Opthal I

Question 1

Describe the clinical features of acute angle closure glaucoma:

Answer 1

• severe pain: may be ocular or headache
• decreased visual acuity
• symptoms worse with mydriasis (e.g. watching TV in a dark room)
• hard, red-eye
• haloes around lights
• semi-dilated non-reacting pupil
• corneal oedema results in dull or hazy cornea
• systemic upset may be seen, such as nausea and vomiting and even abdominal pain

Question 2

Mx of AACG? [4]

Answer 2

− Urgent ophthalmology referral
− Oral/IV Acetazolamide
− IOP lowering drops: timolol, Apraclonidine, Prednisolone, Pilocarpine - reduce the pupil size and create space at iridocorneal angle)

Once IOP managed:
– Peripheral iridotomy
– Clear lens extraction

Question 3

Describe how pilocarpine acts to treat AACG? [2]

Answer 3

Pilocarpine acts on the muscarinic receptors in the sphincter muscles in the iris and causes pupil constriction (it is a miotic agent).
- It also causes ciliary muscle contraction. These two effects open up the pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular meshwork.

Question 4

[] is usually required as a definitive treatment.

Answer 4

Laser iridotomy is usually required as a definitive treatment.

Question 5

How do you differentiate between AACG and anterior uveitis? [3]

Answer 5

While both AACG and anterior uveitis can present with a red, painful eye, the pain in anterior uveitis is usually described as dull or throbbing rather than the severe pain often associated with AACG.

The vision loss in anterior uveitis tends to be less sudden than in AACG. It may also be accompanied by photophobia which is typically absent in AACG.

Ciliary flush (circumcorneal injection) is often seen in anterior uveitis but not typically observed in AACG.

Question 6

How do you ddx AACG and keratitis? [3]

Answer 6

Keratitis presents with a red, painful eye similar to AACG. However, the pain is usually described as sharp or stabbing and may be associated with foreign body sensation which is not typical of AACG.

Visual acuity may be reduced but this change tends to occur more gradually than the rapid onset of visual loss seen in AACG.

A key distinguishing feature is the presence of corneal epithelial defects or infiltrates on slit lamp examination which are not characteristic of AACG.

Question 7

Describe the risk factors for open-angle glaucoma [+]

Answer 7

Increasing age
Family history
Black ethnic origin
Myopia (nearsightedness)
HTN
Corticosteroid use
DM

Question 8

How does open glaucoma present? [

Answer 8

The rise in intraocular pressure may be asymptomatic for a long time and diagnosed by routine eye testing.
- Glaucoma affects the peripheral vision first, resulting in a gradual onset of peripheral vision loss (tunnel vision) - nasal scotomas progressing to ‘tunnel vision’
* Fluctuating pain
* Headaches
* Blurred vision
* Halos around lights, particularly at night

Question 9

Describe the fundoscopy signs of POAG [4]

Answer 9

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

Question 10

At what IOP do you start treatment for PAOG? [1]

Answer 10

Treatment is typically started at an intraocular pressure of 24 mmHg or above.

Question 11

Describe the management plan for PAOG [+]

Answer 11

First line: - 360° selective laser trabeculoplasty is recommended in the NICE guidelines (updated 2022) for all patients needing treatment. - During the procedure, a laser is directed at the trabecular meshwork, improving drainage. It may delay or prevent the need for eye drops. A second procedure may be necessary at a later date.

Medical Mx:
- Prostaglandin analogue eye drops (e.g., latanoprost)
- are the first-line medical treatment. They increase uveoscleral outflow.
- Beta-blockers (e.g., timolol) reduce the production of aqueous humour
- Carbonic anhydrase inhibitors (e.g., dorzolamide) reduce the production of aqueous humour
- Sympathomimetics (e.g., brimonidine) reduce the production of aqueous fluid and increase the uveoscleral outflow

Trabeculectomy surgery may be required where other treatments are ineffective.
- This involves creating a new channel from the anterior chamber through the sclera to a location under the conjunctiva, causing a bleb on the conjunctiva. From here, it is reabsorbed into the general circulation.

