Hx
What do you know about the patient?
- Do they have a family history of same disease?
- Do they have history of trauma?
- History of contact lenses?
- Contact with water, or unknown substances?
- Previous onset of disease?
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- Is it familial history?
- Is it traumatic history?
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Sometimes the questions you choose to ask depend on the appearance you see
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What did they say no to?
- No family history?
- No traumatic history?
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Let's just assume no trauma, and no family history. Potentially there is an involvement of microbes, or it is autosomal recessive.
Family
Non-family
Microbe
AR
This indicates an autosomal dominant condition, and hence a high likelihood of dystrophy.
- Many dystrophy can be identified from appearance
- Some identified based on zones, others based on onset or diurnal pain
- Traumatic, Contact Lens, Surgery, History of microbial disease.
Worse in the morning
No Peripheral sparing
Fuch's Endothelial
* Failure of the endothelial cell pumps cause oedema, which causes blurred and hazy vision in the mornings
* Sometimes AD​
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Lattice Dystrophy
* Whilst less likely, may still occur.
* Spares the periphery (type 1)​
Granular Type II
* Hyaline and amyloid deposits
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Lattice Dystrophy Type III
* Can be AR
* Does not spare the periphery
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Pain, photophobia, glare
Meesmann Dystrophy
* Microcysts may cause glare and discomfort, and pain if cysts rupture
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Granular Type 1
* Discrete white central snowflake/salt and pepper crystals
* Crumb like small deposits in stroma
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It is possible that with no history, it could be dystrophy of autosomal recessive origin, or ectasia.
- Ectasia can be caused by surgery (which may be missed out), or due to unknown reasons, but will require the keratometer or topographer
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AR Dystrophy:
Macular Corneal Dystrophy.
* Characterised by hazy stroma, with keratic precipitates and hazy patches.
* Progressive vision loss, but painless
* GAG and mucopolysaccharide stromal deposits
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Lattice Dystrophy T3:
* Can be AD
* Minimal haze in between lattice lines, but lines are thicker and rope-like
* No sparing of periphery (limbus-limbus)
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Fuch's Endothelial
* Failure of the endothelial cell pumps cause oedema, which causes blurred and hazy vision in the mornings
* Mostly sporadic, can be AD
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Epithelial Basement Membrane Dystrophy:
* Sporadic, involving thickening of BM
* Onset in the 1st/2nd decade
* Map, dot, fingerprint like line patterns appear.
* Spontaneous erosions and pain
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Lattice Dystrophy Type II:
* Meretoja's, and is a false dystrophy
* Lines are delicate but random. Amyloid buildup in trigeminal nerve and corneal stroma
* Is associated with itchy skin, and a puppet like expressionless face
- Most likely an opportunistic microbe, or highly infectious virus.
Focal lesion
Diffuse lesion
No lesion
Bacterial Keratitis:
* Probably staphylococcus, and unlikely to be pseudomonas.
* Lesions are green-yellow and focal
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HSV Keratitis:
* Distinct discrete ulcers with terminal bulbs
Fungal Keratitis:
* Lesions more grey-white
* Diffuse satellite lesions, with feathered edges
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Acanthamoeba Keratitis:
* Has different manifestations, but usually marked by a diffuse immune ring (Wessley Ring)
HZV Keratitis:
* Ulcers are less stainable, and sometimes not present
* May come with skin shingles, or not in zoster sine
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Adenoviral Keratitis:
* Precipitates present, and usually is accompanied by PCF and EKC
* Highly contagious
Contact Lens
Recurrence or previous infection
Surgery and trauma
Bacterial Keratitis:
* Probably pseudomonas cytotoxic strand​
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Fungal and Acanthamoebal Keratitis:
* Whilst they can occur without CL, they are 3-5x more likely in CL wearers. This is due to trauma
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Sterile Keratitis and CLPU:
* Will cause a painful lesion with no discharge, and lesion is fairly small (0.1-2mm)
* No AC reaction either.
* Usually in the periphery to mid-periphery
Graft Rejection:
* Cloudiness appears​
* Leads to failure due to antigen response
* Faint epithelial lines appear
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Bacterial Keratitis:
* Probably pseudomonas invasive strand
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Traumatic Cornea:
* Blunt force to cornea.
* Thickening and folds, very painful, and may need to be sutured together if penetration or laceration
* If chemical trauma, may require intense surgery
* Photokeratitis also possible
Herpes Simplex and Zoster:
* Due to the reactivation of herpes in the trigeminal vein (ophthalmic branch)
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Herpes' Reaction:
* Stromal keratitis may occur, such as non-necrotising and necrotising
* Linear endotheliitis
* Disciform endotheliitis
* Diffuse endotheliitis
* Neutrophic keratopathy
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Thygeson's Punctate Keratitis:
* Unknown cause, but has severe pain with small punctate lesions that recur very often (6-8W)
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Hypersensitivity Reactions:
* Phlyctenulosis -> marching phlyctenules with vessels
* Marginal keratitis -> parallel to limbus
* Interstitial keratitis -> Can have ghost vessels from withdrawn neovascularisation, similar to phlyctenulosis but less severe
(+ve) Topography
Keratoconus
* Munsen's sign, Vogt's striae, Fleischer's ring, is progressive
* Sudden change in astigmatism
* Bending occurs towards periphery
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Pellucid Marginal Degeneration
* Thinning at 4-8 o'clock
* Spares the central, and is 1mm from limbus
* Ulcerification?
* Also astigmatism
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Keratoglobus​
* Limbus to limbus ectasia
* Thins at edges, very steep cornea
* Can have blue sclera, neovascularisation
(-ve) Topography
Posterior Polymorphous
* Is usually AD BUT very rare, so may be missed in family history​
* Generally asymptomatic, asymmetric
* Marked by vesicular endothelial patterns that can be confluent.
* Display of epithelial like characteristics
* Proliferation of band-like lesions
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