Ophthalmology Flashcards
What is the name for transparent conjunctival swelling shown inferior to the cornea in fig.1?
Answer = Chemosis
Chemosis is evident inferior to the cornea. Conjunctival chemoses is due to subconjunctival fluid, reflecting gross conjunctival inflammation, often allergic in origin.
Ectropion describes an outturned eyelid, usually of the lower eyelid and usually age-related. When the lower eyelid is turned out, the exposed tarsal conjunctiva becomes injected, and as the punctum is no longer flush with the globe, tears cannot find their way to the normal tear drainage apparatus and thus run down the cheek.
A hyphaema is a collection of red blood in the anterior chamber, between cornea and iris, which can follow blunt trauma and which requires ophthalmic assessment.
A hypopyon is a collection of white pus in the anterior chamber, between cornea and iris, which should be assumed to indicate endophthalmitis, which can follow cataract surgery or intravitreal injection, and which requires immediate ophthalmic assessment.
Keratitis is the general word for ‘corneal inflammation’, which usually is infection, either bacterial (less common but must be recognised), or herpes simplex (which would get worse if topical steroids are mistakenly given).
If the eye shown is proptotic, and the proptosis is pulsatile with an audible bruit, what diagnosis do you suspect?
These memorable but unusual signs are characteristic of a carotico-cavernous fistula, which can be direct (after trauma, and tends to be ‘high flow’ in which signs are marked), or indirect (occurring spontaneously, which tend to be low flow, with less marked signs).
Its important to remember however that thyroid eye disease (TED) is the most common cause of unilateral or bilateral proptosis. TED can be associated with hyperthyroidism (people tend to remember proptosis as occurring in Graves disease), but also with hypothyroidism. Watch for diplopia (vertical initially as the inferior rectus becomes inflammed and thus restricted), but also for the vision threatening optic neuropathy. In fact as the orbital tissue becomes inflammed and the optic nerve potentially compressed, proptosis is to an extent, protective by decompressing the orbit slightly.
An orbital haemorrhage is usually a sudden event with an obvious cause, like trauma, and ophthalmology trainees should know how to perform an emergency lateral canthotomy to relieve the associated orbital pressure.
Orbital space occupying lesions, such as metastases or a lymphoma, are less common, but which ophthalmologists should be aware of in their differential diagnosis of proptosis.
An 80 year old man has sudden and complete loss of vision in his right eye. The fundal appearance is shown in figure 1.
Which of the following is the most likely diagnosis?
Age-related macular degeneration
Anterior ischaemic optic neuropathy
Central retinal artery occlusion
Central retinal vein occlusion
Retinal detachment
The patient has a central retinal artery occlusion (CRAO). This causes sudden painless loss of vision as an embolus blocks the central retinal artery. For a few days, because the retina is suddenly and completely deprived of blood it becomes pale and swollen looking, in and around the macula, except for the fovea at which there aren’t enough retinal layers to become noticeably swollen. Thus the fovea retains its normal colour, which merely stands out, as a ‘cherry red spot’, in relation to the surrounding pallor.
This case has one unusual feature: a reddish wedge of normal retina from the optic disc’s temporal edge to the edge of the fovea. This is normally perfused retina. Why is it normally perfused if a central retinal artery occlusion has occurred? This patient is lucky enough to have a cilioretinal artery supplying this part of the retina, which up to 20% of the population happen to have. The cilioretinal artery arises from the short posterior ciliary artery rather than the central retinal artery. As the cilioretinal artery is unaffected by the CRAO and supplies a small area of retina adjacent to the optic disc, the patient will have a small area of vision that is preserved. This is interesting, but the essential matter for medical students is to recognise the central retinal retinal artery occlusion.
Treatment for CRAO is usually ineffective, but if the patient presents within 24 hours of loss of vision, and certainly within 6 hours, treatment is worth trying. Vigorous ocular massage will cause large fluctuations in intraocular pressure, and is done with the hope this will dislodge the embolus and cause it to pass further down the retinal arterial tree. Similarly drastically reducing the intraocular pressure by an anterior chamber paracentesis (draining some aqueous humour out of the eye) or by giving intravenous Diamox, may have the same effect.