NB: 360° SLT can delay the need for eye drops and can reduce but does not remove the chance they will be needed at all

Question 12

Describe the pathophysiology of dry age related macular degeneration [+]

Answer 12

Two types:

Wet (also called neovascular), accounting for 10% of cases

Dry (also called non-neovascular), accounting for 90% of cases:
- This phase of AMD is characterised by the presence of asymptomatic drusen formation in Bruch’s membrane.
- Drusen are small yellowish deposits which are visible on fundoscopy
- As AMD progresses, other pathological changes, including pigmentary changes in the retinal pigmentary epithelium (RPE) and geographic atrophy (Figure 3) develop

Question 13

Describe the pathophysiology of wet age related macular degeneration [+]

Answer 13

Wet AMD is characterized by the formation of a choroidal neovascular membrane made up of new, aberrant blood vessels underneath the retina
- This is driven by vascular endothelial growth factor (VEGF)
- more rapidly progressive loss of vision, either by exudate from the new, leaky vessels or by haemorrhage.
- leakage of serous fluid and blood can subsequently result in a rapid loss of vision

Question 14

Describe the clinical features of ARMD

Answer 14

a reduction in visual acuity, particularly for near field objects
* gradual in dry ARMD
* subacute in wet ARMD

AMD is associated with central vision loss and a wavy appearance to straight lines.

difficulties in dark adaptation with an overall deterioration in vision at night

fluctuations in visual disturbance which may vary significantly from day to day

they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects

visual hallucinations may also occur resulting in Charles-Bonnet syndrome

Question 15

How would you investigate ARMD? [4]

Answer 15

slit-lamp microscopy is the initial investigation of choice, to identify any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD.

This is usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time.

fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy.
- This may be complemented with indocyanine green angiography to visualise any changes in the choroidal circulation.

ocular coherence tomography is used to visualise the retina in three dimensions because it can reveal areas of disease which aren’t visible using microscopy alone.

Question 16

Mx of ARMD?

Answer 16

anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib
- the agents are usually administered by 4 weekly injection.

laser photocoagulation does slow progression of ARMD where there is new vessel formation, although there is a risk of acute visual loss after treatment, which may be increased in patients with sub-foveal ARMD. For this reason anti-VEGF therapies are usually preferred.

Question 17

How do you differentiate between ARMD and glaucoma? [2]

Answer 17

TOM TIP: Glaucoma is associated with peripheral vision loss and halos around lights.

AMD is associated with central vision loss and a wavy appearance to straight lines.

Question 18

Answer 18

Retinal detachment

Question 19

Complications of cataracts can be categorised into intraoperative and postoperative.

Describe the intraoperative complications [2]

Answer 19

Capsular Tear:
- A common complication during phacoemulsification, potentially leading to vitreous loss or dislocation of lens fragments into the vitreous cavity.

Zonular Dehiscence:
- This may occur due to pre-existing weak zonules, especially in pseudoexfoliation syndrome or Marfan’s syndrome, leading to unstable lens and possible vitreous prolapse.

Question 20

Complications of cataracts can be categorised into intraoperative and postoperative.

Describe the postoperative complications [2]

Answer 20

Posterior Capsule Opacification (PCO):
- The most frequent postoperative complication, occurring when lens epithelial cells proliferate and migrate onto the posterior capsule. YAG laser capsulotomy is often required for treatment.

Cystoid Macular Oedema (CMO):
- Characterised by fluid accumulation in the macula, it can cause reduced visual acuity postoperatively. It is usually treated with topical non-steroidal anti-inflammatory drugs (NSAIDs) or corticosteroids.

Endophthalmitis:
- A serious but rare complication marked by inflammation within the eye due to bacterial infection. Prompt diagnosis and treatment with intravitreal antibiotics are necessary to prevent permanent vision loss.

IOL Dislocation:
- The intraocular lens may dislocate either immediately after surgery or years later due to zonular weakness or capsular contraction syndrome. Surgical intervention is typically required for correction.

