cardiovascular• Note: disease arterial tortuosityand nephropathy is not typicallystiffening,bottom .expected Grading but due banking schemesto may available cause venous for hypertensive tortuosity retinopathy Requires emergency referral• Typically to the patient’s resolves in 5-7 weeks Hypertension is a chronic medical condition in which arterial blood pressure is elevated. It affects(more over “silver” 1 billion withinA/V people “nicking” the worldwide, vessel) (US) or “nipping”( increasing )(UK) in (B) prevalence with age. It ofis retinalone oftissue the and most visual important •fieldDue changes to ischaemia preventable of the risk RNFL whichever can provide the most urgent care (Mitchell-Wong Scheme used below: Wong & Mitchell, New England Journal of Medicine, 2004;351(22):2310-7), but recent evidence suggestsstiffening, but only banking a modest may cause association venous tortuosity Categorybetween retinopathy• ofGunn sign: and 90 systemic degreeSystolic organvein banked, damage Diastolic, and. tapered (black) general practitioner and/or• May local hospital, have resultant microvascular infarcts with loss LESIONSfactorsHypertension forOF premature isHYPERTENSIVE a chronic death, medical as it increases condition the in riskwhich RETINOPATHY ofLesions ischaemicarterial blood heart of pressure hypertensivedisease, isstroke, elevated peripheral. Itretinopathy• affectsMay vascular beover more 1disease, billion useful• Thickened otherpeople to cardiovascularquantify worldwide, arteriole broadening can increasing disease impinge and uponin prevalencenephropathy the retinal with veins,. Grading Bage . It schemes is one of available the mostSequelae for important• hypertensiveDisruption of preventable ofhypertension retinopathy axoplasmic risk flow manifests in the aswhichever eyea grey- can provide the most urgent careIsolated systolic ≥140 <90 Requires emergency referral to the patient’s Hypertension is a chronic medical condition in which arterial blood pressure is elevated. It affects over 1 billion peopleleading worldwide,to potential veinincreasing occlusions hypertensionin prevalence (below)• Note: with age arterial. It is one tortuosity ofmmHg the most is not important typicallymmHg preventable expected Cotton risk due wool to spots (Moderate retinopathy) factors(Mitchell for-Wong premature Scheme death, used as below it increases: Wong the& Mitchell, risk of ischaemic New England heart Journal disease, of stroke,Medicine, peripheral 2004• ;Can351 vascular( be22): focal2310 disease,-7 or), butgeneralised other recent cardiovascular evidence suggests disease onlyCategory and a nephropathymodest of association. Grading between schemesSystolic retinopathy available, Diastolic, forand hypertensive systemicwhite lesion organ alongretinopathy damage the RNFL. bundles of retinal tissuehypertension and Stagevisual (may be 3field (hypertensive changes ≥180 ≥110 general practitioner and/or local hospital, factors forLESIONS premature death, OF as HYPERTENSIVEit increases the risk of ischaemic RETINOPATHY heart disease, stroke, peripheral vascular disease, other cardiovascular disease and nephropathy. Grading schemes available for hypertensiveSEQUELAE retinopathy OF HYPERTENSION IN THE EYE (Mitchell-Wong Scheme usedVascular below: Wong calibre & Mitchell, changes New England Journal of Medicine, 2004Retinal;351(22 haemorrhages):2310-7),• butSalus’s recent sign: evidence Vein deflected suggests by only arteriole a modest (yellow) associationstiffening, SEQUELAE between but bankingOF retinopathy HYPERTENSION may cause and• systemicUsually venous IN appears organ THE tortuosity damage withinEYE 3 . disc diameters of the ONH normal in elderly)emergency) or Vascular calibre changes (Mild retinopathy)(Mitchell-Wong Scheme used below: Wong & Mitchell, NewRetinal England haemorrhagesJournal of Medicine, (Moderate 2004;351(22): retinopathy)2310-7), but recent evidence suggests onlyhypertension a modest association Hard between exudatesmmHg retinopathy and macularmmHgand systemic oedema organ damage . Optic neuropathy ‘hypertensive or whichever can provide the most urgent care (Mild retinopathy)LESIONS OF HYPERTENSIVE (ModerateA/V RETINOPATHY “nicking” retinopathy) (US)• orBonnet “nipping” sign: Vein (UK) banked (B) (course changed)Hard (blue) exudates andCategory macular of oedema (ModerateTypicallySystolic retinopathy), resolvesDiastolic, in 5-7 weeks Optic neuropathy “hypertensive papillopathy” (Malignant retinopathy) Vascular calibre changes (Mild retinopathy) Retinal haemorrhages (Moderate retinopathy)Hard exudates and macular oedemaNormal (Moderate retinopathy)(ModerateCategory retinopathy) of90 -119 • Due• Systolic to 60ischaemiaOptic, -79 neuropathy Diastolic, of the “hypertensive papillopathy’ RNFL papillopathy (malignant” (Malignant retinopathy) retinopathy) LESIONS OF HYPERTENSIVE RETINOPATHYThickened arteriole• Gunn can sign: impinge 90 degree upon vein thebanked retinal and taperedveins, (black) Categoryhypertension of Systolic• MaymmHg have, resultantDiastolic,mmHg microvascular infarcts with loss • Thickening and loss of elasticity of the arterial wall FlameLESIONS haemorrhage OF HYPERTENSIVE • RETINOPATHY Normal hypertension90-119 •and60Disruption-79mmHg of axoplasmicmmHg flow manifests as a grey- Requires emergencyIsolated systolic referral to the patient’s≥140 <90 A Vascular• Thickening calibre and changes loss of elasticity (Mild of retinopathy) the arterial wall Flame haemorrhageRetinal• Compromised haemorrhages• Note: vessels arterial in (Moderate the tortuosity macula• Compromised leak retinopathy) islipids not (hard typically vessels expected in the maculadue tohypertension leak lipids (hard • InmmHg acuteof retinal hypertension, tissuemmHg vasoconstriction and visual field and changes choroidal ischaemia• In acute results hypertension, in optic vasoconstriction and choroidal ischaemia results in optic • Thickening and loss of elasticity of the arterial wall Vascular calibre changes (Mild retinopathy)Flame haemorrhage leadingRetinal to potential haemorrhages vein occlusions (Moderate retinopathy)(below) • CompromisedNormal vessels in the maculaand white90-119 lesion along60 the-79 RNFL bundles SEQUELAE OF HYPERTENSIONgeneral hypertensionpractitioner and/or (may local IN be hospital, THE EYE • Broadening of light reflex masking the blood vessel Vascular• Broadening calibreA of light changes reflex• maskingOriginate (Mild the retinopathy) blood from vessel column,superficial capillary• Originates bed or from radial superficialRetinalexudates; haemorrhagescapillary hyperstiffening, -reflective (Moderate but on banking OCT,exudates; red retinopathy) mayarrow) cause from hyper thevenous - reflectivedeep tortuosity on OCT, red arrow) from the deep neuropathy and oedema (blue• arrow)In severe as aacute result hypertension, of axoplasmicneuropathy opticflow stasis,neuropathy due and to oedema (blue arrow) as a result of axoplasmic flow stasis, due to • Broadening of light reflex masking• theThickening blood vessel and loss ofrepresents elasticity chronic of the arterial arterial changes wall • Originate from superficial capillaryFlame• haemorrhageSalus’s bed or sign: radialcapillary Vein bed, deflected depositing in by the arterioleOPL. Deposition (yellow) withinHigh normalleak lipids (hardNormal exudates; 120 hyper-reflective-139 the lack90- of119 autoregulation80 -and89 of60 choroidal-79and oedema vasculature (blue (thisarrow) is because results thefrom ONH blood whichevernormal can provide in elderly) the most urgent care column, represents chronic arterial changes parapapillary capillariesA bed or radial parapapillary capillaries capillary bed, depositing in the OPL.Normal Deposition within • Usually90-119 appears60 within-79 3 disc diameters ofthe the lack ONH of autoregulation of choroidal vasculature (this is because the ONH blood or • Thickening and loss of elasticity of the arterial wall Flame haemorrhageHenle’s fibre layer forms a “macular star” High normal on OCT, red arrow120) from-139 theHard deep exudatescapillary80supply -89 isand through macularand the short posterioroedemavasoconstriction ciliary (Moderate arteries) and poor retinopathy) choroidal Optic neuropathy “hypertensive papillopathy” (Malignant retinopathy) column, represents chronic arterial• •changesBroadeningThickening ofand light loss reflex of elasticity masking of the the blood arterial vessel wall parapapillary capillaries • Flame•AppearanceOriginate• haemorrhageBonnet due from to RNFL sign: superficial orientation Vein bankedcapillary (coursebed or radial changed) (blue) and Copper vs. silver wiring (A) A • Appear white-yellow waxy, with a glitterHenle’s due fibre to cholesterin(prehypertension) layer forms a “macularbed, depositing Highstar ”in normal the OPL. Deposition•• orInTypically the 120 chronic-139 phase,resolves the oedema 80in- 589- 7 resolves, weeks leaving ONH pallor/atrophysupply is through the short posterior ciliary arteries) • column,Broadening represents of light reflexchronic masking arterial the changes• bloodAppearance vessel dueA to RNFL orientation• parapapillaryOriginate from capillaries superficial capillary bed or radial (prehypertension) or autoregulation leading to choroidal ischaemia Copper vs. silver wiring (A) • Broadening of light reflex masking the blood vessel• Appearance due to RNFL orientation• •TypicallyOriginate• resolvesGunn from insign: around• superficialLeakage 90 six degree weeks also capillary produces vein macularbed banked or •oedema radialAppear and (hyporeflective tapered white-yellow (black) on waxy, within with Henle’sa glitterHigh fibre due normal layer to formscholesterinSEQUELAE a • Strongly120 OF associated-139 HYPERTENSION with hypertensive80-89 emergency IN(BP: systolic THE• In ≥ 180the EYE orchronic diastolic phase, the oedema resolves, leaving ONH pallor/atrophy Copper vs. silver wiring (A) column, represents • chronic Changes arterial start off aschanges ‘copper wiring’ parapapillary capillaries High(prehypertension) normal • May120-139 have resultantor 80-89 microvascular and axoplasmic flow infarcts stasis. This with is because loss column, represents chronic arterial changes• Resolves in around 6 weeks Dot/blot• parapapillaryAppearance haemorrhage duecapillariesOCT, to RNFLyellow orientationarrow) ‘macular star’ ≥110, and should be managed as such) Requires emergency referral to the patient’s Copper vs. silver wiring (A)(slight broadening of light reflex) (top) • Resolves in around 6 weeks • Note: arterial tortuosity is not typically• Leakage expected alsoStage produces due1 • macular toCompromised oedema(prehypertension) (hyporeflective vessels140 in-159 the on macula leak90- 99lipidsor (hardthe ONH blood supply is •throughStrongly the short associated with • In (BP: acute systolic hypertension, ≥180 or diastolic vasoconstriction and choroidal ischaemia results in optic • Changes start off as •“copperChanges wiring” start off (slight as “copper broadening wiring” (slight of broadening of • ResolvesAppearance in around due to 6RNFL weeks orientation Hard exudatesStage and 1 macular oedema(prehypertension) (Moderate140-159 retinopathy) 90of- 99retinal or tissue and visual field changesOptic neuropathy “hypertensive papillopathy” (Malignant retinopathy) Copper vs. silver wiring (A)‘Silver wiring’, representsDot/blot greater broadening haemorrhageDot/blot of haemorrhage • •OriginatesAppearance from deep due capillary to RNFL bed orientation OCT, yellow arrow) • exudates;Appears white-yellowStage hyper 1 - waxy,reflective with a on OCT,140 red-159 arrow) from90-99posterior the deep ciliary arteries ≥110, and should be managed as such) generalneuropathy practitioner and oedema and/or (blue local arrow) hospital, as a result of axoplasmic flow stasis, due to • CopperChanges vs. start silver off wiring as “copper (A) wiring” (slight broadening of • Resolvesstiffening, in around but 6 weeksbanking may causeVascular venous occlusions/macroaneurysms tortuosity or or Choroidopathy (rare; follows acute hypertensive crisis: systolic >180 mmHg) light reflex) (top) light reflex) (top) reflex (more ‘silver’ within the vessel) (bottom) •Dot/blot(INL,Resolves ONL, orhaemorrhage OPL)in around 6 weeks glitter due toStage cholesterol 1 140-159 or 90-99 • lightChangesChanges reflex) start start (top off off) as as “copper “copper wiring” wiring” (slight (slight broadening broadening• Originate ofof from deep capillary bed (INL, ONL, or OPL)• Compromised vessels in the macula leak lipidscapillary (hard Stage bed, 1 depositing in the140 OPL.-159 Deposition 90- 99within• In• theIn chronicacute hypertension, phase, the oedema vasoconstriction resolves, and choroidal ischaemia resultswhicheverthe in optic lack of can autoregulation provide the most of choroidal urgent care vasculature (this is because the ONH blood • • Originate from deep capillary bedDot/blot (INL, ONL, haemorrhage or OPL) • “Silver wiring” represents greater broadening of reflex • May be more useful to quantify broadening • Dot/blot•DisplacesOriginate retinalhaemorrhage from structures,Vascular deep takes occlusionscapillary (right) bed (INL, ONL, or OPL) Macroaneurysm (right) Elschnig spots (right)or leavingSiegrist ONH streaks pallor/atrophy (right) • “Silver wiring” represents greater broadening of reflex• “Silverlight reflex) wiring” (top represents) greater broadening of reflex exudates; hyper-reflective on OCT,Stage red 2 arrow)• fromLeakage Vascularthe also deep produces occlusions/macroaneurysms160- 179macular oedema100 -109 or neuropathy and oedema (blue arrow)Choroidopathy as a result of(rare; axoplasmic follows flowacute stasis, hypertensive due to crisis: systolic >180 mmHg) light reflex) (top) • Displaces retinal structures,•longer takesOriginate to resolvelonger from to• deep Venous:resolve capillary due to impingement bed (INL, ONL, or OPL) Stage• A localised 2 dilatationHenle’s of fibre aStage layer 2 160forms-179 a “macular • Changes160100 in- 179star RPE-109 due” to 100-109 • Linear hyperpigmented supply is through the short posterior ciliary arteries) (more “silver” within the vessel) (bottom) • Can be focal or generalised• Displaces retinal structures, takes•• longerOriginateDisplaces to fromretinal resolve deep structures, capillary takesbed (INL, longer ONL, to orresolve OPL) (hyporeflective on OCT, yellow arrow) • Strongly associated with hypertensive Images unavailable, though “Silver wiring” represents greater broadening of reflex (more “silver” within the vessel) (bottom) • •(more“Silver “silver” wiring” within represents the vessel) greater (bottom broadening) of reflex by thickenedcapillary artery, bed, depositing in the OPL. retinalDeposition arteriole within (saccular Stage 2 choriocapillaris160-179 infarcts 100-109 thestreaks lack of over autoregulation choroidal of choroidal vasculature (this is because the ONH blood •• DisplacesDisplaces retinalretinal structures, structures, takes takes longer longer toVascular to resolve resolve occlusions (right)• AppearStage white 2 -SEQUELAEyellow waxy,Macroaneurysm with160 aOF- 179glitter (right) HYPERTENSION due 100 to-109 cholesterin emergency (BP: systolic IN ≥ Elschnig180 THE or diastolic spotsnote EYE (right) that the presence of Siegrist streaks• In (right)the chronic phase, the oedema resolves, leaving ONH pallor/atrophy • May be more useful to quantify broadening• May(more(more be “silver” “silver” more usefulwithin within to the the quantify vessel) vessel) broadening( bottom(bottom)) intraretinallyHenle’s (branch fibre layer forms a “macular appearance)star” • Appear as small, black supplyarteries is through the short posteriorthese are ciliary typically arteries) • May be more useful to quantify broadening A/V ‘nicking’B (US) or ‘nipping’ (UK) (B) B Cotton wool spotsCotton (Moderate wool retinopathy) spots • Venous: due to impingement• Leakage also produces• macularA localised oedema dilatation (hyporeflective of a ≥ 110, and on should be managed• Changes as such) in RPE due to • Linear hyperpigmented• Strongly associated with hypertensive emergency (BP: systolic ≥180 or diastolic • Can be focal or generalised • •CanMayMay be be be focal more moreB or useful usefulgeneralised to to quantify quantify broadening broadening (Moderate retinopathy)Cottonocclusion) wool• orAppear spotsposterior white(Moderate to -yellow retinopathy) waxy, withStage a• glitterGradual 3 (hypertensive due leakage to cholesterin of vessels Stage ≥180 3 (hypertensive atrophic≥110≥180 spots, surrounded ≥110• In• theIndicative chronic of fibrinoid phase, the oedemaaccompanied resolves, by leaving systemic ONH pallor/atrophy Images unavailable, though • Thickened arteriole can impinge upon the CottonB wool spots (Moderate retinopathy)lamina (central Hard occlusion) exudates by and thickened macularStage artery, oedema 3 (hypertensive (Moderate retinopathy)≥180 ≥110 necrosis, which thenOptic leads neuropathy “hypertensive papillopathystreaks over choroidal” (Malignant retinopathy) • Can be focal or generalised B CottonCotton wool wool spots spots (Moderate (Moderate retinopathy) retinopathy) compromisesOCT, vision yellow Stage arrow) 3 (hypertensive retinal byarteriole yellow≥180 haloes (saccular ≥110 choriocapillarissymptoms infarcts and signs ≥110, and should benote managed that the aspresence such) of • •CanCan be be focal focal or or generalised generalisedunderlying retinal veins, leading to potential • Leakage also produces macularemergency) oedema (hyporeflective Stage onemergency) 3 (hypertensive or ≥180 or ≥110 • Strongly associated with hypertensive emergency (BP: systolic ≥180 or diastolic • Check for causative artery intraretinally (branch• Appears as deep red • Accelerated hypertension to fibrinous exudation arteries A/V “nicking” (US) or “nipping” (UK) (B)A/V “nicking” (US) or “nipping” (UK) (B) • Ischaemia of the RNFL results in emergency) emergency) appearance) • Appear as small, black these are typically vein occlusions (below) • Due to ischaemia of the RNFL• Due to ischaemia of the OCT,RNFL yellow arrow) haemorrhage +/-exudatesemergency) orcauses choroidalor ischaemiaor ≥110, and should be managed as such) A/V “nicking” (US) or “nipping” (UK) (B) •A/VA/VThickened “nicking” “nicking” arteriole(US) (US) or or “nipping” “nipping”can impinge (UK) (UK) upon (B) (B) the retinal veins, •disruptionDue• toCompromised of ischaemia axoplasmic flow of thewhich vessels RNFL in the maculaocclusion) leak lipids or posterior (hard to • Gradual leakage of vessels • In acute hypertension,atrophic vasoconstrictionspots, surrounded and choroidal• Indicative ischaemia of fibrinoid results in optic • Thickened arteriole can impinge upon the retinal veins,• Salus’s sign: Vein deflected• Due by arteriole to ischaemia• (yellowDisruption) of of the axoplasmic RNFL