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clinical opthalmology > The retina > Flashcards

The retina Flashcards

1
Q

Retinal haemorrhages

A

Flame shaped -RNFL
Dot blot - plexiform layer

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2
Q

Sub retinal haemorrhages

A
  • Darker in colour, retinal vessels visible above, can have arbitrary shape as blood spreads
  • Causes include – wet AMD, choroidal tumours, trauma
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3
Q

Pre retina haemorrhages

A

Subhyaloid haemorrhages – between retina & vitreous – boat shaped
- Vitreous haemorrhages
- Blood is less dense but obscures the underlying retina

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4
Q

Retina Oedema

A
  • Diffuse/localised leakage
  • Forms between the OPL and INL – may involve IPL and NFL
  • Oedema can be shown by an OCT
  • Vision only affected if present at the macula
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5
Q

Exudates

A
  • Exudates are caused by chronic localised oedema and are located at the junction between normal and oedematous tissue – mainly found in the OPL
  • They are spontaneously absorbed into BS after oedema resolves
  • More orange than drusen – larger
  • Associated with Diabetes
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6
Q

Drusen

A
  • Deposits between the RPE (blood/eye barrier) and Buch’s membrane, derived from the deficient metabolism of the photoreceptor outer segments by the RPE
  • Drusen cause damage to photoreceptors and reduce vision
  • Less orange than exudates, associated with AMD
  • Drusen more common at the macula – most activity (cones)
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7
Q

Cotton wool spots

A
  • Accumulation of neuronal debris in the NFL
  • Same appearance of flame shaped haemorrhages, but are white
  • Sign of reduced function of neurons
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8
Q

Abnormal Blood Vessels

A
  • A-V shunts/IRMA (intra retinal microvascular abnormalities)
  • New blood vessels
    o Cross major RBVs and leak on FA
    o 3 ways of describing neovascularization (new blood vessels):
     New vessels at disc – NVD
     New vessels elsewhere – NVE
     New vessels in the iris – NVI
  • Dilated capillaries/collateral vessels/telangiectasias – interchangeable terms
    o do not cross major RBVs and don’t leak on FA
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9
Q

Diabetic retinopathy background info

A

A chronic, complex condition caused by insufficient insulin activity, either due to low production, absence, or insulin resistance. Insulin is made by the pancreas, which has both exocrine (digestive enzyme) and endocrine (hormone-producing) functions—the latter via the islets of Langerhans.
There are two main types:

Type 1 (10%): Autoimmune destruction of islet cells, sudden onset.
Type 2 (90%): Chronic, linked to obesity and aging.
A major global health issue, affecting 366 million people (projected to double by 2030).

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10
Q

Diabetic retinopathy - risk factors

A

Poor control of DM
preganancy
hypertension
neuropathies
hyoperlipidaemia
smoking
cataracts
anaemia
obeasity

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11
Q

DIabetic retinopathy symptoms

A
  • May be asymptomatic
  • Blurred/distorted vision
  • Sudden onset of reduced vision
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12
Q

Diabetic retinopathy signs and features

A

Microaneurysms – tiny red dots, often initially temporal to the fovea. Tend to be the earliest sign of DR
Haemorrhages- both flame shaped and dot blot.
Exudates – sometimes termed hard/soft casued by chronic macular oedema.
microaneurysm:-
* Cotton wool spots
* Venous beading
* New vessels
* Vitreous haemorrhage
* Traction detachment

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13
Q

Diabetic retinopathy scottish grading system

A
  • R0 – no retinopathy – OBSERVE
  • R1 – mild (microaneurysms only) – OBSERVE
  • R2 – moderate (up to 4 haemorrhages) – OBSERVE
  • R3 – severe (haemorrhages, venous beading, IRMA) – REFER
  • R4 – proliferative – REFER
  • M0 – no maculopathy – OBSERVE
  • M1 – early (exudates >1 & <2 DD from fovea) – OBSERVE
  • M2 – advances (Exudates <1 DD from fovea) – REFER
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14
Q

Diabetic retinopathy management

A

Monitor: Annual screening, ensure diabetes/risk factors controlled (via GP).

