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Opthalmology > 4- Ophthalmology (Sudden or subacute deterioration of vision) > Flashcards

4- Ophthalmology (Sudden or subacute deterioration of vision) Flashcards

1
Q

Sudden or subacute loss of vision

A
  • Central retinal artery occlusion (CRAO)
  • Vitreous haemorrhage
  • Wet age related macular degeneration
  • Retinal detachment (rhegmatogenous)
  • Optic neuritis
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2
Q

Central retinal artery occlusion
Background

A
  • Where there is a blockage of blood flow to the central retinal artery
  • The central retinal artery supplies the blood to the retina -> a branch of the ophthalmic artery , which is a branch of the internal carotid artery
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3
Q

Causes of CRAO

A
  • Atherosclerosis
  • Giant cell arteritis
    o Where vasculitis affecting the ophthalmic or central retinal artery causes reduced blood flow
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4
Q

Risk factors for CRAO

A

Risk factors for retinal artery occlusion by atherosclerosis are the same as for other cardiovascular diseases:
* Older age
* Family history
* Smoking
* Alcohol consumption
* Hypertension
* Diabetes
* Poor diet
* Inactivity
* Obesity
Those at higher risk for retinal artery occlusion secondary to giant cell arteritis are white patients over 50 years of age, particularly females and those already affected by giant cell arteritis or polymyalgia rheumatica.

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5
Q

presentation of CRAO

A

Presentation
- Sudden painless loss of vision
- Relative afferent pupillary defect
- Fundoscopy

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6
Q

Relative afferent pupillary defect

A
  • Where the pupil in the affected eye constrict more when light is shone in the other eye compared to when it is shone in the affected eye
  • This occurs because the input is not being sensed by the ischaemic retina when testing the direct light reflex, but is being sensed by normal retina during the consensual light reflex
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7
Q

fundoscopy findings CRAO

A

Pale retina (lack of perfusion with cherry-red spot

Cherry red spots: macula- which has a thinner surface that shows the red coloured choroid below and contrasts with pale retina

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8
Q

immediate management of CRAO

A

If the patient presents shortly after symptoms develop then there are certain things that can be tried to attempt and dislodge the thrombus. None of these have a strong evidence base. Some examples are:
* Ocular massage
* Removing fluid from the anterior chamber to reduce intraocular pressure.
* Inhaling carbogen (a mixture of 5% carbon dioxide and 95% oxygen) to dilate the artery
* Sublingual isosorbide dinitrate to dilate the artery

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9
Q

overall management of CRAO

A

Management
- Referral to ophthalmologist
- Giant cell arteirtiis is an important and potentially reversible cause
o Test for ESR and temporal artery biopsy
o Steroids e.g. prednisolone 60mg

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10
Q

which is more common retinal artery or retinal vein occlusion

A

It is far less common than retinal vein occlusion, and vision deteriorates faster

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11
Q

Retinal vein occlusion
Background

A
  • Occurs when a thrombus forms in the retinal veins and blocks the drainage of blood from the retina
  • Central retinal veins run through the optic nerve and is responsible for draining blood from the retina
  • Four branched veins which come together to form the central retinal vein
    o Blockage of one of the branch veins causes problems in the area drained by that branch, whereas blockage in the central vein causes problems with the whole retina
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12
Q

Pathophysiology
of retinal vein occlusion

A
  • Blockage of a retinal vein causes pooling of blood in the retina
  • This results in leakage of fluid and blood causing macular oedema and retinal haemorrhage
  • This results in damage to the tissue in the retinal and loss of vision
  • Also leads to the release of VEGF , which stimulate neovascularisation
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13
Q

Risk factors for retinal vein occlusion

A
  • Hypertension
  • High cholesterol
  • Diabetes
  • Smoking
  • Glaucoma
  • Systemic inflammatory conditions e.g. SLE
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14
Q

presentation of retinal vein occlusion

A

Presentation
- Sudden
- Painless loss of vision
- Patients can also present with visual field defects, depending on the site of the occlusion.

