Important eye presentations Flashcards
Painful loss of vision
Trauma: corneal foreign body, corneal abrasion, traumatic hyphaema, penetrating injury, globe rupture. Corneal ulcer. Herpes simplex keratitis. Anterior uveitis. Endophthalmitis. Scleritis. Giant cell arteritis.
Acute painless loss of vision
Vitreous haemorrhage.
Wet age-related macular degeneration.
Central or branch retinal vein occlusion.
Central or branch retinal artery occlusion.
Anterior ischaemic optic neuropathy.
Temporal arteritis or giant cell arteritis.
Retinal detachment
Acute painless loss of vision: vitreous haemorrhage
Impaired or no fundal view, ± reduced red reflex.
Causes: retinal detachment, diabetic retinopathy.
Acute painless loss of vision: central or branch retinal vein occlusion
Widespread or hemispheric retinal haemorrhages, ± cotton wool spots, exudates, disc swelling, macular oedema.
Common causes: hypertension, diabetes, hyperlipidaemia.
Other causes: vasculitis (e.g. Behçet’s, sarcoidosis, SLE), clotting disorders (e.g. protein S or C deficiency, antiphospholipid syndrome) multiple myeloma, glaucoma.
Acute painless loss of vision: central or branch retinal artery occlusion
Sudden loss of vision, may have symptoms of GCA, 10% of patients have preceding amaurosis fugax.
Pale retina, cherry red spot, retinal vessel emboli.
Causes: atherosclerotic (hypertension, diabetes, smoking, hyperlipidaemia), embolic (carotid/aortic artery disease, cardiac valve disease), haematological (protein C deficiency, antiphospholipid syndrome, lymphoma, leukaemia), inflammatory (GCA, SLE, polyarteritis nodes, Wegener’s granulomatosis), other (oral contraceptive, trauma, migraine).
Acute painless loss of vision: anterior ischaemic optic neuropathy
May be arteritic (temporal arteritis or GCA) or non-arteritic (hypertension, diabetes, anaemia, smoking, hyperlipidaemia).
Acute painless loss of vision: temporal arteritis or giant cell arteritis
Headache, scalp tenderness, jaw claudication, neck pain, fever, malaise, joint pains.
Tender, non-pulsatile temporal artery, relative afferent pupillary defect, swollen optic disc, ± central retinal arterial occlusion, ± cranial nerve palsies.
Acute painless loss of vision: retinal detachment
Floaters, flashing lights, loss of vision/visual field defect.
Ocular risk factors: history of trauma, cataract surgery, myopia.
Systemic risk factors: Stickler syndrome, Marfan’s syndrome, Ehlers-Danlos syndrome.
Hypertensive retinopathy
Findings depend on classification grade of retinopathy.
Focal/generalised arteriolar constriction and straightening.
Arteriosclerosis leading to changes at arteriovenous crossing points: AV nipping or nicking and silver-wiring of retinal arterioles.
Microaneurysms.
Cotton wool spots indicating ischaemia.
Retinal haemorrhages, usually flame shaped.
Exudate, often in macular star pattern.
Arterial macroaneurysms.
Disc oedema.
Tortuous vessels in malignant hypertension.
Diabetic retinopathy: pathogenesis
Microangiopathy primarily affecting pre-capillary arterioles, capillaries, and post-capillary venules.
There is loss of pericytes, damage to the vascular endothelial cells, deformation of red blood cells with increased aggregation leading to microvascular occlusion and leakage.
Diabetic retinopathy: clinical features
Fundus findings are usually bilateral and broadly symmetrical.
Abnormalities depend on the severity of the disease.
Microaneurysms.
Dot and blot haemorrhages.
Lipid exudates.
Venous beading.
Intraretinal microvascular abnormalities.
Cotton wool spots.
New vessels at the disc or elsewhere.
Tractional retinal detachment.
Macular oedema and thickening (diabetic maculopathy).
Glaucoma: overview
Glaucoma is an optic neuropathy associated with raised intraocular pressures leading to irreversible optic nerve damage.
It is usually asymptomatic and is often detected incidentally, but can lead to blindness.
Glaucoma: applied physiology
Aqueous humour is produced by the ciliary body and mainly drained through the trabecular meshwork but there is also drainage through uveoscleral routes.
Normal intraocular pressure = 8-21mmHg.
Glaucoma: primary angle closure
Narrowing of the anterior chamber drainage angle prevents aqueous fluid outflow resulting in increased intraocular pressure.
Acute: classically a red, painful eye, hazy cornea due to oedema, fixed mid-dilated oval pupil, reduced vision, headache, nausea and vomiting.
Chronic/subacute: may give a history of haloes around lights at night.
Glaucoma: primary open angle
Aqueous fluid outflow is reduced despite anterior chamber angle remaining open.
Most common form of glaucoma in patients >50 years.
Risk factors: increased IOP, reduced central corneal thickness, Afro-Caribbean origin, increased age, affects 1st degree relative, hypertension, diabetes, myopia.