Refer: If clinically significant macular oedema suspected.

Treatment (if referred):
Laser if vision threatened or macular oedema.

PDR:
PRP: 2–4000 burns, reduces VEGF, prevents macular damage, may cause peripheral vision loss.

Vitrectomy: For vitreous haemorrhage or tractional detachment.

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15
Q

Diabetic paillopathy

A

Uncommon AION variant; often bilateral with diffuse, hyperaemic disc swelling.

Likely related to small-vessel disease.

Affects young diabetics, usually painless, unilateral vision loss.

Resolves over months, may leave mild disc pallor.

Good prognosis: 80% retain 6/12 or better vision.

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16
Q

Central aretry vein occlusion signs and symptoms

A

symptoms:-
- sudden profounf vision loss

signs:-
* VA < CF, unless a cilioretinal artery supplying a critical macular area preserves vision
* RAPD is profound
* Fundus
o Pale retina, cherry red spot at fovea
o Peri-papillary retina may appear swollen and opaque
o Occasional small haemorrhage
o Optic atrophy

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17
Q

Central artery vein occlusion management

A

Refer to stroke unit as an emergency

Px should be seen be an ophthalmologist after 3-4 weeks and a minimum of twice subsequently at monthly intervals to detect incipient neovascularisation.

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18
Q

Branch Retinal artery occlusion signs and symptoms

A

Symptoms:

Sudden, profound, painless altitudinal or sectoral visual field loss
May go unnoticed if central vision is spared

Signs:

Visual acuity variable; poor prognosis if central vision affected and not treated quickly
RAPD often present
Fundus:
Arterial/venous attenuation, sludging, segmentation
Cloudy retinal oedema in ischaemic area
Possible visible emboli
Affected artery remains attenuated
Follow-up:

Review at 3 months: fundus, VF, prognosis, and systemic risk management.

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19
Q

Branch vein occlusion signs and symptoms

A

Symptoms:

Central macula: Sudden, painless blurred vision & metamorphopsia
Peripheral occlusion: Often asymptomatic
Signs:

VA variable at presentation
Iris neovascularisation & NVG rare
Most commonly affects supero-temporal vein

20
Q

Branch vein occlusion fundus view

A

Dilated, tortuous vein; flame-shaped & dot-blot haemorrhages
Cotton wool spots, oedema, exudates
Venous nipping (esp. from hypertension)
Acute signs resolve in 6–12 months, may leave venous sheathing, sclerosis
Collateral vessels may develop
Chronic macular oedema = main cause of long-term VA loss
Retinal neovascularisation in ~8% of cases by 3 years

21
Q

Branch vein occlusion management

A
  • If VA reduced, urgent referral for treatment of macular oedema
  • If VA normal, routine referral for management of risk factors
22
Q

Impeding / partial CRVO signs and symptoms

A

Symptoms:

Often absent or mild, transient blurring of vision
Typically worse on waking

Signs:

Mild venous dilation & tortuosity
Scattered dot-blot haemorrhages
Possible mild macular oedema

23
Q

Impeading / partial CRVO management

A
  • Correction of any predisposing systemic conidtions, avoiding dehydration and lowering IOP to improve perfusion
24
Q

Non ischaemic CRVO signs and symptoms

A

Symptoms:

Sudden monocular decrease in vision

Signs:

VA: Impaired, 6/30–6/60; worse than 6/60 suggests significant ischaemia
RAPD: Absent or mild
Fundus:
Tortuous, dilated central retinal vein branches
Dot-blot haemorrhages (mild to moderate)
Cotton wool spots/mild macular oedema
Patchy ischaemic retinal whitening
Acute signs resolve in 6–12 months
Chronic macular oedema & atrophy = main cause of poor vision
Disc collaterals (optociliary shunts) common after CRVO

