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Opthalmology > Acute vision loss > Flashcards

Acute vision loss Flashcards

1
Q

Open angle glaucoma : Definition

A
  1. Optic nerve damage caused by a rise in intraocular pressure.
  2. Raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye.
  3. There are two types of glaucoma:
    ⦁ Open-angle glaucoma
    ⦁ Acute angle-closure glaucoma
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2
Q

Open angle glaucoma : Anatomy

A
  1. Anterior chamber : between the cornea and iris
  2. Posterior chamber : between the lens and iris
  3. Optic disc : ‘Blind’ spot on visual field where optic nerve and blood vessels which supply the retina exit the eye
  4. Optic cup : Indentation within the optic disc where the optic nerve fibres converge
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3
Q

Open angle glaucoma : Aqueous chamber

A

Aqueous humour
1 . MOA : supplies nutrients to the cornea - fills the anterior and posterior chamber of the eye

2 . Supply : Ciliary body -> Posterior chamber -> Iris -> Anterior chamber -> Trabecular network -> Canal of Schlemm -> General circulation

3 . Intraocular pressure : created by resistance to flow through the trabecular network

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4
Q

Open angle glaucoma : Pathophysiology

A
  1. Open-angle glaucoma :
    * Gradual increase in resistance to flow through the trabecular meshwork.
    * The pressure slowly builds within the eye
    Iris is clear of meshwork - funcional increase in outflow pressure from the trabecular network
  2. Cupping of the Optic disc :
    * Increased intra-ocular pressure - damages optic nerve fibres
  • Damage causes indent of the optic cup indent to become wider and deeper, described as “cupping”
  • The optic cup usually is less than 50% of the size of the optic disc.

A cup-disk ratio greater than 0.5 is abnormal

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5
Q

Open angle glaucoma : Risk Factors

A
  1. Increasing age
  2. Family history
  3. Black ethnic origin
  4. Myopia (nearsightedness)
  5. Diabetes / Hypertension
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6
Q

Open angle glaucoma : Clinical presentation

A
  1. Peripheral vision loss : gradual onset - tunnel vision
    Ganglion cells are more densely concentrated in the peripheral (side) region - thus more vulnerable to damage by sudden raised IOP
  2. Blurred vision
  3. Halos around lights, particularly at night
  4. Fluctuating pain
  5. Headaches
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7
Q

Open angle glaucoma : Clinical signs on Fundoscopy

A
  1. Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
  2. Optic disc pallor - indicating optic atrophy
  3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
  4. Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
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8
Q

Open angle glaucoma : Investigation for diagnosis

A
  1. Goldmann applanation tonometry : Gold standard way to measure the intraocular pressure
  2. Slit lamp assessment for the cup-disk ratio and optic nerve health
  3. Visual field assessment for peripheral vision loss
  4. Gonioscopy to assess the angle between the iris and cornea
  5. Central corneal thickness assessment
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9
Q

Open angle glaucoma : Management

A

First line :
1. IOP of ≥ 24 mmHg : 360° selective laser trabeculoplasty (SLT)
Laser at trabecular meshwork, improving drainage - delay/prevent need for eyedrops

Second line :
1. Prostaglandin analogue (PGA) eyedrops : Increases uveoscleral outflow

Third line :
1. Beta-blocker eye drops : Reduces aqueous production

  1. Carbonic anhydrase inhibitors (e.g. Dorzolamide) : Reduces aqueous production
  2. Sympathomimetics (e.g., brimonidine) reduce the production of aqueous fluid and increase the uveoscleral outflow

Fourth line :
Trabeculectomy surgery : creating a new channel from the anterior chamber for reabsorption into general circulation

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10
Q

Acute angle glaucoma : definition

A
  1. Occurs when the iris bulges forward and seals off the trabecular meshwork from the anterior chamber
  2. Prevents aqueous humour from draining
  3. Leading to a continual increase in intraocular pressure.
  4. The pressure builds in the posterior chamber, pushing the iris forward and exacerbating the angle closure.