flow•• DueDisruption manifests to ischaemia of as axoplasmic a ofgrey the- RNFL flow manifests as a grey- Isolated systolic Isolated≥140 systolic <90≥140 <90 accompanied by systemic • •leadingThickenedThickened to potentialarteriole arteriole canvein can impinge occlusionsimpinge upon upon (below) the the retinal retinal veins,veins, •manifestsDisruption as a grey-white of axoplasmic lesion flow manifests aslamina a grey -(central occlusion) IsolatedhypertensionIsolated systolic systolic (may compromises be ≥140Vascular≥140 vision occlusions/macroaneurysms<90 <90 Choroidopathy by yellow haloes necrosis, which then leadsChoroidopathy symptoms (rare; and signs follows acute hypertensive crisis: systolic >180 mmHg) • Thickened arteriole canleading impinge to potential upon the vein retinal occlusions veins, (below) • Bonnet sign: Vein banked• Disruption white of axoplasmic lesion along flow the RNFL manifests•along bundlesDisruptionwhite RNFLexudates; lesion asbundles aof grey alongaxoplasmic hyper- the RNFL- reflectiveflow bundles manifests on OCT,as a grey red- arrow)hypertensionIsolatedVascular from occlusions/macroaneurysms thesystolic (may deepVascular be occlusions/macroaneurysms≥140 <90 (Rare;neuropathy followsChoroidopathy acute and hypertensiveoedema (rare; (blue follows crisis: arrow) acute hypertensiveas a result ofcrisis: axoplasmic systolic >180 flow mmHg) stasis, due to • Salus’sleadingleading sign: to to potential potential Vein deflected vein vein occlusions occlusions by arteriole (below) (below) (yellow) white lesion along the RNFL bundles • Check for causative artery hypertensionhypertension (may (may• beAppears be as deep red • Accelerated hypertension to fibrinous exudation leading to potential •veinSalus’s occlusions sign: Vein (below) deflected by arteriole (yellow) (course changed) (blue) • Usually appears within 3 disc• •Usuallywhite Usuallydiameters appearscapillary lesion appears within ofalong the3bed, discwithin the ONH diameters depositing RNFL 3 disc bundles diameters in the ofOPL. the DepositionONH normalhypertension within in elderly)Vascular (may occlusionsnormal be in (right)elderly)or or Macroaneurysmsystolicthe lack ≥ 180 of mmHg)autoregulation (right) of choroidal vasculature (thisElschnig is because spots the (right) ONH blood Siegrist streaks (right) • •BonnetSalus’sSalus’s sign:sign: sign: Vein Vein Vein deflected bankeddeflected (course by by arteriole arteriole changed) (yellow) (yellow)white (blue) lesion along the RNFL bundles•of theUsually ONH appears withinVascular 3 disc diameters occlusions of(right) the ONH Macroaneurysmnormalnormal in inelderly) elderly) (right) haemorrhage +/-exudatesor or Elschnig spots (right) causes choroidalSiegrist ischaemia streaks (right) • Bonnet sign: Vein banked (course changed) (blue) • Gunn sign: 90 degree vein banked • Typically resolves in 5-7 weeks•• UsuallyTypically Henle’s appears resolves fibre within in layer5- 73 weeksdisc forms diameters a “macular of the ONH star ” supply is through the short posterior ciliary arteries) • Salus’s sign: Vein deflected by arteriole (yellow) • •BonnetBonnet sign: sign: Vein Vein banked bankedand tapered (course (course (black changed) changed)) (blue)(blue) • Typically resolves in 5–7 weeks • Venous: due to impingement normal in• elderly)VascularVenous:• occlusions A due localised to (right)impingement dilatation of a Elschnig• •ChangesA spots localised in RPE duedilatation to of a • Linear hyperpigmented • Changes in RPE due to • Linear hyperpigmented • Gunn sign: 90 degree vein banked •andGunn tapered sign: 90 (black) degree vein banked and• taperedUsually (black) appears within 3 disc diameters•• TypicallyMayTypically have of resolvesresolvesthe resultant ONH in in 5 microvascular5 -7-7 weeks weeks infarcts with loss or Images Images unavailable, though Images unavailable, though • Gunn sign: 90 degree vein banked and tapered (black)• May have resultant microvascular• Appear infarcts whitewith loss-yellow by thickened waxy, withartery, a glitter due to cholesterin retinalRequires arteriole emergency (saccular referral to the patient’s •choriocapillarisIn the chronic infarcts phase, the oedemastreaks unavailable,resolves, over choroidal leaving ONH pallor/atrophy • Bonnet sign: Vein banked (course changed) (blue) • •Note:Gunn arterial sign: 90 tortuosity degree• Note: vein is arterialnot banked typically tortuosity and expectedtaperedis not expected (black) due to • ••MayMayofMay result retinal havehave in loss tissue resultantresultant of retinal and tissue microvascular microvascularvisual field changes infarcts infarcts with with loss loss Requires emergency• byVenous: thickened due toreferral impingement artery, to the by patient’s • Changesretinal in RPE arterioledue to choriocapillaris (saccular infarcts choriocapillarisnote that the presence infarcts of streaks over choroidal note that the presence of • Note: arterial tortuosity is not typically expected due to • Typically resolves in 5-7 weeks and visual field changes intraretinally (branch RequiresRequiresgeneral emergency emergencypractitioner referral referral and/or to tolocalthe the patient’s hospital, patient’s arteriesthough note • •stiffening,Note:Note: arterial arterial but tortuosity bankingtortuositydue may is tois not stiffening,not cause typically typically venous but banking expected expected tortuosity may cause duedue to toof retinal tissue and visual fieldofof • retinalretinalchangesLeakage tissuetissue alsoand and visual producesvisual field field changes macularchanges oedema (hyporeflectiveintraretinally thickenedon appearance) artery, intraretinally(branch (branch • •AppearStrongly as small, associated black with hypertensive emergency (BP: systolicthese ≥ 180are typically or diastolic arteries • Gunn sign: 90 degree vein banked and tapered (black) venous tortuosity general practitioner and/orgeneralgeneral practitionerlocal practitioner hospital, and/or and/or local local hospital, hospital, • Appearappearance) as small, black atrophic spots, that the • Appear as small, black these are typically stiffening, but banking may cause venousstiffening,stiffening, tortuosity but but banking banking may may cause cause venous venous• May tortuosity tortuosity have resultant microvascular infarctsOCT, with yellow loss arrow) occlusion) or posterior to occlusion)• Gradual or posteriorwhichever leakage to lamina canof vessels provide the most urgent care atrophic≥110, spots, and should surrounded be managed• Indicativeas such)presence of fibrinoid accompanied by systemic whicheverRequiresocclusion) can emergency provide or whicheverthe posterior referral most urgentcan toto provide the care patient’sthe most urgent care surrounded• Gradual by yellow leakage haloes of vessels atrophic spots, surrounded • Indicative of fibrinoid • Note: arterial tortuosity is not typically expected due to of retinal tissue and visual field changes lamina (central occlusion) (central occlusion)compromiseswhichever visioncan provide the most urgent care by yellow haloes necrosis,of these which then leads symptoms and signs accompanied by systemic • Accelerated hypertension causes choroidal are typically • Check for causative artery general• laminaMay practitioner be• associated (centralAppears withas and/orocclusion) deep macula red oedemalocal hospital, • Acceleratedcompromises hypertension vision to fibrinous exudation by yellow haloes necrosis, which then leads symptoms and signs stiffening, but banking may cause venous tortuosity Heart Foundation Classification (adults) SEQUELAE OFSystolic, HYPERTENSION mmHg Diastolic, IN mmHgVascular THE EYE occlusions/macroaneurysms ischaemia Choroidopathy (rare; accompaniedfollows acute hypertensive crisis: systolic >180 mmHg) • Check forhaemorrhage causative +/ artery-exudates causes choroidal ischaemia by systemic to fibrinous exudation SEQUELAE OF HYPERTENSIONSEQUELAE OFOF HYPERTENSIONHYPERTENSIONIN THE EYE IN IN THE THE EYE EYE whicheverMacroaneurysm can provide (right) the most urgent care Siegrist• Appears streaks as deep red • Accelerated hypertension Optimal < 120 and < 80 symptoms Hard exudates and macular oedema (Moderate retinopathy) Optic neuropathy “hypertensive• A localised papillopathy dilatation ”of (Malignant a retinal retinopathy) haemorrhage +/-exudates causes choroidal ischaemia HardHard exudates exudates and and macular macular oedemaoedema (Moderate(Moderate retinopathy) Vascular occlusions (right) OpticOptic neuropathy neuropathy “hypertensive “hypertensiveMacroaneurysm papillopathy papillopathy ”(right) (Malignant” (Malignant retinopathy) retinopathy) • LinearElschnig hyper-pigmented spots (right) streaks over choroidal andSiegrist signs streaks (right) Hard exudates and macular oedema (Moderate retinopathy) 120–129Optic neuropathyor “hypertensive80–84 papillopathy” (Malignantarteriole (saccularretinopathy) appearance) Normal • Venous: due to impingement • A localised dilatation of a arteries• Changes in RPE due to • Linear hyperpigmented • Compromised vesselsSEQUELAE in the macula leak lipids OF (hard HYPERTENSION IN THE EYE• In acute hypertension, vasoconstriction and• Gradual choroidal leakage ischaemia of vessels results in optic Images unavailable, though • •CompromisedCompromised vessels vesselsHigh in innormal the the macula macula leak leak lipids lipids (hard(hard by thickened130–139 artery,•• InorIn acute acute hypertension, hypertension,85–89 vasoconstriction vasoconstriction and and choroidal choroidal ischaemia ischaemia results results in opticin optic • Indicative of fibrinoid necrosis, which then streaks over choroidal • Compromised vessels in the macula leakexudates; lipids hyper (hard-reflective on OCT, red arrow) from the deep • In acute hypertension, vasoconstrictionneuropathy and and oedema choroidal (blue ischaemia arrow) as aresults retinalresultcompromises ofin arteriole axoplasmicoptic vision (saccular flow stasis, due to leads choriocapillaristo fibrinous exudation infarcts note that the presence of exudates;exudates; hyper hyper-reflective-reflectiveGrade 1 (mild)on on OCT, OCT, red red arrow) arrow) fromfrom thethe deepdeep 140–159 neuropathyorneuropathy90–99 and and oedema oedema (blue (blue arrow) arrow) as as a resulta result of of axoplasmic axoplasmic flow flow stasis, stasis, due due to to Hardexudates; exudates hyper and-reflective macular on oedemaOCT, redcapillary arrow) (Moderate bed, from depositing the retinopathy) deep in the OPL. Deposition within neuropathyintraretinallyOptic and neuropathy oedema (branch (bluethe “hypertensive lackarrow) of autoregulation as a result papillopathy of ofaxoplasmic choroidal ” vasculatureflow (Malignant• appearance)Appears stasis, as(this due deep retinopathy)is to redbecause the ONH blood • Appear as small, black arteries these are typically capillarycapillary bed, bed, depositing depositing in in the the OPL. OPL. Deposition Deposition withinwithin thethe lack lack of of autoregulation autoregulation of of choroidal choroidal vasculature vasculature (this (this is becauseis because the the ONH ONH blood blood Henle’s fibre layer formsGrade 2a (moderate) “macular star” occlusion)160–179 or posteriororsupply to is through100–109 the short posterior ciliary• Gradual haemorrhagearteries) leakage +/-exudates of vessels atrophic spots, surrounded • Indicative of fibrinoid capillary bed, depositing in the OPL. DepositionHenle’s fibre within layer forms a “macular star” the lack of autoregulation supplyof choroidal is through vasculature the short posterior(this is because ciliary arteries) the ONH blood accompanied by systemic • Henle’sAppear whitefibre layer-yellow forms waxy, a “macular with a glitter star” due to cholesterin lamina (central •occlusion)Insupply the chronic is through phase, the theshort oedema posterior resolves, ciliary leavingarteries) ONH pallor/atrophy necrosis, which then leads • Compromised vessels inHenle’s the macula fibre layer leak forms lipids a “macular (hard • starAppear” white-yellowGrade waxy, 3 (severe) with a glitter due to cholesterin • In acutesupply hypertension, is through the vasoconstriction short• In posterior the chronic ciliary andphase, arteries)choroidal the oedema ischaemia resolves, leavingcompromises results ONH in pallor/atrophy optic vision by yellow haloes symptoms and signs • LeakageAppear white also produces-yellowRequires waxy, macular emergency with oedema a glitter referral (toduehyporeflective the topatient’s cholesterin general on practitioner ≥ 180 • orStronglyIn the chronic associated≥ 110 phase, with the hypertensiveoedema resolves, emergency leaving (BP: ONH systolic pallor/atrophy ≥180 or diastolic Appear white-yellow waxy, with a glitter due to cholesterin In the •chronicCheck phase, for causative the oedema artery resolves, leaving ONH pallor/atrophy• Appears as deep red • Accelerated hypertension to fibrinous exudation exudates; hyper-reflective• on OCT, red arrow) from •the•LeakageOCT,Leakage deep yellow also also arrow) produces producesand/or macular macularlocal hospital, oedema oedema whichever ( (hyporeflectivehyporeflective can provide the most onon urgent care. neuropathy• and oedema (blue•• Strongly≥Strongly 110,arrow) and associated associated shouldas a result be with with managed hypertensiveof hypertensive axoplasmic as such) emergency emergency flow (BP:stasis, (BP: systolic systolic due ≥180 ≥to180 or ordiastolic diastolic • Leakage also produces macular oedemaOCT,OCT, ( yellowhyporeflective yellow arrow) arrow) on • Strongly associated with hypertensive≥≥110,110, and and should should emergency be be managed managed (BP: as systolic as such) such) ≥ 180haemorrhage or diastolic +/-exudates causes choroidal ischaemia capillary bed, depositing in the OPL. Deposition within Isolated systolic hypertension (may be normal in elderly) the lack of autoregulation≥ 140 of choroidalor 180 mmHg) VascularVascular occlusions/macroaneurysms occlusions/macroaneurysms ChoroidopathyChoroidopathy (rare; (rare; follows follows acute acute hypertensive hypertensive crisis: crisis: systolic systolic >180 >180 mmHg) mmHg) • Appear white-yellow waxy, with a glitter due to cholesterinVascular occlusions (right)Chair-side Reference HypertensionMacroaneurysm (right)• In the chronic phase, the oedemaElschnig resolves, spots (right) leaving ONH pallor/atrophySiegrist streaks (right) Chair-side Reference Hypertension VascularVascular occlusions/macroaneurysms occlusions (right) Macroaneurysm (right) ChoroidopathyElschnig (rare; spots follows (right) acute hypertensiveSiegrist crisis: streaks systolic (right) >180 mmHg) Vascular• Venous: occlusions due to impingement (right) Macroaneurysm• A localised dilatation (right) of a •ElschnigChanges spots in RPE(right) due to •SiegristLinear streaks hyperpigmented (right) • Leakage also produces macular oedema (hyporeflective• Venous: on due to impingement • A localised dilatation• Strongly of a associated with hypertensive• Changes in RPEemergency due to (BP: systolic• Linear ≥180 hyperpigmented or diastolic Images unavailable, though Vascular occlusions (right) • byVenous: thickened due toartery, impingement • Aretinal localised arteriole dilatation (saccular of a • choriocapillarisChanges inSiegrist RPE dueinfarcts streaks to (right) • streaksLinear hyperpigmented over choroidal ImagesImages unavailable, unavailable, though though OCT, yellow arrow) by thickened artery,Macroaneurysm (right) retinal arteriole (saccular≥110,Elschnig and should spots (right) be managed choriocapillaris as such) infarcts streaks over choroidal note that the presence of intraretinallyby thickened artery,(branch appearance)retinal arteriole (saccular • Appearchoriocapillaris as small, infarcts black streaksarteries over choroidal notenote that that the the presence presence of of • Venous: due to impingement intraretinally (branch• A localised dilatation of a appearance) • Changes in RPE due to • Appear as small,• Linear black hyperpigmented arteries Images unavailable, thoughthese are typically occlusion)intraretinally or posterior(branch to appearance) • Appear as small, black • arteriesIndicative of fibrinoid these are typically by thickened artery, occlusion) or posteriorretinal to arteriole (saccular • Gradual leakage of vesselschoriocapillaris infarcts atrophic spots,streaks surrounded over choroidal • Indicative of fibrinoid accompaniedthese are typically by systemic occlusion) or posterior to •• GradualGradual leakage of vessels atrophicatrophic spots, spots, surrounded surrounded • Indicative ofnote fibrinoid that the presenceaccompanied of by systemic intraretinallyVascular (branch occlusions/macroaneurysmslaminalamina (central (central occlusion) occlusion) compromises vision Choroidopathy (rare;by yellow follows haloesarteries acute hypertensivenecrosis,necrosis, crisis: which systolicwhich then then leads>180 leads mmHg) symptomsaccompanied and by signs systemic lamina (central occlusion)appearance) compromisescompromises vision • Appear as small, black byby yellow yellow haloes haloes necrosis, whichthese then are leads typically symptoms and signs • •CheckCheck for for causative causative artery artery • Appears as deep red • Accelerated hypertension toto fibrinous fibrinous exudation exudation symptoms and signs occlusion) or posterior to • Check for causative• arteryGradual leakage of vessels •• AppearsAppears as deep red atrophic spots, surrounded•• Accelerated Accelerated• hypertension hypertensionIndicative of fibrinoid to fibrinousaccompanied exudation by systemic Vascular occlusions (right) Macroaneurysm (right) haemorrhagehaemorrhage +/Elschnig-exudates spots (right) causescauses choroidal choroidalSiegrist ischaemia ischaemiastreaks (right) lamina (central occlusion) compromises vision haemorrhage +/-exudates by yellow haloes causes choroidalnecrosis, ischaemia which then leads symptoms and signs • Venous: due to impingement• Check for causative artery • A localised dilatation• Appears of as adeep red • Changes• Accelerated in RPE due hypertension to • Linearto fibrinous hyperpigmented exudation Images unavailable, though by thickened artery, retinal arteriolehaemorrhage (saccular +/-exudates choriocapillariscauses choroidal infarcts ischaemia streaks over choroidal note that the presence of intraretinally (branch appearance) • Appear as small, black arteries these are typically occlusion) or posterior to • Gradual leakage of vessels atrophic spots, surrounded • Indicative of fibrinoid accompanied by systemic lamina (central occlusion) compromises vision by yellow haloes necrosis, which then leads symptoms and signs • Check for causative artery • Appears as deep red • Accelerated hypertension to fibrinous exudation haemorrhage +/-exudates causes choroidal ischaemia Chair-side Reference: Hypertension

