Opthalmology 2

Question 1

What is Corneal Abrasions

Answer 1

Corneal abrasions are scratches or damage to the cornea. They are a cause of red, painful eye

Question 2

Common Causes of Corneal Abrasions

Answer 2

• Contact lenses
• Foreign bodies
• Fingernails
• Eyelashes
• Entropion (inward turning eyelid)

Question 3

Corneal abrasions
If the abrasion is associated with the use of contact lenses there may be infection with ___________

Answer 3

If the abrasion is associated with the use of contact lenses there may be infection with pseudomonas.

Question 4

What is an important differential of Corneal Abrasions

Answer 4

An important differential diagnosis to consider is herpes keratitis as this will require treatment with antiviral eye drops.

Question 5

________ ________ (e.g., from acid) can cause severe damage to the eye and loss of vision.

Answer 5

Chemical abrasions (e.g., from acid) can cause severe damage to the eye and loss of vision.

Question 6

Presentation of Corneal Abrasions

Answer 6

• History of contact lenses or foreign body
• Painful red eye
• Foreign body sensation
• Watering eye
• Blurring vision
• Photophobia

Question 7

Diagnosis of Corneal Abrasions

Answer 7

A fluorescein stain is applied to the eye to diagnose a corneal abrasion. This is a yellow-orange colour. The stain collects in abrasions or ulcers, highlighting them.

Slit lamp examination may be used in more significant abrasions.

Question 8

Corneal Abrasions Management

Answer 8

NICE Clinical Knowledge Summaries on red-eye say patients with potentially sight-threatening causes of red eye should be referred for same-day assessment by an ophthalmologist. Mild, uncomplicated abrasions may be managed in primary care where there is appropriate experience and skill.

Management options include:

• Removing foreign bodies
• Simple analgesia (e.g. paracetamol)
• Lubricating eye drops
• Antibiotic eye drops (i.e. chloramphenicol)
• Follow-up after 24 hours
• **
  Cyclopentolate** eye drops dilate the pupil (they are mydriatics – causing mydriasis, meaning pupil dilation). They may be considered to help relieve symptoms, although evidence is lacking for their use in uncomplicated abrasions.

Chemical abrasions require immediate irrigation for 20-30 minutes and urgent referral to ophthalmology.

Uncomplicated corneal abrasions usually heal over 2-3 days.

Question 9

What is Herpes Keratitis and what is the common causes

Answer 9

Keratitis is inflammation of the cornea. There are a number of causes of keratitis:

• Viral infection with herpes simplex
• Bacterial infection with pseudomonas or staphylococcus
• Fungal infection with candida or aspergillus
• Contact lens acute red eye (CLARE)
  *** Exposure keratitis **is caused by inadequate eyelid coverage (e.g. eyelid ectropion)

Question 10

Herpes keratitis usually affects only the ________ layer of the cornea. If there is inflammation of the stroma (the layer between the epithelium and endothelium), this is called stromal keratitis. This is associated with complications such as ________ ________, ________ and ____________ and can lead to ________ __________.

Answer 10

Herpes keratitis usually affects only the epithelial layer of the cornea. If there is inflammation of the stroma (the layer between the epithelium and endothelium), this is called stromal keratitis. This is associated with complications such as stromal necrosis, vascularisation and scarring and can lead to corneal blindness.

Question 11

Presentation of Herpes Keratitis

Answer 11

• Painful red eye
• Photophobia
• Vesicles around the eye
• Foreign body sensation
• Watering eye
• Reduced visual acuity. This can vary from subtle to significant.

Question 12

Diagnosis of Herpes Keratitis

Answer 12

Staining with** fluorescein** will show a dendritic corneal ulcer. Dendritic describes the appearance of branching and spreading of the ulcer.

Slit-lamp examination is required to find and diagnose keratitis.

Corneal swabs or scrapings can be used to isolate the virus using a viral culture or PCR.

Question 13

Management of Herpes Keratitis

Answer 13

NICE Clinical Knowledge Summaries on red-eye say patients with potentially sight-threatening causes of red eye should be referred for same-day assessment by an ophthalmologist.

Management options in secondary care:

• Aciclovir (topical or oral)
• Ganciclovir eye gel
• Topical steroids may be used alongside antivirals to treat stromal keratitis

A **corneal transplant **may be required after the infection has resolved to treat corneal scarring caused by stromal keratitis.