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15
Q

types of retinal vein occlusion

A

Central retinal vein occlusion (CRVO) occurs when the central retinal vein is occluded by a thrombus
Branch retinal vein occlusion (BRVO) is when one of the central vein’s branches is blocked

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16
Q

fundoscopy findings for retinal vein occlusion

A

The classic fundoscopy description of CRVO is a* ‘stormy sunset’*. Findings include:

  • numerous flame haemorrhages
  • dot and blot haemorrhages
  • cotton wool spots
  • retinal oedema
  • dilated or tortuous retinal veins
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17
Q

other tests for retinal vein occlusion

A
  • Full medical history
  • FBC for leukaemia
  • ESR for inflammatory disorders
  • Blood pressure for hypertension
  • Serum glucose for diabetes
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18
Q

management of retinal vein occlusion

A
  • Patient with suspected retinal vein occlusion should be referred immediately to ophthalmologist
  • Secondary care management to treat macular oedema and prevent neovascularisation (complication) of the retina and iris and glaucoma
    o Laser photocoagulation
    o Intravitreal steroids e.g. dexamethasone intravitreal implant
    o Anti-VEGF therapies (e.g. ranibizumab, aflibercept or bevacizumab
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19
Q

Central retinal artery occlusion vs retinal vein occlusion

A

In CRA occlusion, the retina appears grossly swollen and pale, with a prominent fovea that would otherwise be obscured by a normal, pinkish-red background (see attached - Image 1). In CRV occlusion, the disc is massively swollen with splotches of hemorrhage and cotton wool spots diffusely

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20
Q

Retinal detachment (rhegmatogenous)
Background

A
  • Where the retina separates from the choroid underneath
  • this is usually due to a retinal tear that allows vitreous fluid to get under the retina and fill the space between the retina and choroid
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21
Q

retinal detachment: pathophysiology of loss of sight

A

Rhegmatogenous retinal detachments are often due to retinal tears associated with posterior vitreous detachment or trauma.

  • outer retina relies on the blood vessels of the choroid for its blood supply
  • this makes retinal detachment a sight-threating emergency unless quickly recognised and treatment
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22
Q

Risk factors for retinal deatchment

A
  • Posterior vitreous detachment
  • Diabetic retinopathy
  • Trauma to the eye
  • Retinal malignancy
  • Older age
  • Family history
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23
Q

Presentation of retinal detachment

A
  • Painless
  • Peripheral vision loss
    o Often sudden and like a shadow coming across the vision
    o Blurred or distorted vision
    o Flashes and floaters
24
Q

investigations for Retinal detachment (rhegmatogenous)

A
  • Examination in the eye department will involve a slit-lamp examination, indirect ophthalmoscopy or Goldmann triple mirror examination (which involves a slit lamp and a contact lens applied against the anaesthetised cornea for a few minutes as the peripheral retina is examined).
  • Ultrasound or optical coherence tomography may be used to assess the type and extent of the detachment, any associated tears and any ocular comorbidity.
  • CT and MRI scans have a role if there is a tumour or suspected foreign body.
  • Patients with an exudative RD benefit from a full systemic examination, owing to its association with systemic disease.
25
Q

Management of retinal detachment/ tear

A
  • Referral to someone with appropriate skillset to detect retinal tears or detachment -> if any suspicion -> refer to ophthalmology
  • Management depends if it is a
    o Retinal tear
    o Retinal detachment
26
Q

Management
Retinal tears

A
  • Management aims to create adhesions between the retina and the choroid to prevent detachment
    o Laser therapy
    o Cryotherapy
27
Q

management retinal detachment

A

Aims to reattach the retina and reduce any tract or pressure that may cause it to detach again

Reattaching the retina can be done using one of three option
- Vitrectomy
- Scleral buckling
- Pneumatic retinopexy

28
Q

Vitrectomy

A

Involves removing the relevant part of the vitreous body and replacing it with oil or gas

29
Q

Scleral buckling

A

Involves using a silicone buckle to put pressure on the outside of the eye (the sclera) so that the outer eye indents to bring the choroid inwards and into contact with the detached retina

30
Q

Pneumatic retinopexy

A

Involves injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble creates pressure that flattens the retina against the choroid and close the detachment