Hypertension is a chronic medicalChair condition-side in which arterialReference: blood pressure is elevated Hypertension. It affects over 1 billion people worldwide, increasing in prevalence with age. It is one of the most important preventable risk factors for premature death, as it increases the risk of ischaemic heart disease, stroke, peripheral vascular disease, other cardiovascular disease and nephropathy. Grading schemes available for hypertensive retinopathy Hypertension is a chronic(Mitchell medical condition-Wong Scheme in which usedarterial below blood: pressureWong & is Mitchell,elevated. ItNew affects England over 1 billionJournal people of Medicine, worldwide, 2004 increasing;351 (in22 prevalence):2310-7), with but age recent. It is evidenceone of the suggestsmost important only preventablea modest association risk between retinopathy and systemic organ damage. factors for premature death, as it increases the risk of ischaemic heart disease, stroke, peripheral vascular disease, other cardiovascular disease and nephropathy. Grading schemes available for hypertensive retinopathy (Mitchell-Wong Scheme used below: Wong & Mitchell, New England Journal of LESIONSMedicine, 2004;351 OF(22):2310 HYPERTENSIVE-7), but recent evidence suggests RETINOPATHY only a modest association between retinopathy and systemic organ damage. Category of Systolic, Diastolic, Chair-sideLESIONS Reference: OF HYPERTENSIVE Hypertension RETINOPATHY Category of Systolic, Diastolic, hypertension mmHg mmHg Vascular calibre changes (Mild retinopathy) Retinal haemorrhageshypertension (Moderate retinopathy)mmHg mmHg VascularChair calibre changesChair (Mild- retinopathy)side-side Reference: Reference:Retinal Hypertension haemorrhages Hypertension (Moderate retinopathy) Normal 90-119 60-79 Hypertension is a chronic medical condition in which arterial blood pressure is elevated. It affects over 1 billion people worldwide, increasing in prevalence with age. It is one of the most important preventable risk Normal 90-119 60-79 factors for premature death, as it increases the risk of ischaemic heart disease, stroke, peripheral vascular disease, other cardiovascular disease and nephropathy. Grading schemes available for hypertensive retinopathy and • Thickening and loss of •elasticityThickening of the arterial and loss wall of elasticity of the arterial wallFlame haemorrhage Flame haemorrhage and (Mitchell-Wong Scheme used below: Wong & Mitchell, New England Journal of Medicine, 2004;351(22):2310-7), butA recent evidence suggests only a modest associationA between retinopathy and systemic organ damage. Hypertension is aHypertension chronic medical is a chronic condition• Broadening medical in condition ofwhich light reflex arterialin• which Broadeningmasking bloodarterial the pressure bloodblood of light pressurevessel is reflex elevated is elevated masking. It. affectsIt theaffects blood overover vessel11 billion•billionOriginate people people from worldwide, worldwide,superficial increasing capillary increasing in bed prevalence or• radialinOriginate prevalence with age from. It with is superficialone age of .the It mostis capillary one important of thebed mostpreventable or radial important risk preventable risk factors for premature death,column, LESIONSas it represents increases OF the chronic HYPERTENSIVE risk of arterial ischaemic changes heart RETINOPATHY disease, stroke, peripheral vascular disease,parapapillary other cardiovascular capillariesCategory disease of and nephropathySystolic, . GradingDiastolic, schemes availableHigh for hypertensive normal retinopathy120 -139 80-89 High normal 120-139 80-89 factors for premature death, as it increases the risk of ischaemiccolumn, heart represents disease, stroke,chronic peripheral arterial changes vascular disease, other cardiovascularhypertension disease andmmHgparapapillary nephropathy mmHg capillaries. Grading schemes available for hypertensive retinopathy (Mitchell-Wong Scheme used below: Wong & Mitchell, New England Journal of Medicine, 2004;351(22):2310•-7),Appearance but recent evidencedue to RNFL suggests orientation only a modest association between retinopathy(prehypertension) and systemic organ damage. or (prehypertension) or (Mitchell-Wong Scheme usedVascular below calibreCopper :changes Wong vs.(Mild & silver Mitchell,retinopathy) wiring (A)New England Journal of Medicine,Retinal haemorrhages 2004; (Moderate351(22): retinopathy)2310-7), but recent evidence suggests only• Appearancea modest association due to RNFL between orientation retinopathy and systemic organ damage. Chair-side Reference Copper vs. silver wiring (A) • Resolves in aroundNormal 6 weeks 90-119 60Category-79 of Systolic, Diastolic, • Thickening and loss of elasticity •of theChanges arterial startwall off as “copperLESIONS wiring” OF (slightFlame HYPERTENSIVE broadening haemorrhage of RETINOPATHY • Resolvesand in around 6 weeks Stage 1 140-159 90-99 A• Changes start off as “copper wiring” (slight broadeningDot/blot haemorrhage of hypertensionCategory of mmHg mmHgSystolic , Diastolic, Stage 1 140-159 90-99 • Broadening of light reflex masking lightthe blood reflex) vesselLESIONS (top ) OF HYPERTENSIVE• Originate from superficial capillary RETINOPATHY bed or radial or Vascular calibre changes (Mild retinopathy) Retinal •haemorrhagesOriginate from (Moderate deep High capillary normal retinopathy) bed (INL, ONL,Dot/blot120- 139or OPL) haemorrhage 80-89 or column, represents chronic arterial• “Silver changes wiring” represents lightgreater reflex) broadening (topparapapillary) of reflex capillaries hypertension mmHg mmHg • Appearance due to RNFL orientation • Displaces retinal structures,(prehypertension) takes longer •to resolveOriginateor Normalfrom deep capillaryStage bed 902 (INL,-119 ONL, or60 OPL)-79160 -179 100-109 Copper vs. •silverVascularThickening wiring (A) calibre and loss changes (moreof elasticity “silver” (Mild of withinthe retinopathy) arterial the• vessel)“Silver wall (bottom wiring”) represents greaterFlame broadening haemorrhageRetinal of haemorrhagesreflex (Moderate retinopathy) and Hypertension • Resolves in around 6 weeks Stage 1 140-159 90-99 Stage 2 160-179 100-109 • Changes start off as “copper wiring” (slight broadening of • Displaces retinal structures, takes longer to resolve • May be more useful to quantify broadeningDot/blotA haemorrhage Normal 90-119 60-79 light reflex)• Broadening (top) of light reflex masking the blood vessel(more “silver” within the vessel)B• Originate(bottom from) superficial capillary bed or radial or • Thickening and loss of elasticity of the arterial wall • Originate from deep capillaryFlame bed haemorrhage (INL, ONL, or OPL) Cotton wool spots (Moderate retinopathy)High normal Stage 1203 (hypertensive-139 80-89≥180 and ≥110 • Can be focal or generalised • “Silver wiring”column, represents represents greater broadening chronic arterial of reflex changes May be more useful to quantify broadeningparapapillary capillaries • A • Displaces retinal structures, takes longer to resolve Stage 2 160-179 100-(prehypertension)109 • Broadening(more of “silver” light withinreflex the masking vessel) (bottom the) blood vessel • Originate• Appearance from due superficial to RNFL orientation capillaryB bed or radial emergency) or or Copper vs. silver wiringA/V (A)“nicking” (US) or “nipping” (UK) (B) Cotton wool spots (Moderate retinopathy) Stage 3 (hypertensive ≥180 ≥110 Chair-side Reference: Hypertension• May be more useful to quantify broadening • HypertensionCan be focal is one or of generalised the most important preventable risk factors• Due for to premature ischaemia death, of the as RNFL it increases the risk of ischaemic High normal 120-139 80-89 B • Resolves in around 6 weeks Hypertension is a chronic medicalcolumn, condition represents• Changes chronic start arterial off• asThickened “copper changes wiring” arteriole (slight can broadening impinge upon of the retinal veins,Cotton wool parapapillaryspots (Moderate retinopathy) capillaries Stage 3 (hypertensive ≥180 ≥110Stage 1 Isolated140 systolic-159 90-99≥140 <90 • Can be focal or generalised heart disease, stroke, peripheral vascular disease, other cardiovascular• Disruption of disease axoplasmic and nephropathy.flow manifests The as apresence grey- of emergency) or Dot/blot haemorrhage (prehypertension) or or in which arterial blood pressure is elevated.light reflex) (top) leading to potential veinA/V occlusions “nicking” (below) (US) or “nipping”• (UK)Appearance (B) due to RNFLwhite lesionorientation along emergency)the RNFL bundles • Due orto ischaemia of the RNFLhypertension (may be Copper vs.A/V silver “nicking” wiring (US) or(A) “nipping” (UK) (B) moderate hypertensive retinopathy correlates strongly with acute hypertension. The Mitchell-Wong classification scheme • Due to ischaemia of the RNFL• Originate from deep capillary bed (INL, ONL, or OPL) Chair-side Reference: Hypertension• Thickened• arteriole“Silver wiring”can impinge represents• uponSalus’s the retinalgreater sign: veins,Vein broadening deflected• Thickenedof by reflex arteriole arteriole (yellow) can impinge• Resolves upon the in around retinal• 6Usuallyveins, weeks appears within 3 disc diameters of the ONH normal in elderly) or Hypertension is a chronic medical condition in which arterial blood pressure is elevatedIt affects. It affectsover 1 billion over people 1 billion worldwide, people increasing worldwide, in prevalence increasing with inage. prevalence with age. It is onefor ofhypertensive the most• retinopathyDisruption important of isaxoplasmic detailed preventable flow •belowDisplaces manifests (Wong asretinalrisk &a greyMitchell, -structures, New England takes longer JournalIsolated to resolve of systolic Medicine, 2004;•≥140 351Disruption (22): 2310-7.Stage<90 of axoplasmic 2 Stage flow 1 manifests160-179 as a100 grey-140109- -159 90-99 Isolated systolic ≥140 <90 • Changes startleading off to potential (moreas “copper “silver” vein occlusions wiring”within• Bonnet (below) the (slight vessel) sign: broadening (Veinbottom banked) (courseof changed) (blue) leading to potentialwhite lesion vein along occlusions the Dot/blotRNFL bundles (below)haemorrhage • Typically resolves inhypertension 5-7 weeks (may be white lesion along the RNFL bundles or hypertension (may be factors for premature death, as it increases the risk of ischaemic heart disease, stroke, peripheral vascularChair disease,- otherside cardiovascular Reference:light reflex) disease• Salus’s (top sign:• )and May Vein benephropathydeflected more byusefulHypertension arteriole• Gunn to . quantify (yellow) Gradingsign: 90 broadening degree schemes vein banked available and tapered• Usuallyfor hypertensive (black)appears within 3 disc retinopathy diameters of the ONH • May have resultantnormal microvascular in elderly) infarcts with lossor • Bonnet sign: Vein banked (course changed) (blue) • Salus’s sign: VeinB deflected by• Originatearteriole (yellow)from deep capillary bed (INL, ONL, or OPL) Requires emergency referral to the patient’s Cotton wool spots (Moderate retinopathy) normal in elderly) (Mitchell-Wong SchemeHypertension used below is: aWong chronic & medicalMitchell, condition New England in which Journal arterial ofblood Medicine, pressure 2004is elevated;351(.22Chair It ):affects2310 -7over), but 1- billion siderecent people evidence •Reference: worldwide,“Silver suggests wiring” increasing only•representsCan a bein modest focalprevalence greater orHypertension generalised association• Note: broadening with arterial age . between Ittortuosity ofis reflexone ofis retinopathy notthe typically most important •expected Typicallyand systemic resolvesdue preventable to in 5- 7organ weeks risk damage . of retinal tissue and visual field changes • Usually appearsStage 3 (hypertensivewithin 3 disc diameters≥180 of the ONH≥110 or Chair-side Reference:• Gunn sign: 90 degree vein bankedHypertension and tapered (black) • Bonnet sign: • MayVein have banked resultant (coursemicrovascular• Displaces changed) infarcts retinal with (blue) loss structures, takes longer to resolve emergency) Stage 2 general practitioneror 160 and/or-179 local hospital,100- 109 factors for premature death, as it increases the risk of ischaemic heart disease, stroke, peripheral vascular disease, other cardiovascular• Note: disease arterial tortuosityand nephropathy is not typicallystiffening,bottom .expected Grading but due banking schemesto may available cause venous for hypertensive tortuosity retinopathy Requires emergency referral• Typically to the patient’s resolves in 5-7 weeks Hypertension is a chronic medical condition in which arterial blood pressure is elevated. It affects(more over “silver” 1 billion withinA/V people “nicking” the worldwide, vessel) (US) or “nipping”( increasing )(UK) in (B) prevalence with age. It ofis retinalone oftissue the and most visual important •fieldDue changes to ischaemia preventable of the risk RNFL whichever can provide the most urgent care (Mitchell-Wong Scheme used below: Wong & Mitchell, New England Journal of Medicine, 2004;351(22):2310-7), but recent evidence suggestsstiffening, but only banking a modest may cause association venous tortuosity Categorybetween retinopathy• ofGunn sign: and 90 systemic degreeSystolic organvein banked, damage Diastolic, and. tapered (black) general practitioner and/or• May local hospital, have resultant microvascular infarcts with loss LESIONSfactorsHypertension forOF premature isHYPERTENSIVE a chronic death, medical as it increases condition the in riskwhich RETINOPATHY ofLesions ischaemicarterial blood heart of pressure hypertensivedisease, isstroke, elevated peripheral. Itretinopathy• affectsMay vascular beover more 1disease, billion useful• Thickened otherpeople to cardiovascularquantify worldwide, arteriole broadening can increasing disease impinge and uponin prevalencenephropathy the retinal with veins,. Grading Bage . It schemes is one of available the mostSequelae for important• hypertensiveDisruption of preventable ofhypertension retinopathy axoplasmic risk flow manifests in the aswhichever eyea grey- can provide the most urgent careIsolated systolic ≥140 <90 Requires emergency referral to the patient’s Hypertension is a chronic medical condition in which arterial blood pressure is elevated. It affects over 1 billion peopleleading worldwide,to potential veinincreasing occlusions hypertensionin prevalence (below)• Note: with age arterial. It is one tortuosity ofmmHg the most is not important typicallymmHg preventable expected Cotton risk due wool to spots (Moderate retinopathy) factors(Mitchell for-Wong premature Scheme death, used as below it increases: Wong the& Mitchell, risk of ischaemic New England heart Journal disease, of stroke,Medicine, peripheral 2004• ;Can351 vascular( be22): focal2310 disease,-7 or), butgeneralised other recent cardiovascular evidence suggests disease onlyCategory and a nephropathymodest of association. Grading between schemesSystolic retinopathy available, Diastolic, forand hypertensive systemicwhite lesion organ alongretinopathy damage the RNFL. bundles of retinal tissuehypertension and Stagevisual (may be 3field (hypertensive changes ≥180 ≥110 general practitioner and/or local hospital, factors forLESIONS premature death, OF as HYPERTENSIVEit increases the risk of ischaemic RETINOPATHY heart disease, stroke, peripheral vascular disease, other cardiovascular disease and nephropathy. Grading schemes available for hypertensiveSEQUELAE retinopathy OF HYPERTENSION IN THE EYE (Mitchell-Wong Scheme usedVascular below: Wong calibre & Mitchell, changes New England Journal of Medicine, 2004Retinal;351(22 haemorrhages):2310-7),• butSalus’s recent sign: evidence Vein deflected suggests by only arteriole a modest (yellow) associationstiffening, SEQUELAE between but bankingOF retinopathy HYPERTENSION may cause and• systemicUsually venous IN appears organ THE tortuosity damage withinEYE 3 . disc diameters of the ONH normal in elderly)emergency) or Vascular calibre changes (Mild retinopathy)(Mitchell-Wong Scheme used below: Wong & Mitchell, NewRetinal England haemorrhagesJournal of Medicine, (Moderate 2004;351(22): retinopathy)2310-7), but recent evidence suggests onlyhypertension a modest association Hard between exudatesmmHg retinopathy and macularmmHgand systemic oedema organ damage . Optic neuropathy ‘hypertensive or whichever can provide the most urgent care (Mild retinopathy)LESIONS OF HYPERTENSIVE (ModerateA/V RETINOPATHY “nicking” retinopathy) (US)• orBonnet “nipping” sign: Vein (UK) banked (B) (course changed)Hard (blue) exudates andCategory macular of oedema (ModerateTypicallySystolic retinopathy), resolvesDiastolic, in 5-7 weeks Optic neuropathy “hypertensive papillopathy” (Malignant retinopathy) Vascular calibre changes (Mild retinopathy) Retinal haemorrhages (Moderate retinopathy)Hard exudates and macular oedemaNormal (Moderate retinopathy)(ModerateCategory retinopathy) of90 -119 • Due• Systolic to 60ischaemiaOptic, -79 neuropathy Diastolic, of the “hypertensive papillopathy’ RNFL papillopathy (malignant” (Malignant retinopathy) retinopathy) LESIONS OF HYPERTENSIVE RETINOPATHYThickened arteriole• Gunn can sign: impinge 90 degree upon vein thebanked retinal and taperedveins, (black) Categoryhypertension of Systolic• MaymmHg have, resultantDiastolic,mmHg microvascular infarcts with loss • Thickening and loss of elasticity of the arterial wall FlameLESIONS haemorrhage OF HYPERTENSIVE • RETINOPATHY Normal hypertension90-119 •and60Disruption-79mmHg of axoplasmicmmHg flow manifests as a grey- Requires emergencyIsolated systolic referral to the patient’s≥140 <90 A Vascular• Thickening calibre and changes loss of elasticity (Mild of retinopathy) the arterial wall Flame haemorrhageRetinal• Compromised haemorrhages• Note: vessels arterial in (Moderate the tortuosity macula• Compromised leak retinopathy) islipids not (hard typically vessels expected in the maculadue tohypertension leak lipids (hard • InmmHg acuteof retinal hypertension, tissuemmHg vasoconstriction and visual field and changes choroidal ischaemia• In acute results hypertension, in optic vasoconstriction and choroidal ischaemia results in optic • Thickening and loss of elasticity of the arterial wall Vascular calibre changes (Mild retinopathy)Flame haemorrhage leadingRetinal to potential haemorrhages vein occlusions (Moderate retinopathy)(below) • CompromisedNormal vessels in the maculaand white90-119 lesion along60 the-79 RNFL bundles SEQUELAE OF HYPERTENSIONgeneral hypertensionpractitioner and/or (may local IN be hospital, THE EYE • Broadening of light reflex masking the blood vessel Vascular• Broadening calibreA of light changes reflex• maskingOriginate (Mild the retinopathy) blood from vessel column,superficial capillary• Originates bed or from radial superficialRetinalexudates; haemorrhagescapillary hyperstiffening, -reflective (Moderate but on banking OCT,exudates; red retinopathy) mayarrow) cause from hyper thevenous - reflectivedeep tortuosity on OCT, red arrow) from the deep neuropathy and oedema (blue• arrow)In severe as aacute result hypertension, of axoplasmicneuropathy opticflow stasis,neuropathy due and to oedema (blue arrow) as a result of axoplasmic flow stasis, due to • Broadening of light reflex masking• theThickening blood vessel and loss ofrepresents elasticity chronic of the arterial arterial changes wall • Originate from superficial capillaryFlame• haemorrhageSalus’s bed or sign: radialcapillary Vein bed, deflected depositing in by the arterioleOPL. Deposition (yellow) withinHigh normalleak lipids (hardNormal exudates; 120 hyper-reflective-139 the lack90- of119 autoregulation80 -and89 of60 choroidal-79and oedema vasculature (blue (thisarrow) is because results thefrom ONH blood whichevernormal can provide in elderly) the most urgent care column, represents chronic arterial changes parapapillary capillariesA bed or radial parapapillary capillaries capillary bed, depositing in the OPL.Normal Deposition within • Usually90-119 appears60 within-79 3 disc diameters ofthe the lack ONH of autoregulation of choroidal vasculature (this is because the ONH blood or • Thickening and loss of elasticity of the arterial wall Flame haemorrhageHenle’s fibre layer forms a “macular star” High normal on OCT, red arrow120) from-139 theHard deep exudatescapillary80supply -89 isand through macularand the short posterioroedemavasoconstriction ciliary (Moderate arteries) and poor retinopathy) choroidal Optic neuropathy “hypertensive papillopathy” (Malignant retinopathy) column, represents chronic arterial• •changesBroadeningThickening ofand light loss reflex of elasticity masking of the the blood arterial vessel wall parapapillary capillaries • Flame•AppearanceOriginate• haemorrhageBonnet due from to RNFL sign: superficial orientation Vein bankedcapillary (coursebed or radial changed) (blue) and Copper vs. silver wiring (A) A • Appear white-yellow waxy, with a glitterHenle’s due fibre to cholesterin(prehypertension) layer forms a “macularbed, depositing Highstar ”in normal the OPL. Deposition•• orInTypically the 120 chronic-139 phase,resolves the oedema 80in- 589- 7 resolves, weeks leaving ONH pallor/atrophysupply is through the short posterior ciliary arteries) • column,Broadening represents of light reflexchronic masking arterial the changes• bloodAppearance vessel dueA to RNFL orientation• parapapillaryOriginate from capillaries superficial capillary bed or radial (prehypertension) or autoregulation leading to choroidal ischaemia Copper vs. silver wiring (A) • Broadening of light reflex masking the blood vessel• Appearance due to RNFL orientation• •TypicallyOriginate• resolvesGunn from insign: around• superficialLeakage 90 six degree weeks also capillary produces vein macularbed banked or •oedema radialAppear and (hyporeflective tapered white-yellow (black) on waxy, within with Henle’sa glitterHigh fibre due normal layer to formscholesterinSEQUELAE a • Strongly120 OF associated-139 HYPERTENSION with hypertensive80-89 emergency IN(BP: systolic THE• In ≥ 180the EYE orchronic diastolic phase, the oedema resolves, leaving ONH pallor/atrophy Copper vs. silver wiring (A) column, represents • chronic Changes arterial start off aschanges ‘copper wiring’ parapapillary capillaries High(prehypertension) normal • May120-139 have resultantor 80-89 microvascular and axoplasmic flow infarcts stasis. This with is because loss column, represents chronic arterial changes• Resolves in around 6 weeks Dot/blot• parapapillaryAppearance haemorrhage duecapillariesOCT, to RNFLyellow orientationarrow) ‘macular star’ ≥110, and should be managed as such) Requires emergency referral to the patient’s Copper vs. silver wiring (A)(slight broadening of light reflex) (top) • Resolves in around 6 weeks • Note: arterial tortuosity is not typically• Leakage expected alsoStage produces due1 • macular toCompromised oedema(prehypertension) (hyporeflective vessels140 in-159 the on macula leak90- 99lipidsor (hardthe ONH blood supply is •throughStrongly the short associated with hypertensive emergency• In (BP: acute systolic hypertension, ≥180 or diastolic vasoconstriction and choroidal ischaemia results in optic • Changes start off as •“copperChanges wiring” start off (slight as “copper broadening wiring” (slight of broadening of • ResolvesAppearance in around due to 6RNFL weeks orientation Hard exudatesStage and 1 macular oedema(prehypertension) (Moderate140-159 retinopathy) 90of- 99retinal or tissue and visual field changesOptic neuropathy “hypertensive papillopathy” (Malignant retinopathy) Copper vs. silver wiring (A)‘Silver wiring’, representsDot/blot greater broadening haemorrhageDot/blot of haemorrhage • •OriginatesAppearance from deep due capillary to RNFL bed orientation OCT, yellow arrow) • exudates;Appears white-yellowStage hyper 1 - waxy,reflective with a on OCT,140 red-159 arrow) from90-99posterior the deep ciliary arteries ≥110, and should be managed as such) generalneuropathy practitioner and oedema and/or (blue local arrow) hospital, as a result of axoplasmic flow stasis, due to • CopperChanges vs. start silver off wiring as “copper (A) wiring” (slight broadening of • Resolvesstiffening, in around but 6 weeksbanking may causeVascular venous occlusions/ tortuositymacroaneurysms or or Choroidopathy (rare; follows acute hypertensive crisis: systolic >180 mmHg) light reflex) (top) light reflex) (top) reflex (more ‘silver’ within the vessel) (bottom) •Dot/blot(INL,Resolves ONL, orhaemorrhage OPL)in around 6 weeks glitter due toStage cholesterol 1 140-159 or 90-99 • lightChangesChanges reflex) start start (top off off) as as “copper “copper wiring” wiring” (slight (slight broadening broadening• Originate ofof from deep capillary bed (INL, ONL, or OPL)• Compromised vessels in the macula leak lipidscapillary (hard Stage bed, 1 depositing in the140 OPL.-159 Deposition 90- 99within• In• theIn chronicacute hypertension, phase, the oedema vasoconstriction resolves, and choroidal ischaemia resultswhicheverthe in optic lack of can autoregulation provide the most of choroidal urgent care vasculature (this is because the ONH blood • • Originate from deep capillary bedDot/blot (INL, ONL, haemorrhage or OPL) • “Silver wiring” represents greater broadening of reflex • May be more useful to quantify broadening • Dot/blot•DisplacesOriginate retinalhaemorrhage from structures,Vascular deep takes occlusionscapillary (right) bed (INL, ONL, or OPL) Macroaneurysm (right) Elschnig spots (right)or leavingSiegrist ONH streaks pallor/atrophy (right) • “Silver wiring” represents greater broadening of reflex• “Silverlight reflex) wiring” (top represents) greater broadening of reflex exudates; hyper-reflective on OCT,Stage red 2 arrow)• fromLeakage Vascularthe also deep produces occlusions/macroaneurysms160- 179macular oedema100 -109 or neuropathy and oedema (blue arrow)Choroidopathy as a result of(rare; axoplasmic follows flowacute stasis, hypertensive due to crisis: systolic >180 mmHg) light reflex) (top) • Displaces retinal structures,•longer takesOriginate to resolvelonger from to• deep Venous:resolve capillary due to impingement bed (INL, ONL, or OPL) Stage• A localised 2 dilatationHenle’s of fibre aStage layer 2 160forms-179 a “macular • Changes160100 in- 179star RPE-109 due” to 100-109 • Linear hyperpigmented supply is through the short posterior ciliary arteries) (more “silver” within the vessel) (bottom) • Can be focal or generalised• Displaces retinal structures, takes•• longerOriginateDisplaces to fromretinal resolve deep structures, capillary takesbed (INL, longer ONL, to orresolve OPL) (hyporeflective on OCT, yellow arrow) • Strongly associated with hypertensive Images unavailable, though “Silver wiring” represents greater broadening of reflex (more “silver” within the vessel) (bottom) • •(more“Silver “silver” wiring” within represents the vessel) greater (bottom broadening) of reflex by thickenedcapillary artery, bed, depositing in the OPL. retinalDeposition arteriole within (saccular Stage 2 choriocapillaris160-179 infarcts 100-109 thestreaks lack of over autoregulation choroidal of choroidal vasculature (this is because the ONH blood •• DisplacesDisplaces retinalretinal structures, structures, takes takes longer longer toVascular to resolve resolve occlusions (right)• AppearStage white 2 -SEQUELAEyellow waxy,Macroaneurysm with160 aOF- 179glitter (right) HYPERTENSION due 100 to-109 cholesterin emergency (BP: systolic IN ≥ Elschnig180 THE or diastolic spotsnote EYE (right) that the presence of Siegrist streaks• In (right)the chronic phase, the oedema resolves, leaving ONH pallor/atrophy • May be more useful to quantify broadening• May(more(more be “silver” “silver” more usefulwithin within to the the quantify vessel) vessel) broadening( bottom(bottom)) intraretinallyHenle’s (branch fibre layer forms a “macular appearance)star” • Appear as small, black supplyarteries is through the short posteriorthese are ciliary typically arteries) • May be more useful to quantify broadening A/V ‘nicking’B (US) or ‘nipping’ (UK) (B) B Cotton wool spotsCotton (Moderate wool retinopathy) spots • Venous: due to impingement• Leakage also produces• macularA localised oedema dilatation (hyporeflective of a ≥ 110, and on should be managed• Changes as such) in RPE due to • Linear hyperpigmented• Strongly associated with hypertensive emergency (BP: systolic ≥180 or diastolic • Can be focal or generalised • •CanMayMay be be be focal more moreB or useful usefulgeneralised to to quantify quantify broadening broadening (Moderate retinopathy)Cottonocclusion) wool• orAppear spotsposterior white(Moderate to -yellow retinopathy) waxy, withStage a• glitterGradual 3 (hypertensive due leakage to cholesterin of vessels Stage ≥180 3 (hypertensive atrophic≥110≥180 spots, surrounded ≥110• In• theIndicative chronic of fibrinoid phase, the oedemaaccompanied resolves, by leaving systemic ONH pallor/atrophy Images unavailable, though • Thickened arteriole can impinge upon the CottonB wool spots (Moderate retinopathy)lamina (central Hard occlusion) exudates by and thickened macularStage artery, oedema 3 (hypertensive (Moderate retinopathy)≥180 ≥110 necrosis, which thenOptic leads neuropathy “hypertensive papillopathystreaks over choroidal” (Malignant retinopathy) • Can be focal or generalised B CottonCotton wool wool spots spots (Moderate (Moderate retinopathy) retinopathy) compromisesOCT, vision yellow Stage arrow) 3 (hypertensive retinal byarteriole yellow≥180 haloes (saccular ≥110 choriocapillarissymptoms infarcts and signs ≥110, and should benote managed that the aspresence such) of • •CanCan be be focal focal or or generalised generalisedunderlying retinal veins, leading to potential • Leakage also produces macularemergency) oedema (hyporeflective Stage onemergency) 3 (hypertensive or ≥180 or ≥110 • Strongly associated with hypertensive emergency (BP: systolic ≥180 or diastolic • Check for causative artery intraretinally (branch• Appears as deep red • Accelerated hypertension to fibrinous exudation arteries A/V “nicking” (US) or “nipping” (UK) (B)A/V “nicking” (US) or “nipping” (UK) (B) • Ischaemia of the RNFL results in emergency) emergency) appearance) • Appear as small, black these are typically vein occlusions (below) • Due to ischaemia of the RNFL• Due to ischaemia of the OCT,RNFL yellow arrow) haemorrhage +/-exudatesemergency) orcauses choroidalor ischaemiaor ≥110, and should be managed as such) A/V “nicking” (US) or “nipping” (UK) (B) •A/VA/VThickened “nicking” “nicking” arteriole(US) (US) or or “nipping” “nipping”can impinge (UK) (UK) upon (B) (B) the retinal veins, •disruptionDue• toCompromised of ischaemia axoplasmic flow of thewhich vessels RNFL in the maculaocclusion) leak lipids or posterior (hard to • Gradual leakage of vessels • In acute hypertension,atrophic vasoconstrictionspots, surrounded and choroidal• Indicative ischaemia of fibrinoid results in optic • Thickened arteriole can impinge upon the retinal veins,• Salus’s sign: Vein deflected• Due by arteriole to ischaemia• (yellowDisruption) of of the axoplasmic RNFL flow•• DueDisruption manifests to ischaemia of as axoplasmic a ofgrey the- RNFL flow manifests as a grey- Isolated systolic Isolated≥140 systolic <90≥140 <90 accompanied by systemic • •leadingThickenedThickened to potentialarteriole arteriole canvein can impinge occlusionsimpinge upon upon (below) the the retinal retinal veins,veins, •manifestsDisruption as a grey-white of axoplasmic lesion flow manifests aslamina a grey -(central occlusion) IsolatedhypertensionIsolated systolic systolic (may compromises be ≥140Vascular≥140 vision occlusions/macroaneurysms<90 <90 Choroidopathy by yellow haloes necrosis, which then leadsChoroidopathy symptoms (rare; and signs follows acute hypertensive crisis: systolic >180 mmHg) • Thickened arteriole canleading impinge to potential upon the vein retinal occlusions veins, (below) • Bonnet sign: Vein banked• Disruption white of axoplasmic lesion along flow the RNFL manifests•along bundlesDisruptionwhite RNFLexudates; lesion asbundles aof grey alongaxoplasmic hyper- the RNFL- reflectiveflow bundles manifests on OCT,as a grey red- arrow)hypertensionIsolatedVascular from occlusions/macroaneurysms thesystolic (may deepVascular be occlusions/macroaneurysms≥140 <90 (Rare;neuropathy followsChoroidopathy acute and hypertensiveoedema (rare; (blue follows crisis: arrow) acute hypertensiveas a result ofcrisis: axoplasmic systolic >180 flow mmHg) stasis, due to • Salus’sleadingleading sign: to to potential potential Vein deflected vein vein occlusions occlusions by arteriole (below) (below) (yellow) white lesion along the RNFL bundles • Check for causative artery hypertensionhypertension (may (may• beAppears be as deep red • Accelerated hypertension to fibrinous exudation leading to potential •veinSalus’s occlusions sign: Vein (below) deflected by arteriole (yellow) (course changed) (blue) • Usually appears within 3 disc• •Usuallywhite Usuallydiameters appearscapillary lesion appears within ofalong the3bed, discwithin the ONH diameters depositing RNFL 3 disc bundles diameters in the ofOPL. the DepositionONH normalhypertension within in elderly)Vascular (may occlusionsnormal be in (right)elderly)or or