Which investigation would be most appropriate for visual loss?
Visual fields
Carotid doppler scan
Fluorescein angiography
Ocular ultrasound
CT head
A CRAO must be followed up in the same way a stroke or transient ischaemic attack would be. Remember ‘amaurosis fugax’ is when a clot blocks the central retinal artery, thus vision is completely suddenly painlessly lost in the eye, but within an hour the clot passes on and the vision returns to normal. Thus if vision is lost transiently (migraine can usually be diagnosed from a detailed history), if amaurosis is suspected, follow up as for CRAOs.
Following a CRAO (or amaurosis) a ‘cardiovascular workup’ is appropriate. As part of this, the source of the embolus should be sought, and most often this will be carotid atherosclerosis. Atrial fibrillation, and less commonly heart valve problems would be considered too, depending on the clinical setting. Also its vital to exclude giant cell (temporal) arteritis (GCA), as occasionally temporal arteritis can present with CRAO. Thus a history seeking symptoms of GCA, and ESR and CRP are all essential too.
CT head may be done in due course, to seek evidence of small vessel disease for example, but the other investigations – visual fields, fluorescein angiography and ocular ultrasound, would be uninformative.
A man attended for a Diabetic Eye Screening Programme check. His fundal photo is shown in figure 1.
Which of the following options is correct:
Diabetic macular ischaemia
Diabetic macular oedema
Non-proliferative diabetic retinopathy
Normal fundus
Proliferative diabetic retinopathy
This is a colour photograph of the right eye. The fundal appearances are normal – never be afraid to state this if this is what you think!
While there is no evidence of diabetic retinopathy in this image, a normal fundus does not exclude diabetes. Conversely, up to 20% of people have fundal signs (such as micro aneurysms) at the time of diagnosis of their type II diabetes.
Diabetic macular oedema cannot be appreciated on a 2 dimensional photo, unless there are exudates in the macula. Exudates suggest there ‘is or has been’ fluid. An OCT is the ideal tool to detect macular oedema. Diabetic macular ischaemia has no fundal signs, but might be suspected in someone with diabetes and unexplained poor vision, for example difficulties reading (suggesting a macular problem), i.e. in the absence of diabetic macular oedema.
Which of the following are risk factors for progression of diabetic retinopathy?
Lack of exercise
Not getting an annual eye examination
Poor control of blood pressure
Poor glycemic control
Pregnancy
Its important to ask every patient with diabetes you meet about these risk factors. Good glycaemic and blood pressure control can be difficult, but each are independently important. In pregnancy, diabetic retinopathy can accelerate, and more frequent eye checks are appropriate.
In general, every patient with diabetes should have an annual eye check, and arguably the single most important question you can ask someone with diabetes is ‘Have you had your eyes checked in the last year?’. Most people with diabetes have this annual check through the diabetic eye screening service, but some choose to attend their optician, and this is fine as long as they do so faithfully. Some don’t need to attend screening as they already attend hospital eye clinics. However some don’t have an annual eye check anywhere, and these are probably the people who are hardest to reach, but who most need a check.
Lifestyle factors are probably important both for slowing microvascular and certainly macrovascular complications of diabetes: exercise, weight, dietary factors are crucial and not smoking.
Another patient was referred to the eye clinic by the diabetic retinopathy screening service (fig. 2). What treatment is needed? More than one choice may be correct.
Cataract surgery
Intravitreal anti-VEGFs
Intravitreal steroids
Macular laser
Pan retinal laser photocoagulation
This patient has retinal neovascularisation, and thus has proliferative diabetic retinopathy. The treatment for this is pan retinal laser photocoagulation (PRP), done to induce regression of the new vessels before they bleed (or bleed again) causing vitreous haemorrhage.