31
Q

Wet age macula degeneration
Background

A
  • 2 types of age related macular degeneration
    o Wet- sudden – worse prognosis (10%)
    o Dry- more gradual
  • Degeneration in the macula that causes progressive deterioration in vision
32
Q

Pathophysiology of wet AMD

A
  • Development of new vessels growing from the choroid layer into the retina -> neovascularisation is triggered by VEGF
  • Theses vessels can leak fluid or blood and cause oedema andf more rapid loss of vision
  • Treatment tends to focus on inhibiting VEGF
33
Q

risk factors Wet age macula degen

A

Risk factors
- Age
- Smoking
- White or chinses
- Family history
- CVD disease

34
Q

Presentation Wet age-related macular degeneration

A

Presents more acutely than dry
It can present with a loss of vision over days and progress to full loss of vision over 2-3 years. It often progresses to bilateral disease.
- Central visual field loss
- Reduced visual acuity
- Crooked or wavy appearance to straight lines

35
Q

Examination findings wet age macula degen

A
  • Reduced acuity using a Snellen chart
  • Scotoma (a central patch of vision loss)
  • Amsler grid test can be used to assess the distortion of straight lines
  • Fundoscopy. Drusen are the key finding.
  • Slit-lamp biomicroscopic fundus examination by a specialist can be used to diagnose AMD.
  • Optical coherence tomography is a technique used to gain a cross-sectional view of the layers of the retina. It can be used to diagnose wet AMD.
  • Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to look in detail at the blood supply to the retina. It is useful to show up any oedema and neovascularisation. It is used second line to diagnose wet AMD if optical coherence tomography does not exclude wet AMD.
36
Q

Wet AMD management

A
  • Anti-VEGF medication -> prevent neorevascularisation
  • Medications such as ranibizumab, bevacizumab and pegaptanib are injected into the vitreous chamber of the eye once a month
  • Slow and even reverse progression of the disease
  • Need to be started within 3 months to be beneficial
37
Q

drusen on OCT for macula degeneration

A
38
Q

Optic neuritis
Background

A
  • Optic neuritis is an inflammatory optic neuropathy
  • Affects one eye at a time
  • Typically presents with acute or subacute visual loss
  • Associated with multiple sclerosis (MS)
39
Q

causes of optic neuritis

A
  • MS
  • Antibody mediated
  • non-infectious
  • infectious
  • post-infectious
40
Q

optic neuroitis and MS

A

MOST COMMON cause
- Typical (demyelinating) ON is strongly associated with MS.
- May initially occur as a clinically isolated syndrome without evidence of generalised demyelination -> however this eventually develops in a significant proportion of patients

41
Q

Antibody-mediated optic neuronitis

A

Neuromyelitis Optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody disease

42
Q

Non-infectious optic neuronitis

A

neuroscarcoidosis and SLE

43
Q

infectious optic neuronitis

A

syphilis, lyme disease, cat-scratch disease, herpes zoster, sinus disease

44
Q

Post- infectious neuronitis

A

following an acute infection or immunisation

45
Q

Pathophysiology optic neuronitis

A
  • MS -> autoimmune T cells directed against the CNS myelin antigens which destroys the myelin sheath
  • Contributing factors include
    o Precipitating infectious agents (EBV)
    o Genetic susceptibility
    o The environment (low vitamin D, low UV exposure, smoking and obesity)
46
Q

Risk factors optic neuronitis

A
  • MS (70% of patients with MS have at least one episode) -> often presenting feature
  • Female sex 3:1
  • Young age – 20-50
  • High or low latitude
47
Q

Presentation of optic neuronitis

A
  • Acute to subacute unilateral loss of vision
  • Retrobulbar and peri-ocular pain
  • Photopsia’s -> flashes exacerbated by eye movements
  • Visual field loss
  • Reduced contrast sensitivity and colour vision
  • Vision worsens over hours to days, but recovery starts within 2 weeks with or without treatment
48
Q

Investigations for optic neuronitis

A

All patients with suspected optic neuritis should undergo a comprehensive ophthalmic, cranial nerve and neurological examination.
The ophthalmic examination should include: 4