Macroaneurysmsystolicthe lack ≥ 180 of mmHg)autoregulation (right) of choroidal vasculature (thisElschnig is because spots the (right) ONH blood Siegrist streaks (right) • •BonnetSalus’sSalus’s sign:sign: sign: Vein Vein Vein deflected bankeddeflected (course by by arteriole arteriole changed) (yellow) (yellow)white (blue) lesion along the RNFL bundles•of theUsually ONH appears withinVascular 3 disc diameters occlusions of(right) the ONH Macroaneurysmnormalnormal in inelderly) elderly) (right) haemorrhage +/-exudatesor or Elschnig spots (right) causes choroidalSiegrist ischaemia streaks (right) • Bonnet sign: Vein banked (course changed) (blue) • Gunn sign: 90 degree vein banked • Typically resolves in 5-7 weeks•• UsuallyTypically Henle’s appears resolves fibre within in layer5- 73 weeksdisc forms diameters a “macular of the ONH star ” supply is through the short posterior ciliary arteries) • Salus’s sign: Vein deflected by arteriole (yellow) • •BonnetBonnet sign: sign: Vein Vein banked bankedand tapered (course (course (black changed) changed)) (blue)(blue) • Typically resolves in 5–7 weeks • Venous: due to impingement normal in• elderly)VascularVenous:• occlusions A due localised to (right)impingement dilatation of a Elschnig• •ChangesA spots localised in RPE duedilatation to of a • Linear hyperpigmented • Changes in RPE due to • Linear hyperpigmented • Gunn sign: 90 degree vein banked •andGunn tapered sign: 90 (black) degree vein banked and• taperedUsually (black) appears within 3 disc diameters•• TypicallyMayTypically have of resolvesresolvesthe resultant ONH in in 5 microvascular5 -7-7 weeks weeks infarcts with loss or Images Images unavailable, though Images unavailable, though • Gunn sign: 90 degree vein banked and tapered (black)• May have resultant microvascular• Appear infarcts whitewith loss-yellow by thickened waxy, withartery, a glitter due to cholesterin retinalRequires arteriole emergency (saccular referral to the patient’s •choriocapillarisIn the chronic infarcts phase, the oedemastreaks unavailable,resolves, over choroidal leaving ONH pallor/atrophy • Bonnet sign: Vein banked (course changed) (blue) • •Note:Gunn arterial sign: 90 tortuosity degree• Note: vein is arterialnot banked typically tortuosity and expectedtaperedis not expected (black) due to • ••MayMayofMay result retinal havehave in loss tissue resultantresultant of retinal and tissue microvascular microvascularvisual field changes infarcts infarcts with with loss loss Requires emergency• byVenous: thickened due toreferral impingement artery, to the by patient’s • Changesretinal in RPE arterioledue to choriocapillaris (saccular infarcts choriocapillarisnote that the presence infarcts of streaks over choroidal note that the presence of • Note: arterial tortuosity is not typically expected due to • Typically resolves in 5-7 weeks and visual field changes intraretinally (branch RequiresRequiresgeneral emergency emergencypractitioner referral referral and/or to tolocalthe the patient’s hospital, patient’s arteriesthough note • •stiffening,Note:Note: arterial arterial but tortuosity bankingtortuositydue may is tois not stiffening,not cause typically typically venous but banking expected expected tortuosity may cause duedue to toof retinal tissue and visual fieldofof • retinalretinalchangesLeakage tissuetissue alsoand and visual producesvisual field field changes macularchanges oedema (hyporeflectiveintraretinally thickenedon appearance) artery, intraretinally(branch (branch • •AppearStrongly as small, associated black with hypertensive emergency (BP: systolicthese ≥ 180are typically or diastolic arteries • Gunn sign: 90 degree vein banked and tapered (black) venous tortuosity general practitioner and/orgeneralgeneral practitionerlocal practitioner hospital, and/or and/or local local hospital, hospital, • Appearappearance) as small, black atrophic spots, that the • Appear as small, black these are typically stiffening, but banking may cause venousstiffening,stiffening, tortuosity but but banking banking may may cause cause venous venous• May tortuosity tortuosity have resultant microvascular infarctsOCT, with yellow loss arrow) occlusion) or posterior to occlusion)• Gradual or posteriorwhichever leakage to lamina canof vessels provide the most urgent care atrophic≥110, spots, and should surrounded be managed• Indicativeas such)presence of fibrinoid accompanied by systemic whicheverRequiresocclusion) can emergency provide or whicheverthe posterior referral most urgentcan toto provide the care patient’sthe most urgent care surrounded• Gradual by yellow leakage haloes of vessels atrophic spots, surrounded • Indicative of fibrinoid • Note: arterial tortuosity is not typically expected due to of retinal tissue and visual field changes lamina (central occlusion) (central occlusion)compromiseswhichever visioncan provide the most urgent care by yellow haloes necrosis,of these which then leads symptoms and signs accompanied by systemic • Accelerated hypertension causes choroidal are typically • Check for causative artery general• laminaMay practitioner be• associated (centralAppears withas and/orocclusion) deep macula red oedemalocal hospital, • Acceleratedcompromises hypertension vision to fibrinous exudation by yellow haloes necrosis, which then leads symptoms and signs stiffening, but banking may cause venous tortuosity Heart Foundation Classification (adults) SEQUELAE OFSystolic, HYPERTENSION mmHg Diastolic, IN mmHgVascular THE EYE occlusions/macroaneurysms ischaemia Choroidopathy (rare; accompaniedfollows acute hypertensive crisis: systolic >180 mmHg) • Check forhaemorrhage causative +/ artery-exudates causes choroidal ischaemia by systemic to fibrinous exudation SEQUELAE OF HYPERTENSIONSEQUELAE OFOF HYPERTENSIONHYPERTENSIONIN THE EYE IN IN THE THE EYE EYE whicheverMacroaneurysm can provide (right) the most urgent care Siegrist• Appears streaks as deep red • Accelerated hypertension Optimal < 120 and < 80 symptoms Hard exudates and macular oedema (Moderate retinopathy) Optic neuropathy “hypertensive• A localised papillopathy dilatation ”of (Malignant a retinal retinopathy) haemorrhage +/-exudates causes choroidal ischaemia HardHard exudates exudates and and macular macular oedemaoedema (Moderate(Moderate retinopathy) Vascular occlusions (right) OpticOptic neuropathy neuropathy “hypertensive “hypertensiveMacroaneurysm papillopathy papillopathy ”(right) (Malignant” (Malignant retinopathy) retinopathy) • LinearElschnig hyper-pigmented spots (right) streaks over choroidal andSiegrist signs streaks (right) Hard exudates and macular oedema (Moderate retinopathy) 120–129Optic neuropathyor “hypertensive80–84 papillopathy” (Malignantarteriole (saccularretinopathy) appearance) Normal • Venous: due to impingement • A localised dilatation of a arteries• Changes in RPE due to • Linear hyperpigmented • Compromised vesselsSEQUELAE in the macula leak lipids OF (hard HYPERTENSION IN THE EYE• In acute hypertension, vasoconstriction and• Gradual choroidal leakage ischaemia of vessels results in optic Images unavailable, though • •CompromisedCompromised vessels vesselsHigh in innormal the the macula macula leak leak lipids lipids (hard(hard by thickened130–139 artery,•• InorIn acute acute hypertension, hypertension,85–89 vasoconstriction vasoconstriction and and choroidal choroidal ischaemia ischaemia results results in opticin optic • Indicative of fibrinoid necrosis, which then streaks over choroidal • Compromised vessels in the macula leakexudates; lipids hyper (hard-reflective on OCT, red arrow) from the deep • In acute hypertension, vasoconstrictionneuropathy and and oedema choroidal (blue ischaemia arrow) as aresults retinalresultcompromises ofin arteriole axoplasmicoptic vision (saccular flow stasis, due to leads choriocapillaristo fibrinous exudation infarcts note that the presence of exudates;exudates; hyper hyper-reflective-reflectiveGrade 1 (mild)on on OCT, OCT, red red arrow) arrow) fromfrom thethe deepdeep 140–159 neuropathyorneuropathy90–99 and and oedema oedema (blue (blue arrow) arrow) as as a resulta result of of axoplasmic axoplasmic flow flow stasis, stasis, due due to to Hardexudates; exudates hyper and-reflective macular on oedemaOCT, redcapillary arrow) (Moderate bed, from depositing the retinopathy) deep in the OPL. Deposition within neuropathyintraretinallyOptic and neuropathy oedema (branch (bluethe “hypertensive lackarrow) of autoregulation as a result papillopathy of ofaxoplasmic choroidal ” vasculatureflow (Malignant• appearance)Appears stasis, as(this due deep retinopathy)is to redbecause the ONH blood • Appear as small, black arteries these are typically capillarycapillary bed, bed, depositing depositing in in the the OPL. OPL. Deposition Deposition withinwithin thethe lack lack of of autoregulation autoregulation of of choroidal choroidal vasculature vasculature (this (this is becauseis because the the ONH ONH blood blood Henle’s fibre layer formsGrade 2a (moderate) “macular star” occlusion)160–179 or posteriororsupply to is through100–109 the short posterior ciliary• Gradual haemorrhagearteries) leakage +/-exudates of vessels atrophic spots, surrounded • Indicative of fibrinoid capillary bed, depositing in the OPL. DepositionHenle’s fibre within layer forms a “macular star” the lack of autoregulation supplyof choroidal is through vasculature the short posterior(this is because ciliary arteries) the ONH blood accompanied by systemic • Henle’sAppear whitefibre layer-yellow forms waxy, a “macular with a glitter star” due to cholesterin lamina (central •occlusion)Insupply the chronic is through phase, the theshort oedema posterior resolves, ciliary leavingarteries) ONH pallor/atrophy necrosis, which then leads • Compromised vessels inHenle’s the macula fibre layer leak forms lipids a “macular (hard • starAppear” white-yellowGrade waxy, 3 (severe) with a glitter due to cholesterin • In acutesupply hypertension, is through the vasoconstriction short• In posterior the chronic ciliary andphase, arteries)choroidal the oedema ischaemia resolves, leavingcompromises results ONH in pallor/atrophy optic vision by yellow haloes symptoms and signs • LeakageAppear white also produces-yellowRequires waxy, macular emergency with oedema a glitter referral (toduehyporeflective the topatient’s cholesterin general on practitioner ≥ 180 • orInStrongly the chronic associated≥ 110 phase, with the hypertensiveoedema resolves, emergency leaving (BP: ONH systolic pallor/atrophy ≥180 or diastolic Appear white-yellow waxy, with a glitter due to cholesterin In the •chronicCheck phase, for causative the oedema artery resolves, leaving ONH pallor/atrophy• Appears as deep red • Accelerated hypertension to fibrinous exudation exudates; hyper-reflective• on OCT, red arrow) from •the•LeakageOCT,Leakage deep yellow also also arrow) produces producesand/or macular macularlocal hospital, oedema oedema whichever ( (hyporeflectivehyporeflective can provide the most onon urgent care. neuropathy• and oedema (blue•• Strongly≥Strongly 110,arrow) and associated associated shouldas a result be with with managed hypertensiveof hypertensive axoplasmic as such) emergency emergency flow (BP:stasis, (BP: systolic systolic due ≥180 ≥to180 or ordiastolic diastolic • Leakage also produces macular oedemaOCT,OCT, ( yellowhyporeflective yellow arrow) arrow) on • Strongly associated with hypertensive≥≥110,110, and and should should emergency be be managed managed (BP: as systolic as such) such) ≥ 180haemorrhage or diastolic +/-exudates causes choroidal ischaemia capillary bed, depositing in the OPL. Deposition within Isolated systolic hypertension (may be normal in elderly) the lack of autoregulation≥ 140 of choroidalor 180 mmHg) VascularVascular occlusions/macroaneurysms occlusions/macroaneurysms ChoroidopathyChoroidopathy (rare; (rare; follows follows acute acute hypertensive hypertensive crisis: crisis: systolic systolic >180 >180 mmHg) mmHg) • Appear white-yellow waxy, with a glitter due to cholesterinVascular occlusions (right)Chair-side Reference HypertensionMacroaneurysm (right)• In the chronic phase, the oedemaElschnig resolves, spots (right) leaving ONH pallor/atrophySiegrist streaks (right) Chair-side Reference Hypertension VascularVascular occlusions/macroaneurysms occlusions (right) Macroaneurysm (right) ChoroidopathyElschnig (rare; spots follows (right) acute hypertensiveSiegrist crisis: streaks systolic (right) >180 mmHg) Vascular• Venous: occlusions due to impingement (right) Macroaneurysm• A localised dilatation (right) of a •ElschnigChanges spots in RPE(right) due to Siegrist• Linear streaks hyperpigmented (right) • Leakage also produces macular oedema (hyporeflective• Venous: on due to impingement • A localised dilatation• Strongly of a associated with hypertensive• Changes in RPEemergency due to (BP: systolic• Linear ≥180 hyperpigmented or diastolic Images unavailable, though Vascular occlusions (right) • byVenous: thickened due toartery, impingement • Aretinal localised arteriole dilatation (saccular of a • choriocapillarisChanges inSiegrist RPE dueinfarcts streaks to (right) • streaksLinear hyperpigmented over choroidal ImagesImages unavailable, unavailable, though though OCT, yellow arrow) by thickened artery,Macroaneurysm (right) retinal arteriole (saccular≥110,Elschnig and should spots (right) be managed choriocapillaris as such) infarcts streaks over choroidal note that the presence of intraretinallyby thickened artery,(branch appearance)retinal arteriole (saccular • Appearchoriocapillaris as small, infarcts black streaksarteries over choroidal notenote that that the the presence presence of of • Venous: due to impingement intraretinally (branch• A localised dilatation of a appearance) • Changes in RPE due to • Appear as small,• Linear black hyperpigmented arteries Images unavailable, thoughthese are typically occlusion)intraretinally or posterior(branch to appearance) • Appear as small, black • arteriesIndicative of fibrinoid these are typically by thickened artery, occlusion) or posteriorretinal to arteriole (saccular • Gradual leakage of vesselschoriocapillaris infarcts atrophic spots,streaks surrounded over choroidal • Indicative of fibrinoid accompaniedthese are typically by systemic occlusion) or posterior to •• GradualGradual leakage of vessels atrophicatrophic spots, spots, surrounded surrounded • Indicative ofnote fibrinoid that the presenceaccompanied of by systemic intraretinallyVascular (branch occlusions/macroaneurysmslaminalamina (central (central occlusion) occlusion) compromises vision Choroidopathy (rare;by yellow follows haloesarteries acute hypertensivenecrosis,necrosis, crisis: which systolicwhich then then leads>180 leads mmHg) symptomsaccompanied and by signs systemic lamina (central occlusion)appearance) compromisescompromises vision • Appear as small, black byby yellow yellow haloes haloes necrosis, whichthese then are leads typically symptoms and signs • •CheckCheck for for causative causative artery artery • Appears as deep red • Accelerated hypertension toto fibrinous fibrinous exudation exudation symptoms and signs occlusion) or posterior to • Check for causative• arteryGradual leakage of vessels •• AppearsAppears as deep red atrophic spots, surrounded•• Accelerated Accelerated• hypertension hypertensionIndicative of fibrinoid to fibrinousaccompanied exudation by systemic Vascular occlusions (right) Macroaneurysm (right) haemorrhagehaemorrhage +/Elschnig-exudates spots (right) causescauses choroidal choroidalSiegrist ischaemia ischaemiastreaks (right) lamina (central occlusion) compromises vision haemorrhage +/-exudates by yellow haloes causes choroidalnecrosis, ischaemia which then leads symptoms and signs • Venous: due to impingement• Check for causative artery • A localised dilatation• Appears of as adeep red • Changes• Accelerated in RPE due hypertension to • Linearto fibrinous hyperpigmented exudation Images unavailable, though by thickened artery, retinal arteriolehaemorrhage (saccular +/-exudates choriocapillariscauses choroidal infarcts ischaemia streaks over choroidal note that the presence of intraretinally (branch appearance) • Appear as small, black arteries these are typically occlusion) or posterior to • Gradual leakage of vessels atrophic spots, surrounded • Indicative of fibrinoid accompanied by systemic lamina (central occlusion) compromises vision by yellow haloes necrosis, which then leads symptoms and signs • Check for causative artery • Appears as deep red • Accelerated hypertension to fibrinous exudation haemorrhage +/-exudates causes choroidal ischaemia Chair-side Reference Hypertension