Question 21

Which tissues does orbital cellulits specifically impact? [2]
Which group is it more common in? [1]
How does it occur? [1]

Answer 21

Orbital cellulitis involves infection of the muscle and fat within the orbit, posterior to the orbital septum.
- It is more common in children, with the incidence reported to be 16-fold higher in children compared to adults
- Orbital cellulitis is commonly caused by a local spreading infection from acute bacterial sinusitis, typically from the paranasal sinuses

Question 22

What are the clinical features of orbital cellulitis?

Answer 22

Erythema and swelling around the eye
Proptosis: Forward displacement or bulging of the eye (proptosis) is a cardinal sign of orbital cellulitis
Blurred vision
Painful eye movements
Change in colour vision
Fever
Reduced visual acuity and/or visual fields
Relevant afferent pupillary defect (RAPD)
Marcus-Gunn pupil
Chemosis

Question 23

Bilateral eye signs of orbital cellulitis might indicate .. [1]

Answer 23

Bilateral eye signs may indicate cavernous sinus thrombosis.

Nausea, vomiting, headache, neck stiffness may indicate intracranial involvement.

Question 24

Ix for orbital cellulitis? [1]

Answer 24

**CT scan**: - This is typically the first-line imaging modality due to its accessibility and ability to rapidly visualise bony structures, sinuses, and soft tissue. **It can effectively delineate the extent of infection and identify any associated abscesses.**

Question 25

What imaging would be indicated if ?cavernous sinus thrombosis [1]

Answer 25

**MR venogram** may be required to aid the diagnosis of cavernous sinus thrombosis. If meningeal signs develop, lumbar puncture is indicated.

Question 26

How do you manage orbital cellulitis? [2]

Answer 26

**Patients** with **orbital cellulitis require intravenous antibiotics**, for **seven to ten days** If an **orbital collection** is seen on **imaging, evacuation of orbital pus** or **drainage of paranasal sinus** **pus** may be required.

Question 27

What is Chandler's classification and what does it categorise?

Answer 27

**Chandler’s classification** anatomically categorises orbital complications of **acute rhinosinusitis** (the most common cause of orbital cellulitis). **Group 1**: Pre-septal cellulitis (infection anterior to orbital septum) **Group 2**: Orbital cellulitis (infection posterior to orbital septum) **Group 3:** Subperiosteal abscess (pus collection between bone and periosteum) **Group 4**: Intraorbital abscess (pus collection within the orbit) **Group 5:** Cavernous sinus thrombosis (mural thrombus which may propagate centrally)

Question 28

Describe ocular complications of orbital cellulitis [3]

Answer 28

**Subperiosteal abscess:** - This is an **accumulation of pus between the bone and the periosteum**, often **secondary to bacterial infection**. It can cause **proptosis, impaired ocular motility, and potentially loss of vision** if not treated promptly. **Cavernous sinus thrombosis**: - This is a rare but serious complication, characterised by headache, fever, cranial nerve palsies and decreased consciousness. **It results from the spread of infection from the orbit through emissary veins**. **Optic neuritis:** - Inflammation of the optic nerve can lead to **rapid loss of vision**. Patients may present with reduced visual acuity, relative afferent pupillary defect (RAPD), or abnormal colour vision.

Question 29

What are the intracranial complications of orbital cellulitis? [3]

Answer 29

**Meningitis**: This is inflammation of meninges which presents as fever, neck stiffness and altered mental status. Lumbar puncture is required for definitive diagnosis. **Brain abscess**: A collection of pus within brain parenchyma resulting from contiguous spread or haematogenous dissemination. Symptoms include headache, nausea/vomiting, focal neurological deficits and seizures. **Epidural abscess:** Accumulation of pus between dura mater and skull or vertebral column can lead to severe neurological deficits including paralysis.

Question 30

*distortion of line perception may be noted on Amsler grid testing* this indicates...? [1]

Answer 30

**Normal perception**: All lines appear straight and evenly spaced. **Distorted perception**: Lines may appear wavy, bent, or missing, indicating potential macular pathology. **In wet AMD**, neovascularisation leads to fluid leakage and scarring, exacerbating distortion. In dry AMD, drusen accumulation causes gradual retinal damage. Regular Amsler grid testing can help monitor disease progression and guide treatment decisions.

