Competency 6.1.4 & 6.1.7 Flashcards

1
Q

What is a Limbal Dermoid?

A
  • Presents as a whitish or yellowish lesion at the corneal limbus
  • limbus-sparing dermoids and dermoids involving the entire cornea have been reported
  • Patients with corneal dermoids usually present early in life, as the condition is congenital
  • associated with Goldenhar Syndrome.
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2
Q

Limbal Dermoid Symptoms

A
  • Irritation
  • Dry eye symptoms
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3
Q

Limbal Dermoid Signs

A
  • Young patient age
  • Most are located at the inferior temporal limbus, though can affect only the cornea iself in some cases
  • In terms of appearance:
    o Usually has a dome shape
    o Visible hair follicles
    o Often vascularised
  • May also have coloboma of eyelids, duanes retraction syndrome and microphthalamos
  • May suffer from recurrent conjunctivitis
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4
Q

Limbal Dermoid Non-Surgical Management

A
  • Main concern is visual development and preventing amblyopia
  • Close monitoring of lesion size
  • Close monitoring of VA, stereopsis and refraction
  • If amblyopia proven then treated with patching therapy
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5
Q

When is Surgery indicated for Limbal Dermoid?

A

o Chronic eye rubbing due to irritation and recurrent conjunctivitis
o Amblyopia unresponsive to medical management
o Progressive dellen with corneal surface decompensation
o Growth and encroachment into pupillary area or optical zone
o Aesthetic considerations
o Inadequate lid closure

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6
Q

What is a Conjunctival Inclusion Cyst?

A
  • a benign cyst filled with clear serous fluid containing shed cells or mucoid material
  • constitute 80% of all cystic lesions of the conjunctiva
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7
Q

Conjunctival Inclusion Cyst Risk Factors

A
  • Inflammatory conditions of the conjunctiva
  • Overactive immune system
  • Trauma
  • Surgery
  • Sub-Tenon anesthesia
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8
Q

Conjunctival Inclusion Cyst Symptoms

A
  • If small
    o Generally asymptomatic
    o FB sensation
  • If large
    o Pain
    o Motility disturbances
    o VF defect
    o Induced refractive error
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9
Q

Conjunctival Inclusion Cyst Management

A
  • Generally these cysts disappear spontaneously
  • If persistant:
    o Surgical excision
    o Empyting of cyst using needle
    o YAG laser
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10
Q

What is Conjunctival Papilloma?

A
  • can be benign or malignant and can be found in numerous anatomical locations (eg, skin, conjunctiva, cervix, breast duct)
  • conjunctival papillomas are benign squamous epithelial tumors with minimal propensity toward malignancy
  • A strong association exists between Human Papilloma Virus (HPV) types 6 and 11
  • usually seen in younger patients (HPV related)
  • a slight association exists between UV radiation and limbal conjunctival papilloma so these may be seen in older patients
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11
Q

Limbal Papilloma Signs

A
  • Seen in older patients
  • History of UV exposure
  • Possible decrease in VA
  • Recurrance is not common
  • Almost always single and unilaterial
  • Slowly increase in size
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12
Q

Infectious Papilloma Signs

A
  • Benign and self limiting
  • Commonly seen in children and young adults
  • Most asymptomatic without connjuctvitis
  • No decrease in VA
  • Commonly located in inferior fornix
  • May be bilaterial and mulitiple
  • Appears as a grayish red, fleshy, soft, pedunculated mass with an irregular surface (cauliflowerlike)
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13
Q

What is a Pyogenic Granuloma

A
  • is a common, non-cancerous growth of blood vessels which do not produce pus or involve the chronic inflammation typical of granulomas
  • appear as smooth, red-purple bumps, either flat or on a stalk
  • can recur after removal.
  • PG can appear anywhere on the body, most frequently on the skin, affecting men and women equally
  • ## they are twice as common in the mucous membranes of women, such as the conjunctiva, and are associated with pregnancy
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14
Q

Pyogenic Granuloma Risk factors

A
  • Pregnancy
  • More common in women when conjunctival
  • Linked to inflammation after strabismus surgery
  • Herdeolum/chalazion
  • Young age
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15
Q

Pyogenic Granuloma Symptoms

A
  • Discomfort (depending on location)
  • Lesion will bleed with very little trauma
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16
Q

Pyogenic Granuloma Management

A
  • Topical steroids
  • Cryotherapy
  • Steroid injection
  • Excision
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17
Q

Conjunctival Papillae Characteristics (vs Follicles)

A
  • Can be larger
  • Cobblestone arrangement
  • Flattened top
  • Central vascular cores
  • Commonly caused by allergic immune response or FB/contact lens
  • Structure: Lymphocytes, plasma cells and mast cells in stroma surrounding a central vascular channel
  • Appears more red at surface and pale at the base
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18
Q

Conjunctival Follicles Characteristics (vs Papillae)

A
  • Smaller
  • Dome-shaped
  • May have overlying vessels but lack the prominent central vessel
  • Typically caused by inflammation due to pathogens (e.g. viruses, bacteria and toxins)
  • Structure: Centre of immature proliferating lymphocytes with surrounding corona of more mature lymphocytes and plasma cells.
  • Appears more red at base and paler at surface
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19
Q

Causes of Follicular Reaction

A
  • Toxins (e.g apraclonidine)
  • Viruses (e.g. adenovirus)
  • Chlamydia
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20
Q

Causes of Papillary Reaction

A
  • Allergy (AKC or VKC)
  • Foreign body
  • Superior limbic keratoconjucntivitis
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21
Q

What are Conjunctival Membranes?