Hypertension is a commonly seen and self-reported condition in optometric practice. In cases where there are signs of retinopathy, an optometrist would ideally have the capacity to screen blood pressure in their office. The information below is intended as a guide for measurement of blood pressure status in an optometric practice, and should not be used as a replacement for cardiovascular assessment by a suitably-trained general physician and/or cardiologist.

Establishing blood pressure status in your office

Entering medical history: NOTE: • +/- hypertension (past or present) • Optometric office screening of blood pressure should not be a • Anti-hypertensive medications replacement for evaluation by a trained general physician and/or cardiologist • Cardiovascular co-morbidities (for example DM, cholesterol, stroke, heart disease) • Blood pressure taken at the arm is just one method for determining blood pressure, and does not exclude other cardiovascular diseases • Obesity (BMI ≥ 30 kg/m2) or peripheral vascular disease. • Ongoing communication and co-management with the patient’s general physician is recommended

Entering family history: Cut-off blood pressure levels for referral to GP:

• FHx of hypertension and/or cardiovascular co-morbidities • 140–159/90–99: routine referral • Cause of death of family members? (esp. if premature • 160–179/100–109: within two weeks [< 60 years] death) • ≥ 180/110: emergency referral

Entering ocular history: • Vascular diseases of the eye • Previous intraocular injections

Tips for measuring blood pressure in office

Equipment: • Check to make sure equipment working properly • Too loose • Upside down • Check against another model for accuracy • Sensor not on vessel • Check cuff size appropriate (bladder length should be approximately • Thick clothes 80% of arm circumference [note manufacturer recommendation], especially if circumference > 30cm)

Patient: • Patient should be well-rested and comfortable prior to exam • Patient should be seated straight, feet on the ground, with arm • Good tightness supported at heart level • Sensors correct • Similar to blink rate, consider performing blood pressure while • No/loose sleeve engaging in relaxing activities • 2-3cm above elbow

Measurement: • An average of three readings should be taken, each two minutes apart • Sleeves should not be rolled tightly; if thin clothing, screening blood pressure can be taken over the top, otherwise, removal of sleeved clothing should be considered

Chair-side Reference Hypertension JUNE 2018 17 Chair-side Reference Hypertension Effects of

Hypertension is a commonly seen and self-reported condition in optometric practice. In cases where there are signs of Hypertension retinopathy, an optometrist would ideally have the capacity to screen blood pressure in their office. From page 13 The information below is intended as a guide for measurement of blood pressure status in an optometric practice, and should not be used as a replacement for cardiovascular assessment by a suitably-trained general physician and/or cardiologist. haemorrhages (flame-shaped, dot or blot), microaneurysms, cotton wool spots, hard exudates and/or retinal oedema.9

Establishing blood pressure status in your office Acute blood pressure elevations can lead to optic disc swelling from Entering medical history: NOTE: vasoconstriction, choroidal ischaemia and axoplasmic flow stasis, concurrent • +/- hypertension (past or present) • Optometric office screening of blood pressure should not be a with other clinical signs of hypertensive • Anti-hypertensive medications replacement for evaluation by a trained general physician and/or retinopathy. Once the condition has cardiologist • Cardiovascular co-morbidities (for example become chronic, disc oedema resolves DM, cholesterol, stroke, heart disease) • Blood pressure taken at the arm is just one method for determining and ONH atrophy can develop. blood pressure, and does not exclude other cardiovascular diseases • Obesity (BMI ≥ 30 kg/m2) or peripheral vascular disease. Clinically, generalised arteriolar Figure 1. A 68 year-old male with chronic hypertension, now normalised on treatment, demonstrating features of mild hypertensive retinopathy including arteriolar narrowing • Ongoing communication and co-management with the patient’s narrowing and AV nipping typically (green arrow) and arteriovenous nipping (black arrows). general physician is recommended indicates damage from more chronic hypertension (Figure 1), whereas Entering family history: Cut-off blood pressure levels for referral to GP: haemorrhages, cotton wool spots and hard exudates are likely to indicate • FHx of hypertension and/or cardiovascular co-morbidities • 140–159/90–99: routine referral more recent severe hypertension (Figure 12 • Cause of death of family members? (esp. if premature • 160–179/100–109: within two weeks 2). As detailed in the CFEH chairside [< 60 years] death) reference, and summarised in Table 1 • ≥ 180/110: emergency referral below, hypertensive retinopathy can be graded as mild, moderate or malignant Entering ocular history: using the Mitchell-Wong simplified • Vascular diseases of the eye classification scheme.12 This grading • Previous intraocular injections scale has been found to have similar sensitivity to the older Keith-Wagener- Barker grading scale.13

The presence of hypertensive Tips for measuring blood pressure in office retinopathy is thought to be a marker of other target-organ damage.4 Accelerated Equipment: hypertension (severe HBP associated with retinal haemorrhages and • Check to make sure equipment working properly • Too loose exudates) and malignant hypertension • Upside down • Check against another model for accuracy (accelerated hypertension with • Sensor not on vessel papilloedema) both have poor prognoses • Check cuff size appropriate (bladder length should be approximately • Thick clothes 80% of arm circumference [note manufacturer recommendation], without treatment and require urgent especially if circumference > 30cm) referral for treatment by experienced practitioners.2 Figure 2. A 50 year-old male with acute hypertension, measuring 174/110 mmHg at the time of visit, who had been hospitalised with systolic blood pressure > 200mmHg a Patient: Hypertensive choroidopathy is most week earlier. The retinal photograph shows signs of moderate hypertensive retinopathy • Patient should be well-rested and comfortable prior to exam frequently seen in cases of acute including hard exudates (red arrow), microaneurysms and dot haemorrhages, arteriolar hypertension such as in younger • Patient should be seated straight, feet on the ground, with arm • Good tightness narrowing and arteriovenous nipping. women with pre-eclampsia.14,15 Signs supported at heart level • Sensors correct of choroidopathy include serous retinal • Similar to blink rate, consider performing blood pressure while • No/loose sleeve • 2-3cm above elbow detachment, Elschnig spots (ischaemic visualisation of the retinal vasculature changes are due to acute or chronic engaging in relaxing activities infarcts of the choriocapillaris and for signs of hypertensive retinopathy. hypertension. RPE), and Siegrist streaks (linear photography may be a useful Measurement: hyperpigmentation over choroidal adjunct to detect more subtle changes While optometrists routinely ask their arteries). • An average of three readings should be taken, each two minutes apart in the vasculature. It also provides a diabetic patients about risk factors valuable baseline for future monitoring. for developing diabetic retinopathy • Sleeves should not be rolled tightly; if thin clothing, screening blood pressure can be taken over the top, otherwise, removal of sleeved In cases where hypertensive The role of the optometrist clothing should be considered retinopathy is detected, measuring A comprehensive optometric eye in-office blood pressure may assist the examination typically includes direct optometrist in determining if retinal Continued page 18 Chair-side Reference Hypertension 18 JUNE 2018

Hypertension Management tree when seeing signs suggestive of hypertensive retinopathy From page 17

(for example: HbA1c to gauge the level of glycaemic control), it is Noted on clinical Noted on clinical examination: examination commonly assumed that a patient with • Macular star • Arteriolar narrowing previously-diagnosed hypertension • Optic nerve oedema • A / V crossing changes is well controlled. To complicate • Vitreous haemorrhage • Copper or silver wiring matters, patients will frequently deny • Pre- • Cotton wool spots having ‘high blood pressure’ as they • Neovascularisation • Retinal haemorrhages believe their blood pressure to be normalised on treatment. As a result, using targeted questions – such as: ‘are you on treatment to control high blood pressure?’ and ‘is your GP happy Measure with your blood pressure control?’ Measure in-office BP** in-office BP* – along with a careful exploration of the individual’s medication list, may provide a more accurate hypertension history. BP BP BP It is important to note that adults < 180/110 ≥ 180/110 < 180/110 with presbyopia or refractive error who perceive themselves to be in good general health may visit their optometrist more regularly than their general practitioner (GP). Communicate Immediate contact Consult with GP In the absence of vascular changes, immediately with with GP • Has HTN been early diagnosis of hypertension may be ophthalmologist to determine urgency diagnosed? challenging, particularly as patients are to initiate of management. • Is BP well-controlled? appropriate referral often asymptomatic. Red flags are raised Hospitalisation • Is the patient low-risk may be required. (no other risk factors/ when the medical history uncovers that comorbidities?) an adult patient has not recently seen a GP or is not taking any medications despite having apparent risk factors for hypertension. In these cases, referral to a GP may be indicated and measuring blood pressure at the time of the eye examination can assist with Maintain specialist care NO YES determining the urgency of triage. until stable

A Saudi Arabian-based study found that introducing routine measurement of blood pressure into optometry practices identified 93 of 443 patients Communicate with associated Routine eye exam (21 per cent) with hypertension; of practitioners every 6–12 months those, 68 per cent were unaware of and titrate a and ongoing their HBP. Overall, one previously scheduled review communication undiagnosed hypertensive patient Additional notes: as appropriate with GP * If in-office BP measurement was identified for every eight adults unavailable, prompt review tested and poor control was found with GP in approximately 29 per cent of ** These ophthalmic signs 16 STABLE previously-diagnosed patients. While may be indicative of conditions routine in-office measurement of blood other than hypertensive pressure is not generally indicated retinopathy (e.g. papilloedema) that may also require urgent within optometric practice, the CFEH assessment chair-side reference in this issue of Pharma provides a succinct guide on when to consider taking blood pressure measurement in practice, how to correctly use an automated blood pressure cuff, and interpret and Figure 3. Acknowledgements: Dr Katherine Kalloniatis and Dr Chris Gilbert for their advice regarding measuring blood pressure and medical review periods. JUNE 2018 19

Grade Features information on the procedure itself and None No detectable signs common errors, clinicians may wish to familiarise themselves with appropriate Generalised arteriolar narrowing, focal arteriolar narrowing, arte- guidelines such as the NHF.2 Mild riovenous nicking (nipping), copper wiring (opacity of arteriolar wall) or a combination of these signs Figure 3 (‘Management tree when seeing signs of hypertensive Retinal haemorrhages (blot-shaped, dot-shaped or flame- retinopathy’) is part of the CFEH Moderate shaped), microaneurysm, cotton wool spot, hard exudate or a combination of these signs chair-side reference; it was developed in collaboration with two GPs and an ophthalmologist to assist optometrists Malignant Signs of moderate retinopathy plus swelling of the optic disc in managing patients with signs of hypertensive retinopathy and Table 1. Mitchell-Wong Simplified Hypertensive Retinopathy Grading Scale12 determining the urgency and type of referral required.

In urgent cases, consider speaking directly with the patient’s GP (and manage the results. be obtained with an automated ophthalmologist as necessary) to sphygmomanometer. As further determine the most appropriate course As members of the multidisciplinary expanded on in the CFEH chair- of action. In less urgent cases, written health care team, optometrists can side reference, the patient should communication to the GP may be more make a valuable contribution to patient relax for several minutes in a quiet appropriate. education. Optometrists are likely environment (at room temperature with to have access to a retinal camera legs uncrossed) before measurements Conclusion and images can be a powerful tool in are taken. Factors that can adversely reinforcing the benefits of compliance affect blood pressure measurements Optometrists are skilled at detecting to treatment, lifestyle modification and include: drinking caffeine and smoking vascular changes suggestive of the importance of regular GP visits for within two hours of measurement, hypertensive retinopathy, however those at risk of chronic diseases such as incorrect cuff size or positioning, they may overlook their potential role hypertension and diabetes. presence of peripheral arterial disease, in screening for hypertension and or the presence of a irregularity reinforcing the importance of regular (for example: atrial fibrillation). NHF GP visits and compliance to treatment. Measuring blood pressure and guidelines state that a comprehensive The CFEH chair-side reference aims to initiating referral assessment of blood pressure should provide a practical tool to assist busy Blood pressure measurements in an be based on at least two measurements optometrists in managing hypertensive optometry practice will typically one or more weeks apart. For additional patients in their practice.

1. Australian Bureau of Statistics. Na- Pressure: the JNC 7 report. JAMA 2003; primary open-angle glaucoma: a me- tional Health Survey [internet]. 289: 2560–2572. ta-analysis. Am J Ophthalmol 2014; 158: Canberra: National Health Survey 5. Group SR, Wright JT, Jr., Williamson JD, 615–627.e619. First Results Australia 2014-15 [cited et al. A Randomized Trial of Intensive 11. Chakravarthy U, Wong TY, Fletcher A, 2018 March 3]. Available from: http:// versus Standard Blood-Pressure Control. et al. Clinical risk factors for age-related www.ausstats.abs.gov.au/ausstats/ N Engl J Med 2015; 373: 2103–2116. macular degeneration: a systematic re- subscriber.nsf/0CDA852A349B4CEE- 6. Psaty BM, Smith NL, Siscovick DS, et al. view and meta-analysis. BMC Ophthal- 6CA257F150009FC53/$File/nation- Health outcomes associated with anti- mol 2010; 10: 31. al%20health%20survey%20first%20 hypertensive therapies used as first-line 12. Wong TY, Mitchell P. Hypertensive retin- results,%202014-15.pdf agents. A systematic review and me- opathy. N Engl J Med. 2004; 351(22): 2. National Heart Foundation of Austral- ta-analysis. JAMA 1997; 277: 739–745. 2310-2317. ia. Guideline for the diagnosis and 7. Neal B, MacMahon S, Chapman N. Blood 13. Downie LE, Hodgson LA, Dsylva C, et management of hypertension in adults Pressure Lowering Treatment Trialists al. Hypertensive retinopathy: comparing [Internet]. Melbourne: National Heart C. Effects of ACE inhibitors, calcium an- the Keith-Wagener-Barker to a simpli- Foundation of Australia, 2016 [cited tagonists, and other blood-pressure-low- fied classification.J Hypertens 2013; 31: 2018 March 3]. Available from: https:// ering drugs: results of prospectively 960–965. www.heartfoundation.org.au/images/ designed overviews of randomised tri- 14. Fraser-Bell S, Symes R, Vaze A. Hyper- uploads/publications/PRO-167_Hyper- als. Blood Pressure Lowering Treatment tensive eye disease: a review. Clin Exp tension-guideline-2016_WEB.pdf. Trialists’ Collaboration. Lancet 2000; Ophthalmol 2017; 45: 45–53. 3. World Health Organization. A global 356: 1955–1964. 15. AlTalbishi Aa, Khateb S, Amer R. brief on hypertension. Silent killer, 8. Royal Australian College of General Elschnig’s spots in the acute and remis- global public health crisis [Internet]. Practitioners. Guidelines for preventa- sion stages in preeclampsia: spectral-do- Geneva: World Health Organization, tive activities in general practice, 9th main optical coherence tomographic 2013. [cited 2018 March 3]. Availa- edition. 8.2 Blood Pressure. Melbourne: features. Eur J Ophthalmol 2016; 25: ble from: http://apps.who.int/iris/ RACGP, 2016. [cited 2018 March 3]. e84–e87 bitstream/handle/10665/79059/ Available from: https://www.racgp.org. 16. AlAnazi SA, Osuagwu UL, AlMubrad WHO_DCO_WHD_2013.2_eng.pd- au/download/Documents/Guidelines/ TM, et al. Effectiveness of in-office blood f;jsessionid=7410D6061A1C5958D- Redbook9/17048-Red-Book-9th-Edition. pressure measurement by eye care prac- 56078630277B517?sequence=1 pdf titioners in early detection and manage- 4. Chobanian AV, Bakris GL, Black HR, et al. 9. Wong TY, Mitchell P. The eye in hyper- ment of hypertension. Int J Ophthalmol The Seventh Report of the Joint National tension. Lancet 2007; 369: 425–435. 2015; 8: 612-621. Committee on Prevention, Detection, 10. Zhao D, Cho J, Kim MH, Guallar E. Evaluation, and Treatment of High Blood The association of blood pressure and 20 JUNE 2018

Pharma and Optometry Australia’s official journal Clinical and Experimental Optometry (CXO) are collaborating to bring our readers up to date with some of the most interesting articles, reviews and original research available in the latest issue of CXO.