Question 31

Which tissues does orbital cellulits specifically impact? [2] Which group is it more common in? [1] How does it occur? [1]

Answer 31

**Orbital cellulitis** involves infection of the **muscle and fat within the orbit**, **posterior to the orbital septum**. - It is more **common in children**, with the incidence reported to be 16-fold higher in children compared to adults - **Orbital cellulitis is commonly caused by a local spreading infection** from **acute bacterial sinusitis, typically from the paranasal sinuses**

Question 32

What are the clinical features of orbital cellulitis?

Answer 32

**Erythema** and **swelling** around the **eye** **Proptosis**: Forward displacement or bulging of the eye (proptosis) is a cardinal sign of orbital cellulitis **Blurred vision** **Painful eye movements** **Change in colour vision** **Fever** **Reduced visual acuity and/or visual fields** **Relevant afferent pupillary defect (RAPD)** **Marcus-Gunn pupil** **Chemosis**

Question 33

Bilateral eye signs of orbital cellulitis might indicate .. [1]

Answer 33

Bilateral eye signs may indicate **cavernous sinus thrombosis**. Nausea, vomiting, headache, neck stiffness may indicate intracranial involvement.

Question 34

Ix for orbital cellulitis? [1]

Answer 34

**CT scan**: - This is typically the first-line imaging modality due to its accessibility and ability to rapidly visualise bony structures, sinuses, and soft tissue. **It can effectively delineate the extent of infection and identify any associated abscesses.**

Question 35

What imaging would be indicated if ?cavernous sinus thrombosis [1]

Answer 35

**MR venogram** may be required to aid the diagnosis of cavernous sinus thrombosis. If meningeal signs develop, lumbar puncture is indicated.

Question 36

How do you manage orbital cellulitis? [2]

Answer 36

**Patients** with **orbital cellulitis require intravenous antibiotics**, for **seven to ten days** If an **orbital collection** is seen on **imaging, evacuation of orbital pus** or **drainage of paranasal sinus** **pus** may be required.

Question 37

What is Chandler's classification and what does it categorise?

Answer 37

**Chandler’s classification** anatomically categorises orbital complications of **acute rhinosinusitis** (the most common cause of orbital cellulitis). **Group 1**: Pre-septal cellulitis (infection anterior to orbital septum) **Group 2**: Orbital cellulitis (infection posterior to orbital septum) **Group 3:** Subperiosteal abscess (pus collection between bone and periosteum) **Group 4**: Intraorbital abscess (pus collection within the orbit) **Group 5:** Cavernous sinus thrombosis (mural thrombus which may propagate centrally)

Question 38

Describe ocular complications of orbital cellulitis [3]

Answer 38

**Subperiosteal abscess:** - This is an **accumulation of pus between the bone and the periosteum**, often **secondary to bacterial infection**. It can cause **proptosis, impaired ocular motility, and potentially loss of vision** if not treated promptly. **Cavernous sinus thrombosis**: - This is a rare but serious complication, characterised by headache, fever, cranial nerve palsies and decreased consciousness. **It results from the spread of infection from the orbit through emissary veins**. **Optic neuritis:** - Inflammation of the optic nerve can lead to **rapid loss of vision**. Patients may present with reduced visual acuity, relative afferent pupillary defect (RAPD), or abnormal colour vision.

Question 39

What are the intracranial complications of orbital cellulitis? [3]

Answer 39

**Meningitis**: This is inflammation of meninges which presents as fever, neck stiffness and altered mental status. Lumbar puncture is required for definitive diagnosis. **Brain abscess**: A collection of pus within brain parenchyma resulting from contiguous spread or haematogenous dissemination. Symptoms include headache, nausea/vomiting, focal neurological deficits and seizures. **Epidural abscess:** Accumulation of pus between dura mater and skull or vertebral column can lead to severe neurological deficits including paralysis.