Just for interest, intravitreal injections of anti-VEGFs (or occasionally intravitreal dexamethasone) are the treatment for diabetic macular oedema, not proliferative diabetic retinopathy. (The potential role in future of anti-VEGFs in the management of proliferative diabetic retinopathy is debated as new evidence emerges. Intravitreal anti-VEGFs are sometimes used pre-operatively, if surgery is planned to relieve tractional retinal detachment for example that is occasionally seen in advanced diabetic retinopathy).
Again for interest, macular laser rarely is used in diabetic eye disease, for example for extrafoveal diabetic macular oedema if intravitreal injections aren’t appropriate, for example if someone has a documented allergy to the drugs, or perhaps an extreme needle phobia.
A 25 year old male had gradual deterioration in vision and difficulty driving at night affecting both eyes. His optician was unable to easily visualise his fundi even after dilation.
What are the differential diagnoses for a poor fundal view? More than one answer may be correct.
Age-related macular degeneration
Cataract
Corneal scar
Squint
Vitreous haemorrhage
Cataracts, vitreous haemorrhage, and less commonly corneal scars, each reduce clarity of the ocular media, and thus impair the patient’s view looking out, and the view on examination of someone trying to look in to visualise the fundus.
Age-related macular degeneration (AMD) has three major risk factors: age, smoking, and family history. AMD produces central visual loss, but peripheral vision remains intact, and night vision is not specifically affected. The ocular media remain clear, so the fundus can be visualised. Also this patient is 25 years old!
Squint is an answer. An eye with a constant squint in childhood may lose its visual potential (i.e. is one of the causes of amblyopia). However poor vision due to amblyopia does not gradually worsen after childhood, and does not specifically affect night vision, or the clarity of ocular media (and consequent ability to visualise the fundus).
A common cause of uncertainty in medical students: amblyopia. Ambylopia is poor vision in an eye due to something preventing a clear retinal image being formed in childhood. The eye is anatomically normal, but vision is poor. The degree of visual impairment in amblyopia varies greatly, from almost normal (e.g. 6/9) to very poor (e.g Hand Movements). The most common causes are uncorrected hypermetropia, and constant squint.
A 25 year old male had gradual deterioration in vision and difficulty driving at night affecting both eyes. His optician was unable to easily visualise his fundi even after dilation.
On examination he has cataracts. Which four of the following are associated with cataracts?
Diabetes
Down’s syndrome
Hypertension
Retinitis pigmentosa
Steroids
Cataract causes loss of transparency within the natural lens of the eye, and may produce blurred vision and glare (e.g with oncoming car headlights).
Less than 1% of individuals are born with cataracts, with a variety of causes including being inherited or secondary to an infection in-utero. However most cataracts occur in adult life, and senile cataracts (i.e. simply age-related) account for the vast majority.
Important causes of pre senile cataract (i.e. not simply age-related) include steroids (in any form, from topical to oral to intravenous – cataract development is dose and duration related), uveitis (for which steroids are often needed), diabetes mellitus, high myopia and significant trauma. Cataracts may also occur in association with Down’s syndrome and retinitis pigmentosa.
A 25 year old male had gradual deterioration in vision and difficulty driving at night affecting both eyes. His optician was unable to easily visualise his fundi even after dilation.
He was referred to an ophthalmologist who performed dilated fundoscopy, shown in figure 1. Which three of the following features are present on fundoscopy?
Arteriolar attenuation
Bone–spicule pigmentation of the retina
Retinal detachment
Retinal neovascularisation
Temporal optic disc pallor
In this image, the optic disc rim is pale on the temporal side. There is attenuation of the retinal arteries and bone–spicule pigmentation of the peripheral retina. Even if unsure of the significant of the signs, remember to start with describing what the signs look like: work through ‘colour, contour and cupping’ for the disc, and you could mention lines and patterns of black lines in the retinal periphery, for example.