Question 14

WHat is Subconjunctival Haemorrhage

Answer 14

Subconjunctival haemorrhages are a relatively common condition where one of the small blood vessels within the conjunctiva ruptures and release blood into the space between the sclera and the conjunctiva. They often appear after episodes of strenuous activity such as heavy coughing, weight lifting or straining when constipated. It can also be caused by trauma to the eye.

Question 15

Subconjunctival Haemorrhage
TOM TIP: Most cases are idiopathic and the patient is otherwise healthy, however there are a number of conditions that may have predisposed them to developing a subconjunctival haemorrhage. When a patient turns up with a subconjunctival haemorrhage use it as a clue to think about other conditions that may have contributed:

Answer 15

• Hypertension
• Bleeding disorders (e.g thrombocytopenia)
• Whooping cough
• Medications (warfarin, NOACs, antiplatelets)
• Non-accidental injury

Question 16

Subconjunctival Haemorrhage
Presentation

Answer 16

A subconjunctival haemorrhage appears as a patch of bright red blood underneath the conjunctiva and in front of the sclera covering the white of the eye. It is painless and does not affect vision.

There may be a history of a precipitating event such as a coughing fit or heavy lifting.

They can be confidently diagnosed based on a simple history and examination.

Question 17

Management of Subconjunctival Haemorrhage

Answer 17

Subconjunctival haemorrhages are harmless and will resolve spontaneously without any treatment. This usually takes around 2 weeks.

Think about the possible causes such as hypertension and bleeding disorders. These may need investigating further.

If there is a foreign body sensation lubricating eye drops can help with symptoms.

Question 18

What is Posterior Vitreous Detachment

Answer 18

The **vitreous body **is the gel inside the eye that maintains the structure of the eyeball and keeps the **retina **pressed on the choroid. The vitreous body is made up of collagen and water. With age it becomes less firm and less able to maintain its shape. Posterior vitreous detachment is a condition is where the vitreous gel comes away from the retina. It is very common, particularly in older patients.

Question 19

Presentation of Posterior Vitreous Detachment

Answer 19

Posterior vitreous detachment is a painless condition. It may be completely asymptomatic or patients may present with symptoms of:

• Painless
• Spots of vision loss
• Floaters
• Flashing lights

Question 20

Management of Posterior Vitreous Detachment

Answer 20

No treatment is necessary. Over time the symptoms will improve as the brain adjusts.

Posterior vitreous detachment can predispose patients to developing retinal tears and retinal detachment. They can also present very similarly.

It is essential to exclude and assess the risk of a retinal tear or **detachment **with a thorough assessment of the retina. This is usually done by an optometrist or ophthalmologist.

Question 21

What is Retinal Detachment

Answer 21

Retinal detachment is 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 the choroid.

The outer retina relies on the blood vessels of the choroid for its blood supply. This makes retinal detachment a** sight-threatening** emergency unless quickly recognised and treated.

Question 22

Risk Factors of Retinal Detachment

Answer 22

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

Question 23

Presentation of Retinal Detachment

Answer 23

Retinal detachment is a painless condition that can present with:

• Peripheral vision loss. This is often sudden and like a shadow coming across the vision.
• Blurred or distorted vision
• Flashes and floaters

Question 24

Management of Retinal Tears

Answer 24

Management of retinal tears aims to create adhesions between the retina and the choroid to prevent detachment. This can be done using:

• Laser therapy
• Cryotherapy

Question 25

Management of Retinal Detachment

Answer 25

Any suspicion of retinal detachment requires immediate **referral **to ophthalmology for assessment and management.

Management of retinal detachment aims to reattach the retina and reduce any traction or pressure that may cause it to detach again. This needs to be followed by treating retinal tears as above. Reattaching the retina can be done using one of three options:

• Vitrectomy involves removing the relevant parts of the vitreous body and replacing it with oil or gas.
• Scleral buckling 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.
• Pneumatic retinopexy 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.

Question 26

What is Retinal Vein Occlusion

Answer 26

Central retinal vein occlusion occurs when a blood clot (thrombus) forms in the retinal veins and blocks the drainage of blood from the retina. The central retinal vein runs through the **optic nerve **and is responsible for draining blood from the retina

Question 27

How many branches form central retinal vein

Answer 27

4
There are four branched veins that come together to form the central retinal vein. 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.