It is an ophthalmological emergency requiring rapid treatment to prevent permanent vision loss.

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11
Q

Acute angle glaucoma : Risk factors

A
  1. Family history
  2. Female (four times more likely than males)
  3. Chinese and East Asian ethnic origin
  4. Long-sightedness
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12
Q

Acute angle glaucoma : Medication percipitant

A

Excessive pupil dilatation - cause widening of the iris - resulting in blockage
3. 1. Adrenergic medications (e.g., noradrenaline)

  1. Anticholinergic medications (e.g., oxybutynin and solifenacin)
  2. Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects
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13
Q

Acute angle glaucoma : Clinical presentation

A

A typical patient with acute angle-closure glaucoma presents appearing generally unwell, with a short history of:

  • Severely painful red eye
  • Blurred vision
  • Halos around lights
  • Associated headache, nausea and vomiting
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14
Q

Acute angle glaucoma : Clinical signs on examination

A
  • Hard, red eye
  • Haloes around lights
  • Semi-dilated non reacting pupil
  • Hazy cornea : corneal odema
  • Decreased visual acuity
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15
Q

Acute angle glaucoma : Initial Management

A

1 . Pilocarpine eye drops
* MOA : acts on muscarinic receptors in the sphincter muscles of the iris - causing miosis and ciliary muscle contraction
* Effect : Open up pathway for flow of aqueous humor

2 . Acetazolamide (PO/IV) :
MOA : Carbonic anhydrase inhibitor that reduces the production of aqueous humour.

3 . Hyperosmotic agents (e.g., intravenous mannitol)
MOA : Increase the osmotic gradient between the blood and the eye

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16
Q

Acute angle glaucoma : Definitive Management

A

Laser iridotomy
MOA : Laser used to create a hole in the iris

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17
Q

Posterior vitreous detachment : Definition

A

Posterior vitreous detachment is the separation of the vitreous membrane from the retina.

  • This occurs due to natural changes to the vitreous fluid of the eye with ageing.
  • Posterior vitreous detachment is a common condition that does not cause any pain or loss of vision.

However, rarely the separation of the vitreous membrane can lead to tears and detachment of the retina.

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18
Q

Posterior vitreous detachment : Aetiology

A
  • As people age, the vitreous fluid in the eye becomes less viscous, and thus, does not hold its shape as well.
  • Therefore, it pulls the vitreous membrane away from the retina towards the centre of the eye.
  • Highly myopic (near-sighted) patients are also at increased risk of developing posterior vitreous detachment earlier in life.
  • This is because the myopic eye has a longer axial length than an emmetropic eye.
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19
Q

Posterior vitreous detachment : Clinical features

A
  • The sudden appearance offloaters(occasionally a ring of floaters temporal to central vision)
  • Flashesof light in vision
  • Blurred vision
  • Cobweb across vision

Signs:
Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).

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20
Q

Posterior vitreous detachment : Management

A
  • Posterior vitreous detachment alone does not cause any permanent loss of vision.
  • Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
  • If there is an associated retinal tear or detachment the patient will require surgery to fix this.
21
Q

Retinal detachment : Definition

A
  • Retinal detachment involves the neurosensory layer of the retina (containing photoreceptors and nerves) separating from the retinal pigment epithelium (the base layer attached to the choroid).
  • This separation interrupts the blood supply to the retina, leading to vision impairment
22
Q

Retinal detachment : Pathophysiology

A
  1. Retinal Tears or Holes
    * Allow for the vitreous fluid to pass through and accumulate beneath the retina.
    * Can lift the retina away from the underlying layers, leading to retinal detachment.
    * Distrupt the retina’s blood supply

2 . Non-Rhegmatogenous Retinal Detachment:
* Causes : inflammation, tumors which causes fluid accumulation

3 . Tractional Retinal Detachment:
* Scar tissue on the retina : contracts, pulling the retina away from the underlying layers.
* Scar tissue forms with conditions such as diabetic retinopathy.