  • Visual acuity testing with a Snellen chart
  • Colour vision assessment with an Ishihara test
  • Testing for a relative afferent pupillary defect (RAPD): this will be positive for the affected eye unless there is pre-existing disease in the contralateral eye.
  • Fundoscopy: swelling of the optic nerve may be visible in a third of patients and is typically mild. However, most patients have retrobulbar involvement therefore the optic nerve appears normal. Over time, the optic nerve will develop pallor.
  • Testing extraocular muscle movements: expected to be normal in ON but may detect internuclear ophthalmoplegia (common in multiple sclerosis)

Further tests
- MRI of brain and orbits with gadolinium contrast -> will show enhancement of the optic nerve confirming diagnosis
o May also identify any white matter lesion suggestive of MS
- Lumbar puncture -> to support MS if MRI normal

49
Q

management of optic neuronitis

A

Management
- High dose systemic (IV steroids)
- IV methylprednisolone for 3 days followed by oral prednisolone taper (1mg/kg for 11 days)

50
Q

complications of optic neuronitis

A
  • 90% have vision recovery within 6 months
  • Contrast sensitivity, relative afferent pupil defect and abnormalities of colour perception may persist
  • Recurrence in affected or contralateral eye is 30% at 5 years
  • Does not imply definite conversion to MS
  • 15 year risk of developing MS is 50%
    o 25% in those with normal MRI
51
Q

Vitreous haemorrhage
Background

A
  • Bleeding into the vitreous humour
  • One of the most common causes of sudden painless visual loss
  • Visual loss can vary from
    o Haziness to floaters to complete loss
  • Haemorrhage results in clot formation once the bleeding stops
52
Q

Pathophysiology vitreous haemorrhage

A
  • Proliferative diabetic retinopathy -> due to neovascularisation caused by VEGF
  • Posterior vitreous detachment
  • Ocular trauma (most common caused in children)
    o Open globe injury
    o Close globe injury from blunt trauma
    o Shaking injuries
53
Q

Risk factors

A
  • Neovascularisation e.g. diabetic eye
  • Trauma
  • Anticoagulants and antiplatelets
  • Disorders of coagulation
  • High myopia have increased risk of retinal tears, detachment and associated vitreous haemorrhage
54
Q

High myopia have increased risk of

A

retinal tears, detachment and associated vitreous haemorrhage

55
Q

Presentation of vitreous haemorrhage

A
  • Red hue
  • New onset floaters
  • Symptoms worse in morning if blood settles on macula during sleep
  • Variable visual acquity – may be dramatically reduced
56
Q

Investigations for vitreous haemorrhage

A
  • Intraocular pressures.
  • Best corrected visual acuity.
  • Dilated fundoscopy may reveal haemorrhage spread through the vitreous, or the bleed may conform in shape to the underlying structures.
  • Slit-lamp examination reveals red blood cells in the anterior vitreous.
  • Gonioscopy to look for new vessels in the drainage angle.
  • If there is acute PVD, retinal tear or detachment must be ruled out using scleral depression.
  • The other eye must also be examined.
  • Ultrasonography can be used to detect the blood, PVD, retinal tears, retinal detachment, tractional membranes, intraocular tumours and foreign bodies. This is particularly helpful if the view of the retina is obscured.
  • Fluorescein angiography may help neovascularisation.
  • Orbital CT is indicated in cases of open globe injury, to allow assessment of the integrity of other structures in the orbit and to rule our intraocular foreign body.
  • Blood pressure should also be checked.
57
Q

Management of vitreous haemorrhage

A
  • Referral to ophthalmologist
  • Watch and wait
    o Often clears in days to weeks
    o Patient should rest with head elevated
  • Laser photocoagulation
    o In proliferative vasculopathies as soon as any part of the retina is present
  • Anterior retinal cryotherapy A(RC)
    o In eyes with fresh vitreous haemorrhage
    o Clears liquefied bloods
  • Vitrectomy
    o Indicated when the underlying pathology is likely to progress fast if untreated
  • Intravitreal anti-VEGF agents e.g. bevacizumab
    o To cause regression of neovascularisation in proliferative retinopathies
  • Advice to patients
    o Avoid strenuous activity

Opthalmology (16 decks)

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