Question 28

Blockage of a retinal vein causes pooling of blood in the retina. This results in leakage of fluid and blood causing ______ ______ and _______ ___________ This results in damage to the tissue in the retina and loss of vision. It also leads to the release of ____, which stimulates the development of new blood vessels (neovascularisation)

Answer 28

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 haemorrhages. This results in damage to the tissue in the retina and loss of vision. It also leads to the release of VEGF, which stimulates the development of new blood vessels (neovascularisation)

Question 29

Presentation of Retinal Vein Occlusion

Answer 29

Blockage of one of these retinal veins causes sudden painless loss of vision.

Question 30

Retinal Vein Occlusion Risk Factors

Answer 30

• Hypertension
• High cholesterol
• Diabetes
• Smoking
• Glaucoma
• Systemic inflammatory conditions such as systemic lupus erythematosus

Question 31

Diagnostic examination of retinal vein occlusion

Answer 31

Fundoscopy

Question 32

Retinal vein occlusion Fundoscopy findings

Answer 32

Fundoscopy examination is diagnostic of retinal vein occlusion. It give characteristic findings:

• Flame and blot haemorrhages
• Optic disc oedema
• Macula oedema

Question 33

Other tests of Retinal vein occlusion

Answer 33

The Royal College of Ophthalmologists guidelines from 2015 suggest checking for possible associated conditions in patients presenting with retinal vein occlusion:

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

Question 34

Management of Retinal Vein Occlusion

Answer 34

Patients with suspected retinal vein occlusion should be referred immediately to an ophthalmologist for assessment and management.

Management in secondary care aims to treat macular oedema and prevent complications such as neovascularisation of the retina and iris and glaucoma. The options for this are:

• Laser photocoagulation
• Intravitreal steroids (e.g. a dexamethasone intravitreal implant)
• Anti-VEGF therapies (e.g. ranibizumab, aflibercept or bevacizumab)

Question 35

What is Central Retinal Artery Occlusion

Answer 35

Central retinal artery occlusion occurs where something blocks the flow of blood through the central retinal artery. The **central retinal artery **supplies the blood to the retina. It is a branch of the ophthalmic artery, which is a branch of the internal carotid artery.

Question 36

Most common cause of Central Retinal Artery Occlusion

Answer 36

The most common cause of occlusion of the retinal artery is atherosclerosis. It can also be caused by giant cell arteritis, where vasculitis affecting the ophthalmic or central retinal artery causes reduced blood flow

Question 37

RF of Central Retinal Artery Occlusion

Answer 37

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.

Question 38

Presentation of Central Retinal Artery Occlusion

Answer 38

Blockage of the central retinal artery causes sudden painless loss of vision.

There will be a relative afferent pupillary defect. This is where the pupil in the affected eye constricts more when light is shone in the other eye compared 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 the normal retina during the consensual light reflex.

Question 39

Findings on Fundoscopy of Central Retinal Artery Occlusion

Answer 39

Fundoscopy will show a** pale retina **with a cherry-red spot. The retina is pale due to a lack of perfusion with blood. The cherry-red spot is the macula, which has a thinner surface that shows the red coloured choroid below and contrasts with the pale retina

Question 40

General Management of Central Retinal Artery Occlusion

Answer 40

Patients with suspected central retinal artery occlusion should be referred immediately to an ophthalmologist for assessment and management.

Giant cell arteritis is an important potentially reversible cause. Therefore older patients are tested and treated for this if suspected. Testing involves an ESR and temporal artery biopsy and treatment is with high dose **steroids **(i.e. prednisolone 60mg).

Question 41

Immediate Management of Central Retinal Artery Occlusion

Answer 41

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

Question 42

Long Term Management of Central Retinal Artery Occlusion

Answer 42

Long term management involves treating reversible risk factors and secondary prevention of cardiovascular disease

Question 43

What is Retinitis Pigmentosa

Answer 43

Retinitis pigmentosa is a congenital inherited condition where there is degeneration of the** rods **and cones in the retina. There are many different genetic causes. Some causes involve isolated retinitis pigmentosa whereas others result in systemic diseases associated with the condition. They vary in age at presentation and prognosis.

Question 44

Retinitis Pigmentosa
In most genetic causes the rods degenerate more than cones, leading to ________ ________. They get decreased ________ and ____________ vision.

Answer 44

In most genetic causes the rods degenerate more than cones, leading to night blindness. They get decreased **central **and peripheral vision.

Question 45

Presentation of Retinitis Pigmentosa

Answer 45

The presentation can vary between different underlying causes. Family history is very important. In most causes the symptoms start in childhood.

• Night blindness is often the first symptom
• Peripheral vision is lost before the central vision

Question 46

Findings of Fundoscopy of Retinitis Pigmentosa

Answer 46

Fundoscopy will show pigmentation. This is described as “bone-spicule” pigmentation. Spicule refers to sharp, pointed objects. **Bone-spicule **is used to refer to the similarity to the networking appearance of bone matrix.