25
Ischaemic CRVO signs and symptoms
Symptoms: Sudden, severe, painless monocular vision loss Occasionally pain, redness, photophobia due to neovascular glaucoma (NVG), with prior unnoticed vision reduction Signs: VA: Usually CF or worse; poor prognosis due to macular ischaemia RAPD present NVI (rubeosis iridis) in ~50% of cases, usually within 2-4 months, high NVG risk Gonioscopy: Angular neovascularisation Fundus Findings: Severe tortuosity & engorgement of central retinal vein branches Deep dot-blot & flame-shaped haemorrhages in peripheral retina Cotton wool spots, disc swelling, hyperaemia Acute signs resolve in 9–12 months, potential for atrophic retinal & RPE changes Retinal neovascularisation occurs in 5% of eyes (less than BRVO), but may lead to severe vitreous haemorrhages Optic disc collaterals are common
26
CRVO treating complications
Check IOP Ischaemic CRVO: Urgent referral due to 30% risk of rubeotic glaucoma Non-ischaemic CRVO: Urgent referral if VA reduced or macular oedema If VA good, refer routinely Management is less aggressive than for ischaemic CRVO, so distinguishing is crucial Treatment Options: Macular oedema (VA < 6/9 or central macular thickening): Intravitreal anti-VEGF Steroid Unlikely benefit if VA < 6/120 Rubeosis (NVI): PRP Intravitreal anti-VEGF Glaucoma Management: Shunt surgery Cyclodiode laser
27
Ocular Ischaemic Syndrome signs and symptoms
Symptoms: Gradual vision loss over weeks/months, sometimes sudden or intermittent (amaurosis fugax) Ocular/periocular pain (40%) Persistent afterimages, worsening vision with bright light exposure, slow adaptation Signs: Episcleral injection, corneal oedema Aqueous flare, few cells Iris atrophy, poorly reacting mid-dilated pupil Rubeosis iritis (up to 90%) Cataracts in advanced cases
28
Ocular ischaemic syndrome fundus
Fundus: Venous dilation, arteriolar narrowing Round/flame haemorrhages Occasionally disc oedema, cotton wool spots Proliferative retinopathy with NVD and occasionally NVE Spontaneous arterial pulsation near optic disc Macular oedema Diabetic patients: Retinopathy may be worse ipsilateral to carotid stenosis
29
Ocular ishchaemic syndrome treatment
Anterior segment inflammation: Topical steroid and mydriatics NVG: Surgical/medical management Proliferative retinopathy: PRP Macular oedema: Intravitreal steroid or anti-VEGF Carotid surgery Manage risk factors
30
Hypersensitive Retinopathy
Primary response of retinal arterioles to systemic hypertension is vasoconstriction (less marked in older individuals). Atherosclerosis: Hardening/loss of elasticity of vessel walls, seen as AV nipping at crossing points. Indicates long-standing hypertension. In sustained hypertension, disruption of the inner retinal blood vessels leads to increased vascular permeability, causing flame-shaped haemorrhages and oedema.
31
Hypersensitive Retinopathy Grades
Grade 1: Mild generalised arteriolar narrowing Grade 2: Focal arteriolar narrowing, AV nipping, copper wire appearance Grade 3: Grade 2 plus haemorrhages, exudates, possible macular star and cotton wool spots Grade 4: Severe Grade 3 with optic disc swelling
32
Retinitis pigmentosa signs and symptoms
Symptoms: Night blindness Difficulty with dark adaptation Peripheral vision problems Reduced central vision in later stages Photopsia Signs: VA normal early on; contrast sensitivity affected at early stage Bilateral, mid-peripheral intraretinal 'bone-spicule' pigmentary changes and RPE atrophy with arteriolar narrowing Gradual increase in pigment density with anterior and posterior retinal changes Severe peripheral pigmentation, marked arteriolar narrowing, disc pallor Optic disc drusen Macular atrophy, epiretinal membrane, cystoid macular oedema
33
Retinitis pigmentosa treatment
Treatment * Regular (annual) follow up = essential to detect treatable complications * No specific treatment is yet available * Low vision aids, avoiding smoking, sunglasses, vitamin A supplements
34
Post Vitreous Detachment
