OPH - Retinal Conditions Flashcards

1
Q

Posterior Vitreous Detachment

Vitreous Body
Pathophysiology
Clinical Features
Management

A
  1. ) Vitreous Body - maintains structure of the eyeball
    - holds the retina in place and supports the lens and
    - contains gel: made up of water (99%) and collagen
  2. ) Pathophysiology - vitreous detaches from the retina
    - very common in the elderly (part of ageing process)
    - ↑age –> vitreous body becomes less firm and unable to maintain its shape causing fluid to fill between the potential space between the retina and the vitreous
    - other risk factors: eye trauma, myopia, diabetes
  3. ) Clinical Features - can be asymptomatic or:
    - painless, dark spots of vision loss
    - photopsia (in peripheral vision)
    - floaters (on temporal side of the central vision), moves with eye movements, there constantly
  4. ) Management - no treatment is necessary
    - sx improve overtime as the brain adjusts
    - complications: retinal tears, retinal detachment, vitreous haemorrhage
    - fundoscopy/ocular ultrasound/OCT: to assess the risk of a retinal tear or detachment
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2
Q

Retinal Detachment

Pathophysiology
Risk Factors
Clinical Features
Management

A
  1. ) Pathophysiology - separation of the neural retina from the retinal pigment epithelium (RPE)/choroid)
    - often due to a retinal tear which allows vitreous fluid to enter the space between the retina and the choroid
    - outer retina receives blood supply from the choroid making detachment a sight-threatening emergency
  2. ) Risk Factors
    - ↑age, FH, diabetic retinopathy, myopia
    - eye trauma (rhegmatogenous retinal detachment)
    - posterior vitreous detachment, retinal malignancy
  3. ) Clinical Features - sudden painless loss of vision w/:
    - floaters and flashing lights (spiderweb-like)
    - dense shadow starting peripherally and progressing centrally
    - floaters do not move with eye movements
    - ↓visual acuity, blurred/distorted vision
    - visual field impairment depending on the area
    - straight lines can often appear irregular or curved due to the retina sagging away from the choroid
    - may have absent red (fundal) reflex
  4. ) Management - ophthalmological emergency
    - permanent blindness if progresses to the macula
    - fundoscopy/ocular ultrasound/OCT: for imaging
    - requires surgery to reattach the retina and fix any retinal tears
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3
Q

Surgical Methods for Retinal Detachment

Vitrectomy
Scleral Buckling
Pneumatic Retinopexy
Management of Retinal Tears

A
  1. ) Vitrectomy - removing the relevant parts of the vitreous body and replacing it with oil or gas
    - safest and most common procedure
  2. ) Scleral Buckling - use a silicone “buckle” to apply pressure on the sclera so the outer eye indents
    - this brings the choroid into contact w/ the retina
    - used in younger patients (30s) and in patients that do not have posterior vitreous detachment
  3. ) Pneumatic Retinopexy - inject gas bubble into the vitreous body to create pressure flattening the retina
    - dangerous outdated method, rarely used
  4. ) Management of Retinal Tears - create adehsions between retina and choroid to prevent detachment
    - can be done using laser therapy or cryotherapy
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4
Q

Retinal Vein Occlusion

Pathophysiology
Risk Factors
Clinical Features
Management

A
  1. ) Pathophysiology - thrombus forms, blocks drainage of blood from the retina –> blood pooling in the retina
    - leakage of fluid and blood causes macular oedema and retinal haemorrhages, causing damage to tissue in the retina and also causing neovascularization (↑VEGF)
    - can be one of 4 branched veins or the central retinal vein which causes problems with the whole retina
  2. ) Risk Factors
    - smoking, hypertension, diabetes, high cholesterol
    - glaucoma, polycythaemia, inflammatory conditions e.g. SLE
  3. ) Clinical Features - sudden painless loss of vision
    - fundoscopy: severe flame and blot haemorrhages, cotton wool spots, tortuous veins, optic disc oedema and macula oedema

4.) Management - emergency referral to ophthalmology
- other tests: full medical history, FBC (leukaemia),
ESR (inflammatory disorders), BP (HTN), BM (diabetes)
- laser photocoagulation, intravitreal steroids (e.g. a dexamethasone intravitreal implant)
- Anti-VEGF therapies (e.g. ranibizumab, aflibercept)

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5
Q

Central Retinal Artery Occlusion

Pathophysiology
Clinical Features
Immediate Management
Long Term Management

A
  1. ) Pathophysiology - blockage of central retinal artery occludes blood supply to the retina
    - ICA –> ophthalmic artery –> central retinal artery
    - most common cause is atherosclerosis but can also be caused by giant cell arteritis
    - risk factors: ↑age, FH, smoking, alcohol, HTN, DM, obesity, GCA: PMR, women, white-caucasian
  2. ) Clinical Features - sudden painless loss of vision
    - fundoscopy: pale retina (↓perfusion) with a cherry-red spot (thinner macular surface shows red choroid below)
    - relative afferent pupillary defect: pupil in the affected eye constricts more when light is shone in another eye
  3. ) Immediate Management - emergency referral to ophthalmology, exclude GCA: especially older patients
    - attempt to dislodge the thrombus:
    - ocular massage
    - remove fluid from the anterior chamber to ↓IOP
    - inhaling carbogen (5% CO2, 95% O2) to dilate artery
    - sublingual isosorbide dinitrate to dilate the artery

4.) Long Term Management - treating reversible risk factors and secondary prevention of CVD

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6
Q

Optic Neuritis

Pathophysiology
Clinical Features
Management

A
  1. ) Pathophysiology - damage to the optic nerve
    - most common cause is MS (more common in women)
    - other causes include:
    - diabetes, SLE, sarcoidosis
    - syphilis, Lyme disease, measles, mumps
  2. ) Clinical Features
    - unilaterally reduced visual acuity over hours to days
    - periocular pain: pain on eye movement, the pain feels like it is behind the eye
    - dyschromatopsia: deficiency in colour perception
    - absent direct light reflex (pupils do not constrict)
    - RAPD, central scotoma (enlarged blind spot)
    - may have papilledema
    - ?MS sx: paraesthesia, weakness etc…
  3. ) Management
    - high-dose PO (or IV) methylprednisolone for 5 days
    - contrast sensitivity, colour vision and visual fields can remain impaired even after recovery of visual acuity
    - 50% of patients with a single episode of optic neuritis will go on to develop MS over the next 15 years
    - referral to neurology for an MRI contrast of the brain and spinal cord
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7
Q

Vitreous Haemorrhage

Pathophysiology
Clinical Features
Investigations

A
  1. ) Pathophysiology - bleeding into the vitreous humour from disruption of retinal vessels or nearby vessels
    - causes: diabetes (PDR), vitreous detachment, trauma
    - other RF: HTN, anti-coagulants, bleeding disorders, severe myopia
  2. ) Clinical Features - sudden painless loss of vision
    - typically an acute or subacute onset
    - floaters or shadows/dark spots in the vision
    - ↓visual acuity, red hue to vision
    - visual field defect if severe
    - may have absent red (fundal) reflex
  3. ) Investigations
    - fundoscopy: haemorrhage in the vitreous cavity
    - slit-lamp: RBCs in the anterior vitreous
    - ultrasound: exclude retinal tear/detachment
    - fluorescein angiography: identify neovascularization
    - orbital CT: used if open globe injury
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