Question 40

What is Amsler grid testing? [1] What does it help detect? [1]

Answer 40

**Normal perception**: All lines appear straight and evenly spaced. **Distorted perception**: Lines may appear wavy, bent, or missing, indicating potential macular pathology. - In **wet AMD,** neovascularisation leads to fluid leakage and scarring, exacerbating distortion. - In dry AMD, drusen accumulation causes gradual retinal damage. **Regular Amsler grid testing can help monitor disease progression and guide treatment decisions.**

Question 41

**Purulent discharge** x **eyes may be 'stuck together' in the morning)** = ? [1] How do you tx? [1]

Answer 41

**Bacterial conjunctivitis** normally a self-limiting condition that usually settles without treatment within 1-2 weeks topical antibiotic therapy is commonly offered to patients, e.g. Chloramphenicol. Chloramphenicol drops are given 2-3 hourly initially whereas chloramphenicol ointment is given qds initially

Question 42

Describe the presentation of viral conjunctivitis [4]

Answer 42

Unilateral (that can then spread) UTRI Watery discharge Normal vision Swelling around eye in morning - oedema settles throughout day due to gravity

Question 43

Ix for viral conjunctivitis? [1]

Answer 43

- PCR swab

Question 44

Mx for viral conjunctivitis? [3]

Answer 44

Conservative Mx - Wash hands etc to avoid further spread - Cold compress - Lubricants

Question 45

Presentation of bacterial conjunctivitis? [3]

Answer 45

**Unilateral** - Yellow / green discharge **Severe purulent discharge** **Eyes may be 'stuck together' in the morning)**

Question 46

Where would you get lymphadenopathy in viral conjunctivitis? [1]

Answer 46

**Palpable preauricular lymphadenopathy**, particularly in viral conjunctivitis.

Question 47

Mx for bacterial conjunctivitis? [2]

Answer 47

**topical antibiotic therapy** is commonly offered to patients, e.g. **Chloramphenicol** * Chloramphenicol drops are **given 2-3 hourly initially** where as **chloramphenicol ointment is given qds initially** * **topical fusidic acid** is an alternative and should be used for **pregnant women**. Treatment is twice daily

Question 48

**Patients** with **allergic conjunctivitis** typically present with the **following signs and symptoms:** [5][

Answer 48

* Bilateral ocular itching and redness * Watery or stringy, mucoid discharge * Conjunctival chemosis and hyperemia * Eyelid oedema and erythema * Tearing and photophobia

Question 49

Mx for mild, moderate and severe allergic conjunctivitis? [3]

Answer 49

* **Mild**: Topical lubricants, Oral antihistamines * **Moderate**: Topical antihistamines/mast cell stabiliser: G Olopatidine * **Severe**: Topical steroids, Steroid-sparing agents: G Ciclosporin

Question 50

Describe what is going on here [1]

Answer 50

**Subepithelial opacities** seen in **adenoviral keratitis**. These typically are non-staining and can persist even after the acute episode of conjunctivitis has resolved.

Question 51

# Lecture Viral conjuctivitis: - If adenospots: treat with? [1]

Answer 51

− If adenospots...**topical steroids**

Question 52

# Lecture Management of episcleritis? [2]

Answer 52

- **Lubricants** − Oral NSAIDs: **Flurbiprofen** **100 mg three times daily**

Question 53

Mx of scleritis? [3]

Answer 53

**NSAIDs** (oral) **Steroids** (topical or systemic) **Immunosuppression** appropriate to the underlying systemic condition (e.g., methotrexate in rheumatoid arthritis)

Question 54

What is shown? [1]

Answer 54

**Microbial Keratitis:** - AKA ‘corneal ulcer’, infection of the cornea

Question 55

What is a typical case of a person with microbial keratis? [1]

Answer 55

− **CL wearer who wears their contact lenses for extended periods. Presents with pain, redness, discharge and reduced vision** ## Footnote **NB**: Careful history! Always ask: do you wear CLs to swim/steam room?