Symptoms * Floaters – described as cobwebs * Flashes – single flashes, not like fortification spectra * Asymptomatic Signs * Weiss ring o Glial tissue from around disc o Usually not an obvious ring o Best seen with bright light, slightly oblique, in front of/below disc * Posterior hyaloid o Crinkly grey membrane behind lens
35
PVD management
* Mainly reassurance * Px’s are initially very symptomatic * Most will find that symptoms get much less over a few months a * A few will remain symptomatic * Options include: vitrectomy, Nd:YAG vitreolysis
36
Retinal tears - Lattice degeneration
Signs: Spindle-shaped retinal thinning Sclerosed vessels forming arborizing white lines (classic sign) Snowflakes (degenerated Müller cell remnants) RPE hyperplasia is common Small retinal holes frequently present Prevalence: Found in 6–8% of normal eyes Present in 30% of eyes with retinal detachment Management: Routine prophylaxis not justified
37
Retinal tears - Horseshoe tears
Key Points: Caused by posterior vitreous detachment (PVD) Requires same-day referral Risk of Retinal Detachment (RD): Symptomatic U-tears: 90% risk of RD Asymptomatic U-tears: 5% risk Ongoing RD risk remains for affected eye U-tears have higher RD risk than round holes Treatment: Laser photocoagulation (primary treatment) Cryotherapy may be used Does not relieve symptoms (e.g., floaters); purpose is RD prevention
38
Retinal tears - round hole
Prevalence: Found in ~6% of normal eyes Not all cases require referral Risk of Retinal Detachment (RD): Very low risk: Study of 235 eyes over 11 years: 1 clinical RD 19 subclinical detachments Management: Routine prophylaxis not justified
39
Retinal detachment types
Rhegmatogenous = Rupture Tractional = Tugging Exudative = Excess fluid
40
Retinal detachment signs and symptoms
Symptoms: Flashes and floaters (often with acute PVD) Curtain/shadow-like visual field defect, usually noticed as it approaches the macula Sudden vision loss if the macula is involved Signs: ↓ IOP (typically ~5 mmHg lower) RAPD (Marcus Gunn pupil) Mild iritis Tobacco dust (pigment cells in anterior vitreous) Retinal appearance varies depending on duration of detachment
41
Tractional retinal detachment
Causes: Proliferative retinopathies (e.g. diabetic retinopathy, retinopathy of prematurity) Penetrating posterior segment trauma Symptoms: Typically no flashes or floaters (no acute PVD) Slowly progressive visual field defect, can be stable for months or years Signs: Concave RD with no retinal breaks Reduced retinal mobility, no shifting subretinal fluid Maximum elevation at points of vitreoretinal traction If a break occurs, it may convert to rhegmatogenous RD and progress quickly
42
Exudative retinal detachment
Symptoms: No flashes (no vitreoretinal traction) Floaters (if vitritis present) Rapidly progressing visual field defect Signs: Convex RD with a smooth, mobile surface Shifting fluid depending on head position (e.g., supine → fluid shifts → new area detaches) Leopard spots (pigmented clumping) may appear after detachment resolves Treatment: Based on underlying cause Some cases resolve spontaneously Others may need corticosteroids
43
Retinoblastoma
Presentation: Bilateral: within 1st year of life Unilateral: around 2 years old Symptoms: Leukocoria, strabismus, red painful eye (secondary glaucoma), poor vision, inflammation Signs: Dome-shaped white lesion with calcification Endophytic: grows into vitreous Exophytic: subretinal masses causing RD Differentials: congenital cataract, ROP, toxocariasis, PFV, Coats disease, uveitis
44
Astrocytoma
Rare, usually asymptomatic Associated with tuberous sclerosis Signs: yellowish/white, semi-transparent plaque or nodule, often calcified centrally
45
Capillary Haemangioma
Rare, can threaten vision Symptoms: macular exudates, RD Signs: Early: small red lesion Established: red-orange mass in temporal periphery with dilated vessels from optic disc Treatment: observation, laser photocoagulation, cryotherapy

clinical opthalmology (5 decks)

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