The pigmentation is most concentrated around the **mid-peripheral **area of the retina.

There can be associated narrowing of the arterioles and a waxy or pale appearance to the optic disc.

Question 47

Associated Systemic Diseases with Retinitis Pigmentosa

Answer 47

There are several genetic systemic diseases that involve retinitis pigmentosa. It is not worth learning the names and details but it is worth being aware they exist. Some examples are:

• Usher’s Syndrome causes hearing loss plus retinitis pigmentosa
• Bassen-Kornzweig Syndrome is a disorder of fat absorption and metabolism causing progressive neurological symptoms and retinitis pigmentosa
  ** Refsum’s Disease* is a metabolic disorder of phytanic acid causing neurological, hearing and skin symptoms and retinitis pigmentosa

Question 48

Management of Retinitis Pigmentosa

Answer 48

General management involves:

• Referral to an ophthalmologist for assessment and diagnosis
• Genetic counselling
• Vision aids
• Sunglasses to protect the retina from accelerated damage
• Driving limitations and informing the DVLA
• Regular follow up to assess vision and check for other potentially reversible conditions that may worsen the vision such as cataracts

Question 49

Retinitis Pigmentosa
There isn’t a huge amount of evidence supporting options to slow the disease process. Some options that may be considered by a specialist in certain scenarios include:

Answer 49

• Vitamin and antioxidant supplements
• Oral acetazolamide
• Topical dorzolamide
• Steroid injections
• Anti-VEGF injections

Gene therapy is a potential future treatment that could alter the disease process and lead to better outcomes.

Question 50

WHat is Optic neuritis

Answer 50

Optic neuritis (ON) is an inflammatory optic neuropathy usually affecting one eye at a time and typically presents with acute or subacute visual loss. It frequently occurs in association with multiple sclerosis (MS).

Question 51

What is the risk factors of optic neuritis

Answer 51

• Known diagnosis of MS: up to 70% of patients with MS will have at least one episode. Optic neuritis can be the presenting feature of MS in up to 20% of cases.
• Female sex: there is a female predominance by a ratio of 3:1
• Young age: most patients are aged 20-50 years
• Higher latitude: the incidence is higher for populations at higher or lower latitudes (the northern United States, northern and western Europe, southern Australia and New Zealand) compared with areas closer to the equator

Question 52

Clinical features of Optic Neuritis

Answer 52

Typical symptoms of demyelinating ON include:5,6,7

• Acute to subacute unilateral loss of vision: the visual acuity upon testing can vary from being normal (6/6) to rarely becoming ‘no perception of light’, i.e. inability to tell when a bright flashlight is being shone into the affected eye.
• Retrobulbar and peri-ocular pain: this is present in >90% of cases and is exacerbated by eye movements and may precede or occur with visual loss. The pain is believed to occur due to close proximity of rectus muscle insertions to the inflamed optic nerve sheath at the orbital apex.
• Photopsias (flashes) exacerbated by eye movements
• Visual field loss: any pattern of field loss may be seen including diffuse, altitudinal, central and sectoral losses.
• Reduced contrast sensitivity and colour vision (red).

The vision worsens over hours to days, but recovery starts within two weeks with or without treatment. The visual acuity may recover to near normal but permanent abnormalities of colour perception, contrast sensitivity and visual field may occur.

Question 53

Clinical Examination of optic neuritis

Answer 53

• 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)

Question 54

Differential Diagoses of Optic Neuritis

Answer 54

• Atypical causes of ON (see aetiology section)
• Ischaemic: giant cell arteritis must be considered in a patient over the age of 50
• Hereditary: Leber’s hereditary optic neuropathy
• Compressive/infiltrative: secondary to an orbital infection, malignancy or inflammatory disease (e.g. sarcoidosis).
• Nutritional/toxic: B12/folate deficiency and alcohol
• Trauma/radiation

Question 55

Ix of optic neuritis

Answer 55

MRI of the brain and oribits

Question 56

What is the medical management of optic neuritits?

Answer 56

Patients with typical ON should be started on high-dose corticosteroid therapy.

The typical regimen is intravenous methylprednisolone 1g daily for three days followed by an oral prednisolone taper (1mg/kg for 11 days).

Oral methylprednisolone 500mg once a day for five days has been suggested as an alternative to intravenous steroids, but its use remains controversial.