Sheela E Kumaran MPhil Optom Patient-reported outcome

Jyoti Khadka measures in and PhD strabismus: a systematic Rod Baker BSc Optom review Konrad Pesudovs PhD FAAO Summary and comment provided by Maria Markoulli Optometry and Vision Science, PhD MOptom GradCertOcTher FBCLA FAAO Flinders University, Adelaide, Deputy Editor, Clinical and Experimental Optometry South Australia

identified early on, treatment can eight ophthalmic quality of life be initiated to minimise the impact domains: activity limitation, concerns, of these developmental conditions. emotional well-being, social well- Starting with this issue, Pharma and The resulting functional deficits being, economic, convenience, Optometry Australia’s official journal of impaired stereoscopic depth symptoms and mobility. Clinical and Experimental Optometry perception and defective sensory, will collaborate to bring our readers motor and visual cognition translate They identified both non-disease and up to date with some of the most to difficulties in activities such as disease specific questionnaires that interesting articles, reviews and reading, grasping and driving as well have been used to assess amblyopia original research available in the pages as the psycho-social and emotional and strabismus impact. Non-disease of CXO. well-being of those affected, for specific questionnaires identified example, in the case of perceivable include the Short Form (SF-36) and Published in Australia since 1919, strabismus. Understandably, this the Paediatric Quality of Life Inventory CXO is the leading peer-reviewed can significantly impact on quality (PedsQL) which are widely used in journal of original optometric and of life. In order to determine if the adults and children respectively; vision science research and reviews screening and treatment regimens that both assess quality of life domains in the Asia-Pacific region. In each we implement are effective relative to such as physical functioning, role new issue of Pharma, CXO Deputy the cost and inconvenience, we need limitations and social functioning. Editor Maria Markoulli will confer to have a robust and validated tool to These questionnaires offer a superficial with Pharma Clinical Editor Mark measure quality of life. understanding of a person’s well-being Roth to select a stand-out article as they are not specific to a disease, from a recently-published issue of Ms Sheela Kumaran and colleagues lacking the sensitivity to evaluate CXO. An overview of the article and from Flinders University undertook the impact of amblyopia and/or a discussion on its relevance to the a systematic review which aimed to strabismus. practice of optometry will be provided identify the patient-reported outcome by Dr Markoulli. measures currently used to determine When the authors explored disease the impact of amblyopia and/or specific questionnaires, 32 patient- strabismus on quality of life and to reported outcome measures were Patient-reported outcome measures determine the robustness of existing identified that were specific to in amblyopia and strabismus: a questionnaires. amblyopia and/or strabismus, 12 systematic review were specific to amblyopia and 18 CXO. July 2018 doi: 10.1111/cxo.12553 In order to do this, they conducted were strabismus specific, while two a systematic search of electronic addressed both conditions. Of the 12 Amblyopia and strabismus are two databases such as PubMed and amblyopia questionnaires, only two conditions commonly encountered Cochrane and assessed the quality assessed the impact of amblyopia itself in clinical practice that can of all patient-reported outcome have a significant impact on an measures identified and their individual’s quality of life. When comprehensiveness in terms of the Continued page 21 JUNE 2018 21

Outer retinal tubulations AMD management requires a collaborative approach

responded to multiple injections CASE REPORT Abhishek Sharma with different agents for macular degeneration. MBBS DPhil(Oxon) FRANZCO One such patient, an active 74-year- Brisbane Retina old, had been fitting in her monthly Queensland Eye Institute Medical management of wet macular degeneration has vastly improved injections for the past two years with intravitreal injections of anti- between her yoga, local community VEGF agents. work and overseas travelling. The frequent injections were cramping In Australia, we are in an enviable her style and there was a three-month position where our government cruise trip planned for winter with provides specialists with access to her group of friends. She was referred these medications. for a second opinion to see whether there was an alternative treatment for However, quoting Spider-Man’s Uncle her wet macular degeneration. Ben: ‘With great [injecting] power, comes great responsibility’, and not At her appointment, she mentioned all nails respond to the same hammer. that vision had stabilised in her As retinal specialists, we commonly treated eye for the past year, at 6/24 in receive referrals for second opinions regarding patients who have not Continued page 22

surgery. The Effect of Diplopia use based on the presenting patient and CXO review Questionnaire was the only tool the overall question we wish to have identified to measure the impact answered. If we are interested to know From page 20 of post-operative diplopia. The how their condition is impacting their Intermittent Questionnaire psychosocial well-being as an adult, was the only questionnaire validated we will choose a questionnaire that (Amblyopia Survey and the Socio- for child-specific strabismus, with differs from one we would select if we Professional Integration Questionnaire, most of the strabismus instruments were interested in following up on the while the other 10 assessed the impact measuring the impact of strabismus impact of patching on an amblyopic of treatment. on appearance in adults. These child. questionnaires generally measured Most of the amblyopia instruments concerns relating to appearance and Future work needs to be done to measured the impact on children; treatment outcome. develop appropriate questionnaires to only the Amblyopia Survey targeted enable us to assess all eight ophthalmic the psychosocial impact on adults. Kumaran and colleagues conclude that domains of quality of life and to track Of these 12 questionnaires, only none of the questionnaires summarised the impact of our treatment on the one has been validated via modern address quality of life comprehensively overall well-being of our patients. psychometric tests (Children’s Vision based on the eight identified ophthalmic for Living Scale). These questionnaires domains. Although there are many predominantly measure activity questionnaires available, all current limitation and emotional impact as a instruments used to measure quality result of treatment. of life in those with amblyopia and/or strabismus are flawed in some way. Each quarter, CXO’s Deputy Editor Maria Mark- Of the 18 strabismus surveys oulli and Pharma’s Clinical Editor Mark Roth select a stand-out article from a recently-pub- identified, six were developed to Discussion lished issue of CXO to appear in Pharma. determine the impact of strabismus on quality of life and the remaining As clinicians we need to be selective To access CXO, please go to: www.optometry. 12 measured the impact of strabismus about which questionnaire we wish to org.au/cxo-journal/ 22 JUNE 2018

AMD management From page 21

her left pseudophakic eye. Intravitreal treatment had been extended at one stage but had returned to monthly injections due to her OCT scans, with no recent change in vision. She was otherwise healthy, did not smoke and took her AREDS2 vitamin pills religiously, along with some other herbal therapies.

The fundus examination showed areas of and Figure 1. Defining features of outer retinal tubulations on OCT: hyper-reflective some disciform scar changes, but border, hypo-reflective core, in outer nuclear layer there was no acute haemorrhage. Her OCT scan demonstrated a significant cystic-looking structure but no signs of subretinal fluid. The fluorescein angiogram also did not reveal an active choroidal neovascular membrane. Her findings were consistent with outer retinal tubulations, which was nicely demonstrated on our OCT.

Outer retinal tubulations were first described in very similar scenarios: patients who had long-term injections with no apparent resolution of cystic fluid. Outer retinal tubulations are formed due to chronic retinal injury, damaging the inner and outer segments of photoreceptors, in the ellipsoid zone on the OCT.

Over a period of time the damaged cells form a circular rearrangement. On OCT, this appears as a hyper- reflective outer ring and a hypo- reflective core, which is not consistent with a cyst. The tubulations are Figure 2. On fundus examination, there was no sign of an active choroidal neovas- in the outer nuclear layer. Outer cular membrane retinal tubulations do not respond to anti-VEGF injections; however, these patients still require long-term monitoring for occurrence of new subretinal fluid and new wet AMD signs. private systems. It allows several she would be sent to us for a retinal After another couple of visits with no minds to attack a problem, especially assessment straight away. Her next goal new changes on her OCT scans and no when a condition is not changing or is to rustle up an OCT scanner on her further injections, I sent her back to improving and through collaboration cruise ship, for a year-long cruise. her referring optometrist, requesting we entertain other diagnoses. regular OCT scans. This collaborative approach is important in providing Although we could not improve her our patients with the best treatment vision, our patient was happy that pathways, minimising unnecessary she could be monitored locally by her interventions, and should be optometrist, and if there was ever a encouraged in both the public and concern about new wet AMD changes, JUNE 2018 23

Therapeutic NEWS of note

The impact of supplemental bilateral in the same time span. antioxidants on patients with non- Associate Professor advanced AMD To assess the five-year progression Mark Roth from unilateral to bilateral age-related Researchers at the Waterford Institute macular degeneration (AMD) and of Technology, Ireland conducted a BSc(Pharmacology) associated risk factors, researchers two-year study to evaluate the impact BAppSc(Optom) PGCertOcTher conducted pooled data analyses of three of supplemental macular carotenoids NEWENCO FAAO OAM prospective population-based cohorts, (including versus not including meso- the Blue Mountains Eye Study, Beaver zeaxanthin) in combination with Dam Eye Study and Rotterdam Study. co-antioxidants on visual function in patients with non-advanced age-related Retinal photography and interview macular degeneration. with comprehensive questionnaires were conducted at each visit of three The study involved 121 participants, The retinal signs of cognitive decline studies. AMD was assessed following randomly divided into two groups. the modified Wisconsin AMD grading Researchers from the Atherosclerosis (Group 1: Age-Related Eye Disease protocol. Progression to bilateral Risk in Communities (ARIC) study Study 2 formulation with a low dose [25 any (early and late) or late AMD was have found that vascular changes are mg] of zinc and an addition of 10 mg assessed among participants with associated with an increased risk for meso-zeaxanthin; n = 60). Group 2: Age- unilateral involvement only. cognitive decline and dementia. Related Eye Disease Study 2 formulation with a low dose [25 mg] of zinc; n = 61). The researchers found that, in any five- Drawing on data from a 20-year period year duration, 19–28 per cent of any among 12,313 men and women between Visual function was assessed using unilateral AMD cases became bilateral ages 50 and 73 at baseline, researchers best-corrected visual acuity, contrast and 27–68 per cent of late unilateral calculated composite cognitive scores sensitivity (CS), glare disability, AMD became bilateral. that included memory, language retinal straylight, photostress recovery and executive function/attention time, reading performance, and the The authors concluded that one in tasks. Participants were classified as National Eye Institute Visual Function four to one in five unilateral any AMD having no, mild or moderate/severe Questionnaire-25. Macular pigment cases, and up to one in two unilateral retinopathy based on the presence of was measured using customised late AMD cases progressed to bilateral microaneurysms, retinal haemorrhages, heterochromatic flicker photometry. in five years. Known AMD risk factors, or soft exudates on retinal fundus including smoking, are significantly photography at visit 3 (4–8 years after Statistically-significant improvements associated with the progression to baseline). in the primary and several secondary bilateral involvement. outcome measures were observed. Also The study authors found that all statistically significant increases in Br J Ophthalmol. Sept 2017 doi: retinopathy components, especially macular pigment at all eccentricities 10.1136/bjophthalmol-2016-309729. retinal haemorrhages, were associated were observed over time, and the with greater 20-year cognitive decline. degree of augmentation was statistically Arteriolar changes were not associated comparable between interventions. Should there be only two types of with significant 20-year cognitive diabetes? decline in fully adjusted models. The study authors concluded that According to a study published in The Estimated rates of cognitive decline supplementation with a formulation Lancet: Diabetes & Endocrinology: no. were similar between those with and that contains the macular carotenoids In fact, they propose classifying five those without diabetes mellitus and (with or without meso-zeaxanthin), types of diabetes. between blacks and whites. in combination with co-antioxidants, results in improvements in contrast In the introduction to their study, ‘Novel The authors wrote that their study’s sensitivity and other measures of visual subgroups of adult-onset diabetes findings support the exploration of function in patients with non-advanced and their association with outcomes: more sensitive measures in the eye AMD. a data-driven cluster analysis of six such as optical coherence tomography variables,’ the team of international angiography, which may provide Invest Ophthalmol Vis Sci. Oct 2017. researchers wrote that they believe that surrogate indexes of microvascular doi: 10.1167/iovs.16-21192 the two existing variations of diabetes lesions relevant to cognitive decline (type 1 and type 2) is overly simplistic. in older adults. The results also draw Progression from unilateral to They argue that ‘a refined classification attention to the importance of routine bilateral AMD could provide a powerful tool to funduscopic examinations in optometric individualise treatment regimens and clinical practices. One in four to one in five unilateral identify individuals with increased risk AMD cases progress to bilateral in Neurology. Feb 2018. doi.org/10.1212/ five years, and up to one in two late WNL.0000000000005205 unilateral AMD cases progressed to Continued page 24 24 JUNE 2018

between seven and eight per cent, change of ONSD at lateral gaze and TNoN rather than 6.5–7 per cent according to thicker retinal nerve fibre layer. the recently-released evidence-based From page 23 guidance statement from the American The researchers concluded that College of Physicians (ACP). retinal nerve fibre layer thickness can potentially be used to detect moderate- of complications at diagnosis.’ Published in March in the Annals to-severe papilloedema. A-scan of Internal Medicine, the guidance may further assist differentiation Analysing data from the records of statement was based on a search of the of mild papilloedema from 15,000 people across five patient literature for English-language national pseudopapilloedema. registries, the researchers behind guidelines that addressed HbA1c the study found that the disease can targets for type 2 diabetes in non- Optom Vis Sci. Dec 2017 doi: 10.1097/ actually be grouped into five distinct pregnant outpatient adults. OPX.0000000000001148. clusters, according to variables such as Body Mass Index (BMI), age of diagnosis Based on their review, the ACP put New guidelines for hay fever and degree of insulin resistance: forward four major recommendations for clinicians: US-based publication Annals of Cluster 1: severe autoimmune diabetes, Internal Medicine convened a work which overlaps with type 1 diabetes, Personalise goals for glycaemic control group of representatives of the and is ‘characterised by early-onset in patients with type 2 diabetes on the American Academy of Allergy, Asthma disease, relatively low BMI, poor basis of a discussion of benefits and and Immunology (AAAAI) and the metabolic control, insulin deficiency, harms of pharmacotherapy, patients’ American College of Allergy, Asthma and presence of antibodies.’ preferences, patients’ general health and Immunology (ACAAI), to provide and life expectancy, treatment burden, specific guidance on pharmacologic Cluster 2: severe insulin-deficient and costs of care. treatment for seasonal allergic rhinitis, diabetes (SIDD), which is similar to including for initial therapy. the first cluster (people were relatively Aim to achieve an HbA1c level young at diagnosis and were not between seven and eight per cent in Following a systemic review, the overweight) without the presence most patients with type 2 diabetes. workgroup made two ‘strong’ and one of antibodies. ‘People in this cluster ‘weak’ recommendations. looked for all the world like [they had] Consider deintensifying pharmacologic type 1 diabetes, but they didn’t have therapy in patients with type 2 diabetes 1. For initial treatment of seasonal “autoantibodies” that indicate type 1.’ who achieve HbA1c levels less than 6.5 allergic rhinitis in persons aged per cent. 12 years or older, monotherapy Cluster 3: severe insulin-resistant with an intranasal corticosteroid diabetes (SIRD), marked by insulin Treat patients with type 2 diabetes is preferred; combining it with an oral resistance and high BMI. (Their bodies to minimise symptoms related to antihistamine confers no additional were making insulin, but the cells were hyperglycemia and avoid targeting benefit. (Strong recommendation). not responding to it). an HbA1c level in patients with a life expectancy less than 10 years due 2. For initial treatment of seasonal Cluster 4: mild obesity-related diabetes to advanced age (80 years or older), allergic rhinitis in persons aged (MOD), characterised by obesity but not residing in a nursing home, or with 15 years or older, an intranasal by insulin resistance. other chronic conditions. corticosteroid should be chosen over a leukotriene-receptor antagonist Cluster 5: mild age-related diabetes Ann Intern Med. March 2018 doi: such as montelukast. (Strong (MARD): which is similar to diabetes 10.7326/M17-0939 recommendation). of the fourth cluster (MOD), but found in patients older than those in other 3. For treatment of moderate-to-severe A-scan and OCT to differentiate categories. The most common form of seasonal allergic rhinitis in persons papilloedema from diabetes, affecting 40 per cent of the aged 12 years or older, the clinician pseudopapilloedema people in the study. may recommend the combination of Researchers conducted a an intranasal corticosteroid and an The authors acknowledged that their retrospective cross-sectional intranasal antihistamine for initial study can’t confirm whether all five analysis on papilloedema and treatment. (Weak recommendation). clusters of diabetes have different pseudopapilloedema patients causes or whether the classifications to determine the utility of Finally, the work group suggested will change over time. Future research, A-scan ultrasound and spectral that although patients tend to prefer they suggested, is required. domain OCT retinal nerve oral medications over nasal sprays, fibre layer (RNFL) thickness in if an intranasal corticosteroid is The Lancet. March 2018 doi: 10.1016/ differentiating papilloedema from used regularly, it is the most effective S2213-8587(18)30051-2 pseudopapilloedema. medication for addressing all allergic rhinitis symptoms, with no need The study found that compared with to add an oral antihistamine. New guidelines for type 2 diabetics pseudopapilloedema, papilloedema Most patients with type 2 diabetes eyes showed larger mean optic nerve Ann Intern Med. Nov 2017 doi: should aim for an HbA1c target sheath diameter (ONSD), greater 10.7326/M17-2203 JUNE 2018 25

Looking into the future: the biological contact lens bandage

The ProKera bandage contact lens1 is discharge and swelling around her Dr Emily Glover a therapeutic device used to promote eyes. She has a previous ocular history OD healing of a damaged corneal or of microbial after sleeping in conjunctival surface.2 It is used widely her coloured contact lenses, and OS in The United States of America, with recurrent corneal erosion (REE). Clinical Resident Optometrist, FDA approval,3 to treat diseases such The Australian College of as severe dry eye, chemical injury, Optometry, Australia Clinical Findings keratitis, herpetic ulcers and recurrent corneal erosions.2 Unaided visual acuity (VA): right eye The University of Melbourne (OD) 20/60, pin-hole (PH) 20/40+ Optometry and Vision Sciences The device works by inserting a small and OS 20/200 (with bandage contact portion of amniotic membrane* onto lens), PH 20/40. Anterior slitlamp Dr J James Thimons the posterior surface of a ProKera examination revealed OS superior OD FAAO ABO conformer between two polycarbonate recurrent corneal erosion and inferior rings. This is then applied to the corneal neovascularisation. Diagnosis Chairman National Glaucoma patient’s eye, where the amniotic was a REE of the OS. A ProKera Society, USA membrane interacts with the anterior Amniotic bandage contact lens was surface to promote healing and placed on the patient’s eye. Artificial regeneration. The amniotic membrane tears as needed, both eyes and Medical Director, Ophthalmic eventually dissolves, usually in about Besivance for the left eye every night Consultants of Connecticut, USA one week, and the ProKera device can before dinner was chosen as the most be removed by the optometrist. beneficial treatment strategy.

Figure 1A-1F. Biological contact lens insertion. (Images courtesy of Bio-tissue, Inc.)

Figure 1A. Apply topical Figure 1B. The clinician Figure 1C. Ask the patient to Figure 1D. Insert the bandage Figure 1D. Gently hold the Figure 1F. Confirm centration anesthesia prepares the bandage lens for look down. The superior eyelid lens into the superior bulbar inferior eyelid surface and in- with slitlamp. Review the insertion by removal from pro- is held by the clinician. . sert the inferior portion of the patient in approximately tective packaging and rinsing bandage lens onto the ocular one week to confirm wound vigorously with sterile saline. surface. Ask patient to close healing and bandage contact The superior eyelid is held. close their eyes, allowing the lens removal. bandage to rest on the ocular surface.