Question 56

Keratitis refers to inflammation of the **[]**, which is commonly secondary to an infectious cause

Answer 56

Keratitis refers to inflammation of the **cornea**, which is commonly secondary to an infectious cause ## Footnote **NB**: Infectious keratitis is often used interchangeably with the term corneal ulcer as the two commonly present together

Question 57

**Keratitis** occurs when there is **inflammation of the cornea**. The cause of keratitis is broadly divided into which two categories? [2] - Describe things that cause each [2]

Answer 57

**Infectious keratitis**: - bacterial, viral, fungal, protozoal **Non-infectious keratitis**: - autoimmune, exposure, vitamin A deficiency

Question 58

What are the risk factors for keratitis? [5]

Answer 58

Anything that **damages the integrity of the corneal epithelium** can increase the risk of keratitis. Important risk factors include: * **Contact lens use** * **Trauma** * **Immunosuppression** * **Dry eyes** * **Corticosteroid eye drops** * **UV light exposure** * **Swimming in contaminated waters**

Question 59

Describe this finding [1]

Answer 59

**Dendritic ulcer** under **fluorescein staining** - pathognomic for hepatic keratitis

Question 60

What are the clinical features of herpatic keratitis? [+]

Answer 60

**Keratitis** is characterised by **eye redness, pain, blurry vision, and photophobia.** * Eye redness * Eye pain * Blurred vision * Photophobia (sensitivity to light) * Increased lacrimation (excess tear production) * Difficulty opening the eye * Foreign body sensation * Eye discharge * Associated conjunctivitis

Question 61

Describe this finding an the clinical significance of the finding [1]

Answer 61

A **corneal ulcer** refers to a **defect** in the **epithelium** that involves the **stroma**. It should be considered an **ophthalmic emergency** because it can be **sight-threatening if untreated.**

Question 62

Describe the mx of keratitis [+]

Answer 62

**Viral**: * **Epithelial HSV keratitis** is treated with topical aciclovir. * **adenovirus keratitis**, treatment is usually supportive and personal hygiene is very important. **Acanthamoeba** **keratitis** should be treated with a **combination of topical polyhexamethylene biguanide and chlorhexidine** that may be combined with **pentamidine** **Bacterial keratitis** - is treated with **topical antibiotics** - severe infections and specific pathogens may require the addition of **systemic antibiotic therapy to the treatment regimen** - typical choice is the use of **topical** **Ciprofloxacin** **every 2-6 hours.** **Also**: − Dilating eye drop **(G Cyclopentolate 1%)** to **alleviate pain** − **Once epithelial defect heals** can give **topical steroids to reduce scarring**

Question 63

Ix for keratitis? [2]

Answer 63

Investigations: **Corneal scrape and conjunctival swab**

Question 64

Describe the typical case of uveitis [1]

Answer 64

* Typical case: **Photophobia, dull ache, slightly reduced vision (if presenting early) and a red eye.**

Question 65

The uvea is divided into which three components? [3]

Answer 65

**Iris**: the coloured part of the eye. It controls the size of the pupil which helps regulate the amount of light entering the eye. **Ciliary body**: a ring-shaped structure located behind the iris. It has important functions in accommodation, allowing us to focus on objects at different distances by changing the lens shape. It has several parts including the ciliary muscle, ciliary process, and zonular fibres. **Choroid**: this is a thin, dark brown/black layer that extends from the ciliary body to the optic nerve head. Its dark colour is due to melanocytes in its outermost layer. It contains a network of blood vessels that help support the health of the retina.