Retinal detachments typically present with a shadow in one eye, gradually progressing from the edge of vision across the visual field of the affected eye, after days affecting the whole visual field. The appearance is like that of wallpaper peeling off a wall, as the neural retina gradually separates from the underlying retinal pigment epithelium. The most common cause is the normal process of posterior vitreous detachment (pvd). PVD is worth knowing about as cases of ‘flashes and floaters’ present every day to any Eye Casualty. In pvd, the vitreous collapses in on itself, causing new floaters (which remain for life) and flashes (occurring as the collapsing vitreous pulls on the retina, and which should stop when the vitreous finally separates from the retina). Usually pvd occurs without complication. Occasionally the vitreous traction on the retina is enough to pull a tear in the retina. This allows fluid in through the tear, underneath the retina, and hence the retinal detachment begins.
Retinal neovascularisation is the process of new blood vessel formation, occurring most commonly in diabetic retinopathy (defining the proliferative phase of diabetic retinopathy). It is usually secondary to retinal ischaemia and the production of excess vascular endothelial growth factor (VEGF). These new vessels are prone to bleeding – into the vitreous. Vitreous haemorrhage presents with a sudden painless onset of floaters in the vision, often enough floaters over 10 to 20 minutes to obscure the vision completely. Effectively its like a liquid bruise. It usually settles over weeks and months, gradually clearing over weeks and months allowing the patient to see out and the ophthalmologist to see in.
A 25 year old male had gradual deterioration in vision and difficulty driving at night affecting both eyes. His optician was unable to easily visualise his fundi even after dilation.
Diabetic maculopathy
Papilloedema
Primary open angle glaucoma
Proliferative diabetic retinopathy
Retinitis pigmentosa
Retinitis pigmentosa is characterised by the following clinical triad: ‘arteriolar attenuation, bone–spicule peripheral retinal pigmentation and waxy optic disc pallor’. Although the appearance is characteristic and striking, and the condition interesting for clinicians and importantly it is impactful for families affected, its probably not a condition most medical students would be expected to be familiar with.
Diabetes can cause a) retinopathy (i.e changes in the retinal periphery) and b) maculopathy (i.e. changes in the macula): both retinopathy and maculopathy usually coexist and the signs overlap. Non-proliferative diabetic retinopathy (NPDR) causes dot and blot haemorrhages and with time, cotton wool spots, and then can progress in some cases to proliferative DR characterised by new vessel formation (neovascularisation) at the optic disc, or elsewhere. In diabetic maculopathy dot and blot haemorrhages are seen in the macula, and in some cases exudates, the presence of which suggests macular oedema.
Primary open angle glaucoma causes increase in the cup to disc ratio: over 0.6 is probably glaucoma, while 0.6 or less is probably normal, as a general rule of thumb.
If the optic disc contour is indistinct, or blurry, then the optic disc is swollen. There are many causes for this, such as optic neuritis (in a younger patient with multiple sclerosis for example), anterior ischaemic optic neuropathy (including temporal arteritis, never to be missed), papilloedema (which means optic disc swelling specific to raised intraocular pressure) and severely raised blood pressure.
A 25 year old male had gradual deterioration in vision and difficulty driving at night affecting both eyes. His optician was unable to easily visualise his fundi even after dilation.
Diplopia
Family history
Night blindness
Retinoblastoma
Visual field defect
Features of retinitis pigmentosa include night blindness (nyctalopia) and loss of peripheral vision (tunnel vision may be detected using confrontational visual field techniques). Both eyes are usually affected and there are three possible patterns of inheritance:
Autosomal recessive
Autosomal dominant
X–linked recessive.
The recessive forms occur earlier in life and are usually more visually debilitating. X–linked recessive forms will have female carriers and affected males in their pedigree.
Retinoblastomas are malignant retinal tumours that present in childhood. There is no association between retinoblastoma and retinitis pigmentosa.
Retinitis pigmentosa does not affect eye movements and so it is not associated with diplopia (double vision).