The convenience and efficiency of Discussion the biological contact lens makes it desirable to use in clinical practise ProKera is an alternative treatment and has been shown to work option to increase the rate and healing successfully in managing recurrent of the corneal surface in recurrent corneal erosions. corneal erosion. This patient was slow to respond to previous treatment regimens of artificial tears, antibiotics, Case study steroids and rigid contact lenses, A 56-year old Caucasian female therefore this strategy was employed. presented at Ophthalmic Consultants Figure 2. A temporary tape-tarsorrhaphy of Connecticut for review of a An amniotic membrane is an over the lid crease, narrows the eye open- avascular, sterile, fetal membrane ing, keeps the bandage lens centered and persistent left eye (OS), minimises discomfort. Exposure may also managed with a bandage contact lens. cause undesirable thinning of the amniotic On this occasion she reported waking membrane tissue. with her ‘lids were glued shut,’ with Continued page 26 26 JUNE 2018

Figure 3A-F. Biological contact lens removal. (Images courtesy of Bio-tissue, Inc.)

Figure 3A. Apply topical Figure 3B. Pull the lower eyelid Figure 3C. Lift the lower edge Figure 3D. Ask the patient to Figure 3E. Apply gentle pres- Figure 3F. Slide the bandage anesthesia down of the bandage lens using a look down sure on the upper eyelid lens out cotton swab or blunt-tipped tweezers

expression and therefore decreasing of the eye conditions in 20 per cent Lens bandage inflammation4 and angiogenesis.2 and 30 per cent reported ocular From page 25 It is also believed that the amniotic discomfort and headache. Discomfort membrane displays antimicrobial is most likely due to the ProKera properties which is useful in polycarbonate ring, especially from found deep within the placental decreasing the chance of corneal the superior eyelid.2,5 Researchers tissues during embryological infection. suggest that the application of a softer development. It contains an ring may be a way to improve ocular epithelium, stroma and basement How the amniotic membrane provides comfort.5 membrane. The basement membrane anti-microbial defence is still a topic contains collagen, including collagen of controversy, but it is suggested that Although currently unavailable in type VII,2 which is common to the it is due to components within the Australia, the use of biologic corneal corneal basement membrane and tissue and the bandage contact lens bandage devices in the US have conjunctiva. Amniotic membranes itself acting a physical barrier between provided safe and effective healing are extracted from donors the eye and the environment.2,4 to with less scarring and undergoing caesarean delivery and inflammation, less pain and improved are analysed for any transmissible Implantation of the ProKera from a clinical outcomes. diseases and treated with broad- donor to recipient does not mount an spectrum antibiotics prior to ocular immune response as it lacks major ProKera offers clinicians a safe and application.2 histocompatibility antigens HLA-A, effective alternative approach to B and/or DR.2,4 Despite this, with manage ocular surface disorders such When applied to the cornea, the inefficient sterilising of the amniotic as RCE. It may be useful for patients amniotic membrane – either cryogenic membrane prior, there is still a with chronic eye diseases where or dehydrated – interacts with the possibility of transmitting a viral or traditional therapeutic approaches are surface to promote epithelial growth bacterial infection to the host if the not enough. through cell migration, differentiation donor amniotic membrane is not and adhesion to the ocular surface.2,4 accurately screened or stored correctly.4 1. ProKera [Internet]. Miami: Bio-Tissue; 2016 [cited on 2017 Nov 30]. Availa- It also promotes limbal stem cell ble from: http://www.biotissue.com/ regeneration and repair of the corneal In 2009, a study investigated the safety patients/our-products/patients-prokera. epithelium. and efficacy of ProKera for patients aspx. 2. Mcgaughy AG, Gupta PK. In-Office Use with anterior eye disease. Out of the of Amniotic Membrane. Fekrat S, Scott The stromal portion of the amniotic twenty participants (twenty eyes), IU (eds.). American Academy of Oph- 60 per cent recovered visual acuity thalmology. 2015. [cited on 2017 Nov membrane contains hyaluronic 30]. Available from: https://www.aao. acid which is effective in inhibiting over an average of twenty-five days. org/eyenet/article/in-office-use-of-amni- fibroblast growth, decreasing cytokine Possible side effects were recurrence otic-membrane 3. Department of Health & Human Ser- vices. 510(k) SUMMARY ProKeraT M Bio-Tissue, Inc. [Internet]. Washington: U.S. Food and Drug Administration; 2003 Dec 12 [cited 2017 Nov 30]. Avail- able from: https://www.accessdata.fda. gov/cdrh_docs/pdf3/k032104.pdf. 4. Malhotra C, Jain AK. Human Amniotic Membrane Transplantation: Different Modalities of its use in Ophthalmology. World J Transplant 2014: 4; 111-121. 5. Pachigolla G, Prasher P, Di Pascuale MA, et al. Evaluation of the role of ProKera in the management of ocular surface and orbital disorders. Eye Con- tact Lens 2009; 35: 172-175.

*Amniotic membranes currently do not have widespread, private practice, commercial availability in Australia compared with the USA. Access in some states is via the cornea Figure 4. Biological contact lens in place. (Image courtesy of Bio-tissue, Inc.) bank or major eye hospitals. JUNE 2018 27

A new glaucoma treatment Latanoprostene bunod and the trabecular meshwork

In 1977, Murad found that it was, in Latanoprostene bunod Professor Leo Semes fact, NO release that accounts for the A new focus for the management of OD FAAO vasodilatory effect of nitroglycerin glaucoma has become the trabecular and related compounds.6,7 NO is meshwork. The hypothesis is also a biologically active molecule at that impaired aqueous drainage School of Optometry the cellular level during metabolic is the initiation of the cascade of University of Alabama at processes. The discovery of exogenous glaucomatous damage. It is thought that Birmingham, USA NO’s vasodilatory effect raised, for this then results in increased intraocular the first time, the question about pressure. While this hypothesis appears endogenous NO’s potential role in contrary to much of the conventional cardiovascular physiology. concept of glaucoma, the primary risk factor for glaucoma remains elevated Lowering intraocular pressure (IOP) Several years later, while studying IOP. In fact, the only means to minimise has been the mainstay of glaucoma vasodilation in response to glaucomatous damage is to reduce and management acetylcholine, Robert Furchgott that primary risk factor. The 2015 for decades. The Centre for Eye observed that, in the absence of the version of the American Academy of Health recommends beginning with endothelial lining, the smooth muscle Ophthalmology’s Preferred Practice the simplest topical strategy, a cells of vessels were unable to relax in Pattern does not even include elevated prostaglandin analogue (PGA) or beta- response to acetylcholine.8 IOP as part of the definition.12 This blocker (BB).1 This recommendation leads to newer thinking, suggesting follows setting a target pressure based He postulated that some substance that there may be some non-IOP related on a number of clinical findings that produced by the endothelium was insult that occurs to raise IOP. This is are beyond the scope of this article. required for the relaxation of vessels, what has pinpointed the trabecular setting off an intense search to meshwork as that potential site and Four specific PGAs are available for identify this substance, known then as has brought about the development of use by optometrists in Australia. endothelium-derived relaxing factor latanoprostene bunod. Latanoprost became commercially- (EDRF). This designation remained for available over 20 years ago. An the rest of the decade. Development of the specific molecule emerging chemical modification of included clinical trials that resulted in the latanoprost molecule includes the In 1987, nearly a decade after the FDA-approval in the United States. The addition of a nitric-oxide (NO) moiety. elucidation of NO’s role in nitrate- mechanism of action to lower IOP for Vyzulta (latanaprostene bunod 0.024% induced vasodilation, Moncada and latanoprost is well known as enhancing ophthalmic solution) was approved by Ignarro discovered independently uveoscleral outflow.13 Addition of the the US Food and Drug Administration that NO is in fact the mystery EDRF NO moiety to the latanoprost chain is in November 2017.2 The mechanism that had long been sought after thought to bolster IOP reduction by and site of action are both interesting by researchers.9,10 To honour their two means. First, enlarging pores of the and will be detailed below. pioneering work ‘concerning nitric trabecular meshwork as well as activity oxide as a signaling molecule in at the endothelial-cell level of the the cardiovascular system’, the trabecular vasculature to enhance blood NO 1998 Nobel Prize in Physiology of flow.2,14 These combined actions are Nitric oxide (NO) was named ‘molecule Medicine was awarded to Furchgott, thought to be responsible for enhanced of the year’ in 1992.3 Its history, Ignarro, and Murad.11 The discovery IOP-lowering compared to latanoprost however, begins well over 200 years of endothelial-cell-derived NO’s alone.15 earlier. NO was discovered in the critical role in vasodilation marked a 1770s by Joseph Priestly, in England.4 major advancement in the history of The side-effect profile of latanoprostene Until the culmination of research into physiology. bunod is similar to that of the NO’s capacity for vasodilation, it was latanoprost formulation alone. These regarded as a reactive free radical and Thereafter, researchers began to explore include predominantly reversible air pollutant. Although nitroglycerin the messenger molecule’s functions growth and largely permanent was synthesised and found to have a beyond the vessel wall, and they soon increased and periocular vasodilatory effect in the 1840s, and, by recognised that NO was a remarkably pigmentation.2 The adverse events the 1870s, had been widely used along versatile messenger playing a complex reported from the initial clinical with related nitrate compounds to treat role in physiological activities of trials are also familiar—conjunctival patients with angina and hypertension, multiple human body systems.3 hyperemia, eye irritation and pain and no one connected these chemicals’ This then became the focus of the effects on vascular tissues with NO for application of NO-donating compounds the next century.5 in glaucoma management. Continued page 28 28 JUNE 2018

Glaucoma From page 27 pain at the instillation site.2,16,17 These occurred at rates greater than two per cent but all were observed to occur in fewer than 10 per cent of patients enrolled in the clinical trials.

Non-IOP related factors continue to emerge as components of the glaucoma risk spectrum. Looking to the future, we may find ourselves investigating blood flow to the optic nerve, inner retina and perhaps even the trabecular meshwork. These directions may also include the larger sphere of systemic blood flow Figure 1. Latanoprost acid works within the uveoscleral pathway to increase aqueous humor as well as such extrinsic factors such outflow. Butanediol mononitrate releases NO to increase outflow through the trabecular mesh- as cerebrospinal fluid pressure.18 We work and Schlemm’s canal. (Image courtesy of B+L) have known that systemic absorption of topically applied medications has systemic implications. Specifically, the beta-blockers slow heart rate and have 1977; 74: 3203–3207. al. Latanoprostene bunod 0.024% versus the potential for significant adverse 7. Katsuki S, Arnold W, Mittal C, et al. Stim- timolol maleate 0.5% in subjects with 19,22 ulation of guanylate cyclase by sodium open-angle glaucoma or ocular hyper- pulmonary effects. So we should nitroprusside, nitroglycerin and nitric tension: the APOLLO study. Ophthal- exercise caution in those scenarios oxide in various tissue preparations mology 2016; 123: 965–973. and recognise that these effects can be and comparison to the effects of sodium 17. Medeiros FA, Martin KR, Peace J, et al. 23,24 azide and hydroxylamine. J Cyclic Nu- Comparison of latanoprostene bunod identified and minimised. Newer cleotide Res 1977; 3: 23–35. 0.024% and timolol maleate 0.5% in compounds such as latanoprostene 8. Furchgott RF, Zawadski JV. The obligatory open-angle glaucoma or ocular hyper- bunod may offer alternatives. role of endothelial cells in the relaxation tension: the LUNAR study. Am J Oph- of arterial smooth muscle to acetylcho- thalmol 2016; 168: 250–259. line. Nature 1980; 288: 373–376. 18. Charters, Lynda. Ocular perfusion pres- The prevalence of glaucoma continues 9. Palmer RM, Ferrige AG, Moncada S. sure, cerebrospinal fluid pressure: New to be underestimated. In fact, a greater Nitric oxide release accounts for the players in glaucoma. Ophthalmology biological activity of endothelium-de- Times [Internet]. 2017 Dec [Cited 2017 proportion of high-risk patients may be rived relaxing factor. Nature 1987; 327: Dec 10]. Available from: http://oph- overlooked than previously thought.25 524–526. thalmologytimes.modernmedicine.com/ 10. Ignarro LJ, Byrns RE, Buga GM, et al. En- ophthalmologytimes/news/ocular-perfu- dothelium-derived relaxing factor from sion-pressure-cerebrospinal-fluid-pres- As optometrists on the front line pulmonary artery and vein possesses sure-new-players-glaucoma. of primary eye care, we can work pharmacologic and chemical properties 19. Nieminen T, Lehtimäki T, Mäenpää J, et identical to those of nitric oxide radical. al. Ophthalmic timolol: plasma concen- together to lessen the vision- and Circ Res 1987; 61: 866–879. tration and systemic cardiopulmonary sight-threatening burden of glaucoma. 11 The Nobel Prize in Physiology or Med- effects. Scand J Clin Lab Invest 2007; 67: Now we will have new weapons in that icine 1998. [Internet]. [Cited 2017 Dec 237–245. 15]. https://www.nobelprize.org/nobel_ 20. Uusitalo H, Niño J, Tahvanainen K, et fight. prizes/medicine/laureates/1998/ al. Efficacy and systemic side-effects of 12. Primary Open-Angle Glaucoma Suspect topical 0.5% timolol aqueous solution 1. Chair-side Reference: Glaucoma Med- Preferred Practice Pattern [Internet]. and 0.1% timolol hydrogel. Acta Oph- ications for Optometrists. Centre for American Academy of Ophthalmology thalmol Scand 2005; 83: 723–728 Eye Health [Internet]. [Cited 2017 Dec Preferred Practice Pattern Glaucoma 21. Gandolfi SA, Chetta A, Cimino L, et al. 9]. Available from: https://centrefo- Panel. [Internet]. [Cited 2017 Dec Bronchial reactivity in healthy indi- reyehealth.com.au/wp-content/up- 15]. Available from: https://www. viduals undergoing long-term topical loads/2016/09/chairside_reference_glau- aao.org/preferred-practice-pattern/ treatment with beta-blockers. Arch coma_treat.pdf primary-open-angle-glaucoma-sus- Ophthalmol 2005; 123: 35–38. 2. vyzulta.com [Internet] Bausch & Lomb In- pect-ppp-update-201 22. Inan UU, Ermis SS, Orman A, et al. The corporated. [Cited 2017 Dec 9]. Available 13. Digiuni M, Fogagnolo P, Rossetti L. A comparative cardiovascular, pulmonary, from: http://www.vyzulta.com/hcp/ review of the use of latanoprost for ocular blood flow, and ocular hypoten- 3. Culotta E, Koshland DE Jr. NO news is glaucoma since its launch. Expert Opin sive effects of topical travoprost, bimato- good news. Science 1992; 258: 1862– Pharmacother 2012; 13: 723–745. doi: prost, brimonidine, and betaxolol. J Ocul 1865. 10.1517/14656566.2012.662219. Pharmacol Ther 2004; 20: 293–310. 4. Steinhorn BS, Loscalzo J, Michel T. Nitro- 14. Semes, L. Nitric oxide: Historic perspec- 23. Snape JP, Waldock A. Spirometry for pa- glycerin and Nitric Oxide-A Rondo of tive and recent developments. In, Tsai tients prescribed topical beta-blockers. Themes in Cardiovascular Therapeutics. JC, Gray MJ, Cavallerano AC, Nitric Ox- Nurs Stand 2000; 15: 35–38. N Engl J Med 2015; 373: 277–280. ide in glaucoma: What clinicians need to 24. Hepsen IF, Yildirim Z, Yilmaz H, et al. 5. Murrell W. Nitro-glycerine as a remedy know. Candeo Clinical/Science Commu- Preventive effect of lacrimal occlusion for angina pectoris. Lancet. 1879; 80-81: nications. White Plains, NY; 2017. on topical timolol-induced bronchoc- 113–115; 151-152; 225-227. http://www. 15. Weinreb RN, Ong T, Scassellati SB, et al. onstriction in asthmatics. Clin Exp thelancet.com/journals/lancet/issue/vol- A randomised, controlled comparison Ophthalmol 2004; 32: 597–602. 113no2890/PIIS0140-6736(00)X8912-X] of latanoprostene bunod and latano- 25. Waisbourd M, Pruzan NL, Johnson D, et 6. Arnold WP, Mittal CK, Katsuki S, et al. prost 0.005% in the treatment of ocular al. The Philadelphia Glaucoma Detec- Nitric oxide activates guanylate cyclase hypertension and open angle glaucoma: tion and Treatment Project: Detection and increases guanosine 3’:5’-cyclic the VOYAGER study. Br J Ophthalmol Rates and Initial Management. Oph- monophosphate levels in various tissue 2015; 99: 738–745. thalmology 2016; 123: 1667–1674. doi: preparations. Proc Natl Acad Sci USA 16. Weinreb RN, Sforzolini BS, Vittitow J, et 10.1016/j.ophtha.2016.04.031. Vision Australia. Your partners in the circle of care.

When is the best time to refer to us?

Diagnosis of a permanent, 1 non-correctible or progressive eye condition. or

Visual Acuity is 6/24 or less (BCVA/BEO) or Visual Fields 2 of 30 degrees or less with both eyes open (BEO). or

Vision impairment is 3 putting your patient at risk. or

Support adjusting to vision 4 impairment is needed.

At Vision Australia we work together with optometrists to ensure the best outcomes for people who are blind or have low vision. With 28 locations around Australia, it’s easy to refer to us. Just visit visionaustralia.org or call 1300 84 74 66.

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