23
Q

Retinal detachment : Risk factors

A
  1. Lattice degeneration (thinning of the retina)
  2. Posterior vitreous detachment
  3. Trauma
  4. Diabetic retinopathy
  5. Retinal malignancy
  6. Family history
24
Q

Retinal detachment : Clinical presentation

A
  1. Painless condition - retina lacks pain receptors

2 . Sudden Peripheral vision loss - ‘shadow’ appears and progresses towards mental vision
* Peripheral retina is affected first as : thinner and fewer supportive structures
* Veil over field of vision

3 . Distortions of vision
* Straight lines appear curved
* Blurring
* Flashes and floaters

25
Q

Retinal tears : Management

A

Management of retinal tears aims to create adhesions between the retina and the choroid. The options are:
* Laser therapy
* Cryotherapy

26
Q

Retinal detachment : Management

A

Aims : Reattach the retina + reduce any traction or pressure that may cause it to detach again.

Options;
1. Vitrectomy : Keyhole surgery to fix the tear

  1. Pneumatic retinopexy : Injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble presses the separated layer back into place.
27
Q

Retinal vein occlusion : Definition

A

Retinal vein occlusion (RVO) is a vascular disorder involving the blockage of a retinal vein,
* leading to impaired blood flow and potential damage to the retina.

28
Q

Retinal vein occlusion : Anatomy

A
  1. Branch retinal veins drain into the central retinal vein,
  2. Central retinal vein exits via the Optic nerve
  3. Drain into either the superior ophthalmic vein or cavernous sinus.
  • Blockage of one of the branch veins affects the area drained by that branch.
  • Blockage in the central vein causes problems with the whole retina.
29
Q

Retinal vein occlusion : Pathophysiology

A

1 . Blockage of a retinal vein :
* causes venous congestion in the retina, preventing drainage

2 . Increased venous pressure
* macular oedema / retinal haemorrhages : fluid and blood leaking into the retina
* This results in retinal damage and vision loss.

Ischaemic vs non-Ischaemic.

3 . Ischaemia
* The occlusion of a retinal vein leads to
* impaired blood flow, causing ischemia (lack of oxygen supply) in the affected area of the retina.

4 . Neovascularisation : * Retinal ischaemia leads to the release of vascular endothelial growth factor (VEGF)
* new blood vessel development

30
Q

Retinal vein occlusion : Clinical presentation

A

Clinical presentation varies - dependant on visual loss, location, occlusion etc

  1. Painless vision loss - corresponds to affected area
31
Q

Retinal vein occlusion : Clinical examination findings

A
  1. Opthalmoscopy examination
    blood and thunder appearance
  • Dilated tortuous retinal veins
  • Flame and blot haemorrhages
  • Retinal oedema
  • Cotton wool spots
  • Hard exudates
32
Q

Retinal vein occlusion : Management

A
  1. Urgent opthalmologist referral
  2. Management in secondary care aims to treat macular oedema and prevent neovascularisation. The options are:
  • Anti-VEGF therapies (e.g., ranibizumab and aflibercept)
  • Dexamethasone intravitreal implant (to treat macular oedema)
  • Laser photocoagulation (to treat new vessels)
33
Q

Central Retinal artery occlusion : Definition

A

Central retinal artery occlusion occurs due to obstruction to blood flow through the central retinal artery.

  • The central retinal artery is a branch of the ophthalmic artery, which is a branch of the internal carotid artery
34
Q

Central Retinal artery occlusion : Causes

A
  1. Atherosclerosis : Most common cause
  2. Vaculitis : (affecting ophthalmic/central retinal artery : Giant cell arteritis
35
Q

Central Retinal artery occlusion : Risk factors

A
  1. Cardiovascular disease :
    * smoking, hypertension, diabetes and raised cholesterolincrease the risk of atherosclerosis
  2. Hx of Vasculitis : Giant cell arteritis, Polymyalgia Rheumatica
36
Q

Central Retinal artery occlusion : Clinical presentation

A
  1. Sudden painless loss of vision
    * described as like a “curtain coming down” over the vision.
37
Q

