Diseases of the anterior segment in horses Flashcards

1
Q

What structures are located in the anterior segment?

A
  • Cornea
  • Anterior chamber
  • Posterior chamber
  • Iris
  • Ciliary body
  • Lens
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2
Q

What produces aqueous humour? What is the main component? How is it sampled?

A

Ciliary body

98% water

Sampling
* Sedation
* Topical anaesthesia
* Retrobulbar block

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3
Q

What are the most common aqueous humour abnormalities? How are they characterised? What causes them?

A

Flare - increased opacity
* ↑↑↑ [protein]/fibrin
* Uveitis

Hypopyon
* Pus in anterior chamber
* Falls to the bottom by gravity
* Uveitis

Hyphaema
* Blood in anterior chamber
* Uveitis
* Trauma
* Coagulopathy

Glaucoma
* Increase in IOP
* Mainly of Aqueous Humour

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4
Q

What IOP is associated with glaucoma? How does it present? What are the advanced stages?

A

IOP >30mmHg

Presentation
* Variable pain
* Corneal oedema
* Often zonal
* Haabs striae - linear opacity in the cornea
* DM injury
* Mydriasis/myosis - mostly myosis
* Buphthalmos

Advanced stages
* Progressive mydriasis
* Lens: luxation/cataracts
* Retinal degeneration
* Loss of vision

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5
Q

How is glaucoma treated?

A

Treat underlying disease

Medical
* Topical treatment
* Beta blockers
* 0.25% timolol TID
* Carbonic anhydrase inhibitors
* 2% dorzolamide TID
* Mydriatics
* Atropine
* Treat concurrent disease
* Uveitis -> corticosteroids

Surgical
* Laser cyclophotocoagulation - destroys part of the ciliary body to slow down AH production
* (Gonio implants - poor success)
* Enucleation

Goal - reduce IOP to 20 mmHg

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6
Q

What are congenital diseases affecting the iris?

A
  • Aniridia - no iris
  • Iridal hypoplasia - underdevelopment or incomplete development of the iris
  • Iris coloboma - missing part of iris
  • Persistent pupillary membrane
  • Dysplasic pupillary membrane
  • Heterochromia
  • Congenital miosis
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7
Q

What are acquired diseases of the iris?

A
  • Uveitis
    • Secondary, ERU
    • Discolouration
  • Synechiae
    • “Stuck” pupil - because iris is stuck to the lens
    • Dyscoria
  • Cysts
  • Neoplasia
    • Melanoma
  • Rubeosis iridis/iritis - discoloaration of the iris as a consequence of inflammation
    • new blood vessel formation may occur due to ischemia
  • Prolapse
    • with perforation
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8
Q

What are synechiae usually secondary to? How are they managed?

A

Often secondary to uveitis, may cause the pupil to be stuck in position and therefore affect vision

Treatment
* Mydriatics
* Tissue Plaminogen Activators - help break down fibrin

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9
Q

Where can iris cysts be located? What is a common differential? How can you differentiate? How are they treated?

A

Often an incidental finding, but may obscure pupil (worse in sunlight)

Location
* Granula iridica
* Pupillary margin
* Ciliary body
* Iris stroma

Melanoma is main differential - need to ultrasound to differentiate

Treatment
* Laser deflation
* Aspiration

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10
Q

When does iris prolapse occur? How does it present? How can you confirm it? How is it treated?

A
  • Subsequent to globe rupture/perforation
  • Brown spot on cornea indicates prolapse
  • Ultrasound
  • Treatment: enucleation or transposition of the cornea
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11
Q

What are the stuctures in the uvea? What are their functions?

A

Middle vascular layer of the eye -> Blood Ocular Barrier
Provides support and nourishment

Iris
- Shutter function

Ciliary body
- continuous production of AH
- Regulation of IOP via drainage at ICA

Choroid
- Provide blood supply to the retina

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12
Q

What is uveitis? How can i present depending on location? What structures are involved?

A

Inflammation of the structures part of the Uvea

Anterior
* Iris, Ciliary body
* Aqueous flare, myosis, hypopyon, hyphaema
* Also conjunctival hyperemia, episcleral injection, corneal oedema, keratic precipitates
* fibrin clots

**Posterior **
* Choroid and retina
* Vitreal cloudiness
* Retinal degeneration
* peripapillary degeneration, aka butterfly lesion

Panuveitis
* Anterior and posterior uveitis combined

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13
Q

What is the pathogenesis of anterior uveitis?

A

Acquired uveitis
* Systemic disease
* Infections, sepsis
* Neoplasia
* Trauma (blunt)
* Equine Recurrent Uveitis (ERU)

Reflex uveitis (secondary)
* Corneal ulceration
* Conjunctivitis
* Glaucoma

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14
Q

What drives inflammation in posterior uveitis? What can be consequences?

A
  • Neutrophilic infiltration of iris and ciliary body, then replaced by lymphocytes, plasma cells and macrophages
  • Given that the choroid is the primary vascular supply to the retina, choroidal inflammation (choroiditis) can lead to retinopathy.

Consequences
* Retinal damage
* Serofibrinous exudate in the vitreus
* Cataracts

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15
Q

What is equine recurrent uveitis (ERU)? What are the different steps?