Question 66

Describe the clinical features of anterior uveitis [+]

Answer 66

* **acute onset** * **ocular discomfort** & pain (may increase with use) * pupil may be irregular and small * **photophobia** (often intense) * blurred vision * **red eye** * lacrimation * ciliary flush * **hypopyon**; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level * visual acuity initially normal → impaired

Question 67

Describe how you Ix anterior uveitis [2]

Answer 67

**Ocular examination**: - **Slit-lamp biomicroscopy** is critical for detecting **anterior chamber cells, flare, keratic precipitates, and posterior synechiae** - **Intraocular pressure measurement** and d**ilated fundus examination** should be performed to assess posterior segment involvement and potential complications. **Laboratory investigations**: - Based on the patient's history and clinical presentation, specific tests can be ordered, such as serologic tests for syphilis, Lyme disease, and toxoplasmosis, and quantiFERON-TB Gold for tuberculosis. - Autoimmune markers, such as HLA-B27, antinuclear antibody (ANA), and rheumatoid factor, may be considered if an underlying systemic disease is suspected.

Question 68

Tx for anterior uveitis? [2]

Answer 68

**PM**: **Topical corticosteroids**: - First-line treatment for anterior uveitis includes **potent topical corticosteroids (e.g., prednisolone acetate 1% or dexamethasone 0.1%)** administered frequently in the **acute phase and tapered according to clinical response.** **Cycloplegic agents**: - **Topical cycloplegics** (e.g., **tropicamide** or **homatropine**) help relieve **ciliary spasm and pain**, reduce the **risk of posterior synechiae**, and maintain the **depth of the anterior chamber.** **Systemic therapy**: - **Oral corticosteroids or immunosuppressive agents** (e.g., methotrexate, azathioprine, or mycophenolate mofetil) may be indicated for severe or refractory cases, or when posterior segment involvement is present. **Lecture**: − **Topical steroids** – tapered – **G Dexamethasone 0.1%** − **Topical dilating drops** – **G Cyclopentolate 1%** − Investigate individuals with multiple episodes

Question 69

Anterior uveitis is characterised by inflammation in the anterior chamber that can lead to the formation of a **hypopyon**. What is this? [1]

Answer 69

**Hypopyon**: fluid level of white cells within the anterior chamber. This is a sign of severe inflammation

Question 70

This patient has uveitis. Explain what is seen in the slit lamp photo [1]

Answer 70

**Keratic precipitates**: cellular deposits on the corneal endothelium)

Question 71

Describe what is meant by Post-operative Endophthalmitis [1]

Answer 71

* **Inflammation of internal eye tissues** – usually **secondary to infective an organism** * Typically occurs following **ophthalmic surgery**

Question 72

Presentation of post-operative endophthalmitis? [4]

Answer 72

**Increasing pain, redness, photophobia and reduced vision/floaters** - Typically occurs following ophthalmic surgery

Question 73

Mx for Post-operative Endophthalmitis? [3]

Answer 73

**Management**: − Urgent same-day referral to **ophthalmology** − **Slit lamp review** − **Intravitreal biopsy** − **Intravitreal antibiotics**

Question 74

Describe this finding in PVD [1]

Answer 74

**The Weiss ring**, a circular floater that can be seen following PVD, may also be visible during this examination.

Question 75

How do you differentiate PVD from retinal detachment? [1]

Answer 75

The **presence of photopsia, floaters and a sudden decrease in vision are common to both PVD and retinal tear/detachment**. - However, patients with retinal tears often **report an increase in the number of floaters compared to those with PVD.** - A crucial differentiating factor is the onset of symptoms. In **PVD, symptoms manifest gradually as the vitreous humour shrinks and detache**s from the retina over time. Conversely, symptomatic onset in **retinal tear or detachment is typically rapid.** - **Ophthalmoscopic** examination may **reveal subretinal fluid or a greyish retina in cases of retinal detachment**, distinguishing it from PVD where these signs are absent.

Question 76

How do you differentiate PVD from vitreous haemorrhage? [1]

Answer 76

Vitreous haemorrhage shares similar initial symptoms with PVD such as **floaters**; however, these tend to be **more diffuse and numerous due to blood dispersion** within the **vitreous cavity.** - Patients with vitreous haemorrhage **may also experience blurred vision or complete loss of sight if bleeding is substantial,** whereas visual acuity remains relatively unaffected in PVD. - On fundoscopy, **red blood cells can be seen floating in gel-like substance in cases of vitreous haemorrhage**. This sign is not present in PVD.