Central Retinal artery occlusion : Clinical signs

A

1 . Relative afferent pupillary defect:
* where the pupil in the affected eye constricts more when light is shone in the contralateral eye

  • Due to ischaemic damage to optic nerve

2 . Fundoscopy :
* Pale retina - lack of perfusion
* Cherry red spot : Fovea has a thinner surface, exposed red coloured choroid below

38
Q

Central Retinal artery occlusion : Management

A

**Poor prognosis as management is difficult **

  1. Giant cell arteritis -potentially reversible cause.
    * Ix :ESR blood test + temporal artery biopsy.
    * Tx : high-dose systemic steroids.
  2. Intraarterial thrombolysis may be attempted but currently, trials show mixed results.
39
Q

Vitreous haemorrhage : Definition

A
  1. Abnormal presence of blood within the vitreous humor, the gel-like substance that fills the central cavity of the eye.
  2. This condition can arise from various underlying causes.
40
Q

Vitreous haemorrhage : Pathophysiology

A

1 . Haemorrhaging of Neovascular vessels

Neovascular vessels form which are more prone to haemorrhaging

  • Diabetic Retinopathy
  • Wet Age related macular degeneration

2 . Retinal blood supply disruption

  • Retinal vein occlusion + Retinal artery occlusion
    Disruption of blood flow to retinal vessels may lead to bleeding into the vitreous
  • Vitreous Detachment
    Traction on retinal vessels from separation of the vitreous from the retina can cause bleeding
41
Q

Vitreous haemorrhage : Clinical features

A

Blood in the vitreous hummer obstructs transmission of light resulting in;

  1. Sudden vision loss } Large bleeds prevent any light tramission
  2. Blurred vision } Moderate bleeds
  3. Floaters } Small bleeds
42
Q

Vitreous haemorrhage : Management

A
  1. Observation:
    * Small vitreous hemorrhages may resolve spontaneously
  2. Surgery (Vitrectomy):
    : significant or persistent bleeding
  • Vitrectomy surgery : remove the blood from the vitreous cavity and address underlying issues.
  1. Treatment of Underlying Conditions:
43
Q

Optic neuritis : Definition

A
  • Optic nerve transmits visual information from the eye to the brain
  • Inflammation and damage to the optic nerve, leading to vision impairment
    *associated with autoimmune processes : Multiple Sclerosis
44
Q

Optic neuritis : Pathophysiology

A
  1. Autoimmune Inflammation:
    • Immune system inflammation targets the myelin sheath surrounding the optic nerve fibers.
  2. Demylination:
    • Loss of myelin sheath is essential for the efficient transmission of electrical signals along nerve fibers.
  3. Infiltration of Immune Cells:
    • Immune cell infiltrate the optic nerve.
    • These cells contribute to the inflammatory response and play a role in the demyelination process.
  4. Edema and Swelling:
      • Inflammation leads to edema (fluid accumulation) and swelling within the optic nerve.
    • The increased pressure can further compromise nerve function.
  5. Impaired Nerve Conduction*
    • Demyelination disrupts the normal conduction of electrical impulses along the optic nerve.
    • As a result, visual signals are not transmitted efficiently from the eye to the brain.
  6. Axonal Damage:
    • Permanent vision loss : Prolonged inflammation and demyelination can lead to damage to the nerve fibers (axons) themselves.
45
Q

Optic neuritis : Clinical features

A
  1. Onset : Unilateral Central vision loss over hours or days
  • Pain:
    • Eye pain with eye movement } common symptom.
  • Color Vision Deficits:
    • poor discrimination of colours, ‘red desaturation’
  • Central Visual Field Deficits:
    • Central stomata
  • Relative afferent pupillary defect
46
Q

Optic neuritis : Investigation

A
  • MRI of the brain and orbits
47
Q

Optic neuritis
: Causes

A
  • Multiple sclerosis: the commonest associated disease
  • Diabetes
  • Syphilis
48
Q

Optic neuritis: Management

A
  • High-dose steroids
  • Recovery usually takes 4-6 weeks

Prognosis
* MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%

Opthalmology (5 decks)

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