A

Immuno-mediated, recurrent, pan-uveitis

  • Leading cause of blindness in horses (2-25%)
  • Acquired condition
  • Breed predisposition (eg Appaloosas, WB, Draft)
  • Unilateral vs bilateral (80:20)
  • Easily confuse with other ocular disease

Steps
1. First episode of acquired ocular disease
1. Blood ocular barrier compromised
1. Leakage of antigens in the eye
1. Recurrent inflammatory episodes (antigen recognition by immune system)

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16
Q

Describe pathogenesis of ERU

A
  • Infection bypassing BOB, leakage of antigens within the eye
    • Bacteria: Leptospira, salmonella, rhodococcus,…
    • Viruses: EHV, EIV, EVA, EIA, …
    • Parasites: strongyles, onchocerca, toxoplasma, …
    • Fungi
  • Genetics (appaloosa - increased susceptibility)
  • Trauma
  • Immuno-mediated processes
17
Q

What are the 3 forms of ERU? What clinical signs are associated?

A

Classical
* Alternates acute episodes with quiescent periods
* panuveitis

Insidious
* Low grade, persistent, gradual progression
* Appaloosas

Posterior
* Vitreous cloudiness
* Chorioretinopathy
* Retinal detachment
* Cataracts
* WB, draft

Clinical signs
* Pain, epiphora, blepharospasm
* Corneal oedema
* Aqueous flare, hyphaema, hypopyon
* Myosis
* Rubeosis iridis
* Corpora nigra degeneration
* Synechiae
* Cataracts
* Chorioretinopathies
* Glaucoma
- Ultimately vision loss

18
Q

How is ERU treated?

A

Medical - Aim is to control pain and inflammation
- Mydriatics (Atropine & Phenylephrine/Tropicamide)
- Steroids - dexamethasone/prednisolone
- NSAIDs - Topical (bromfenac, flurbiprofen, etc) or Systemic (flunixin)
- ± Antimicrobials - Topical – if corneal ulceration is present or Systemic (if one suspects bacterial pathogenesis)

Surgical
* Suprachoroidal Cyclosporin A device implant
* Release medication directly into ciliary body
* Surgery performed during quiescent phase only
* Prevents recurrence for ~5 years
* Pars plana vitrectomy
* Involves removal of the vitreous
* Aims at removing vitreal particles
* Before surgery need to confirm that there are vitreal antibodies (eg against Leptospira) as success rate is better for those cases
* Enucleation
* Uncontrollable pain
* Non visual eye

19
Q

What is the prognosis of ERU? What are the complications?

A

Guarded to poor – vision loss most likely in the long term
It is lifelong!!!

Complications
- Synechiae, fundus lesions and iris discolouration associated with poorer outcome

Early and aggressive treatment is key
Cyclosporine A implants most successful to delay progression

20
Q

What is the function of the lens?
What are the clinical signs of disease of the lens?

A

Function:
* Refraction
* Accommodation
* Image quality
* Protection of the retina

Clinical signs:
* Changes in vision
* ± Discomfort
* Epiphora
* Blepharospasm
* Photophobia
* Changes in eye appearance
* Changes in performance
* Owner may notice an opacity in the eye

21
Q

How can you evaluate the lens?

A
  • Sedation
  • Palpebral nerve block
  • Mydriatics (take 30min to work)
    • Tropicamide
    • Phenylephrine
  • Ophthalmoscopy
    • Ophthalmoscope
    • Slit light
    • Transillumination
    • Retroillumination
    • Slit-lamp biomicroscopy

Ultrasonography

22
Q

What diseases affect the lens?

A

Congenital
- Cataracts ~35% of congenital ocular defects
- Aphakia - absence of the lens.
- Coloboma - notch-like defect at the lens equator
- Ectopia lentis - disordered lens tissue in a shallow anterior chamber
- Some luxations
- Sperophakia - abnormally spherical lens.
- Lenticonus/lentiglobus - conical or globular contour

Acquired
- Cataracts
- Luxations/subluxations
- Capsular perforation
- Expansion
- Rupture

23
Q

What is a suture line on the lens?
What do they look like?

A

A line where the growing tissue of the lens is meeting
can be y shapped, often see the posterior suture line
not abnormal

24
Q

What are the causes of cataracts?
Acquired
Confenital
Age related

A

Acquired (secondary)
* Uveitis
* Trauma
* Glaucoma
* Intra-ocular neoplasia
* After intra-ocular surgery

Congenital
* Breed
* Belgian draft, Morgan, QH, TB), Rocky mountain horse, American saddlebred
* With other ocular disorders
* Embryonic disruption

Age related
* Senile cataracts
* Nuclear sclerosis
* Slowly progressive, >18yo

25
Q

What is the character of congenital cataracts?

A
  • Diagnosed before 6 months
  • Uni or bilateral
  • Complete, nuclear, perinuclear, extranuclear
  • Involving anterior and posterior suture lin (very rarely progress)
  • Lenticular (nuclear) rarely progress, may actually decrease in size
26
Q

What is the character of non-progresive cataracts?

A
  • Usually nuclear or perinuclear
  • May become smaller overtime
  • Seldom compromise vision
  • Periodic examination to ensure non-progressiveness
27
Q

What is the character of progressive cataracts?

A
  • Usually secondary to other disease (uveitis), therefore monitor for other extra-lenticular abnormalities
  • Equatorial, anterior cortex
  • Progress slowly over months/years
  • With uveitis may progress rapidly
  • Frequent monitoring
  • May lead to loss of vision
28
Q

What is the treatment of cataracts?

A
  • Control uveitis or other underlying process
  • Phacoemulsification - Very specialised intraocular procedure
29
Q

What are the clinical signs of lens luxation?
What is the treatment?

A
  • Zonular fibre damage:
    • Inflammation
    • Glaucoma
    • Trauma
    • Hypermature cataracts
  • Congenital

Clinicla signs:
* Aphakic crescent
* Iridodonesis (iris vibration)
* Corneal oedema
* Elevated IOP
* Visual impairment/blindness

Treatment
* Enucleation
* Lens removal
* Phacoemulsification