Question 77

Describe the typical presentation of vitreous haemorrhage [2]

Answer 77

Patients with vitreous haemorrhage typically present with **sudden, painless vision loss or floaters.** On examination, the **affected eye may have reduced visual acuity, and the red reflex may be absent or diminished.**

Question 78

Describe the tx for vitreous haemorrhage [3]

Answer 78

**Observation**: **Mild**, **non-threatening vitreous haemorrhages** may be managed conservatively, with observation and follow-up to monitor for spontaneous resolution. **Treatment of underlying cause**: Addressing the primary cause of the haemorrhage, such as laser photocoagulation for diabetic retinopathy or intravitreal injections for wet AMD, can help prevent further bleeding and vision loss. **Vitrectomy**: In cases of **severe** or **persistent vitreous haemorrhage**, surgical intervention with pars plana vitrectomy may be necessary to remove the blood and restore vision. This procedure also allows for the treatment of underlying retinal pathology, such as retinal detachment or proliferative retinopathy.

Question 79

Describe the pathophysiology of retinal detachment [3]

Answer 79

**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 is usually due to a **retinal tear**, allowing **vitreous fluid to get under the neurosensory retina and fill the space between the layers.** - The **neurosensory retina relies on the blood vessels of the choroid for its blood supply**. - Therefore, retinal detachment can **disrupt the blood supply and cause permanent damage** to the **photoreceptors**, making it **sight-threatening.**

Question 80

Describe the typical features of retinal detachment [+]

Answer 80

**new-onset floaters or flashes** - as these indicate pigment cells entering the vitreous space or traction on the retina respectively **Sudden onset, painless and progressive visual field loss,** described as a **curtain or shadow progressing to the centre of the visual field from the periphery** should also raise suspicion of detachment

Question 81

How may retinal detachment present in infants? [2]

Answer 81

In **infants**, retinal detachment may present with a **squint or a white pupillary reflex**. It should be suspected if there is a history of ocular trauma with older children, as they are unlikely to comment on visual changes.

Question 82

Describe the examination findings of retinal detachment [3]

Answer 82

On examination, **peripheral visual fields** may be **reduced**, and **central acuity may be reduced** to **hand movements if the macula is detached**. The **swinging light test may highlight a relative afferent pupillary defect** if the **optic nerve is involved.** **On fundoscopy, the red reflex is lost** and **retinal folds** may **appear as pale, opaque or wrinkled forms**. If the break is small, however, it may appear normal.

Question 83

Describe the treatment of retinal tears [2] and detachment [3]

Answer 83

**Retinal tear Management** Patients presenting with painless flashes and floaters should have a detailed assessment to detect retinal tears and retinal detachment. Any suspicion of retinal detachment requires immediate ophthalmology referral. Management of **retinal tears** aims to create **adhesions** between the **retina and the choroid**. The options are: * **Laser therapy** * **Cryotherapy** **Management of retinal detachment** aims to reattach the retina and reduce any traction or pressure that may cause it to detach again. - The options for reattaching the retina are **vitrectomy, scleral buckle or pneumatic retinopexy.** **Vitrectomy** - involves keyhole surgery on the eye, removing the vitreous fluid, fixing the tear, and then inserting gas or oil into the eye to hold the retina in place. **Scleral buckling** - involves using a silicone “buckle” to put pressure on the sclera from outside the eye, squashing the eye inwards to reconnect the layers of the retina. It acts like a corset, squeezing the eye contents together. **Pneumatic retinopexy** - involves injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble presses the separated layer back into place.

Question 84

Describe how you manage refractive error problems? [2]

Answer 84

**Management** depends on the suspected underlying cause: **if gradual onset** & **corrected by pinhole occluder** and **no other associated symptoms** - then an **optician review would be the next step** **other patients should be seen by ophthalmology**. - If there are **associated symptoms such as visual loss or pain this should be urgent**

Question 85

What investigation can help to determine if blurred vision is due to refractive error or not [1]

Answer 85

**pinhole occluders** are a useful way to check for whether the blurred vision is due to a refractive error or not