A
  • True membrane formation occurs when the fibrinous deposit secreted by the invading microorganisms or ocular tissues adheres to the conjunctiva’s epithelial surface due to capillaries’ growth into the membrane
  • Peeling membranes in membranous conjunctivitis causes bleeding and leaves behind a raw surface, representing more intense inflammation.
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22
Q

Conjunctival Membranes Causes

A

Causes of Membranous conjunctivitis include:
- Bacterial infections can cause true membrane formation. Bacterial infections include Chlamydia.
- Viral causes include adenovirus (most common) and potential for fibrosis. Herpes simplex virus (HSV) and Epstein-Barr virus (EBV) may also be implicated.
- Drug reactions including hypersensitivity spectrum reactions, Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), often in response to adverse drug reactions.
- Autoimmune diseases
- Eye-limited inflammatory etiologies include ocular cicatricial pemphigoid and chemical or thermal injury.

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23
Q

What are Conjunctival Pseudomembranes?

A
  • Pseudomembranous conjunctivitis membranes are more superficial, with no growth into the conjunctival epithelium, and can be removed with minimal bleeding.
  • bleeding may still be observed in pseudomembranous conjunctivitis due to severe inflammation and friability of the underlying conjunctiva
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24
Q

Conjunctival Pseudomembranes Causes

A
  • Bacterial causes include Chlamydia
  • Viral causes include adenovirus but COVID-19 has also been implicated
  • Inflammatory etiologies include hypersensitivity reactions, such as SJS,
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25
Q

What is a Subconjunctival Haemorrhage?

A

Subconjunctival haemorrhage (S-CH) results from rupture of conjunctival or episcleral blood vessels causing bleeding into the subconjunctival space
- Two main causes:
- spontaneous (higher incidence in adults over 50 years)
- Traumatic (higher incidence in younger adults)

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26
Q

Subconjunctival Haemorrhage Spontaneous Causes

A
  • idiopathic (most common)
  • Valsalva manoeuvre (e.g. coughing, lifting, straining, vomiting) producing increase in central venous pressure
  • systemic vascular disease (e.g. hypertension, diabetes)
  • medication (anticoagulants, NSAIDs)
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27
Q

Subconjunctival Haemorrhage Traumatic Causes

A
  • injury
  • eye rubbing
  • ocular surgery/procedure (cataract surgery, refractive surgery, anaesthesia technique such as sub-Tenon’s anaesthetic or peribulbar block and intravitreal injection)
  • contact lens handling injury
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28
Q

Subconjunctival Haemorrhage Risk Factors

A
  • Older age (highest incidence at 60-80 years)
  • Trauma (including contact lens-related injury)
  • Anticoagulant medication (e.g. aspirin, warfarin, clopidogrel, rivaroxaban, apixaban)
  • Hypertension, diabetes and other systemic vascular disorders
  • Bleeding abnormality (leukaemia, clotting disorders)
  • Long-term topical steroid treatment
  • Conjunctival vascular lesion
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29
Q

Subconjunctival Haemorrhage Symptoms

A
  • Mild ache or irritation (if extensive haemorrhage, otherwise painless)
  • May be asymptomatic
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30
Q

Subconjunctival Haemorrhage Signs

A
  • Red area on eye, location usually temporal or inferior, caused by blood beneath the conjunctiva of which the posterior border can be seen
  • Haemorrhage-localised or diffuse
  • Usually unilateral
  • No discharge
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31
Q

Subconjunctival Haemorrhage Management

A
  • Reassure patient
  • Condition usually clears within 5-10 days
  • Tear supplement / ocular lubricant if mild ocular irritation is present
  • Cold compresses for any discomfort
  • Consider ocular/orbital involvement in patients on anticoagulation
    o Retinal haemorrhage
    o Diplopia
    o Proptosis
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32
Q

What is a Pingecula?

A
  • Elastotic degeneration of the conjunctiva
  • appears as a yellow white raised lesion in the interpalpebral bulbar conjunctiva
  • Pinguecula does not progress to become pterygium; they are two distinct conditions
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33
Q

Pingecula Predisposing Factors

A
  • Increasing age (seen in most eyes by age 70)
  • Long term exposure to UV radiation
  • Sunlight (residence at or near the equator, outdoor work, especially on reflective surfaces e.g. sand, concrete, water, snow)
  • Welding and other occupational exposure
  • Male gender (likely to be related to occupational exposure)
  • Chronic irritation from wind or dust
  • Contact lens wear
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34
Q

Pingecula Symptoms

A
  • Usually asymptomatic
  • Possible mild foreign body sensation and redness when inflamed (pingueculitis)
  • Occasional cosmetic concern
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35
Q

Pingecula Signs

A
  • Area of conjunctival thickening
  • Located in the palpebral aperture, usually situated horizontally at the limbus and more common nasally
  • usually bilateral
  • Elevated and less transparent than normal conjunctiva
  • White to yellow colour, fat like appearance, calcification sometimes present
  • Sometimes slightly more hyperaemic than surrounding conjunctiva
  • May lead to Dellen in adjacent cornea
  • Decreased tear break-up time (TBUT)
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36
Q

Pingecula Management

A
  • Advice
    o Reassure patient about benign nature of the lesion
    o Advise on UV protection to minimise risk of inflammation
    o Brimmed hat
    o Sunglasses in wrap-around style for side protection
  • Treatment
    o Cold compresses when inflamed
    o Ocular lubricants for symptomatic relief (drops for use during the day, unmedicated ointment for use at bedtime)
    o PoM Pingueculitis usually responds to a brief course of a ‘non-penetrating’ topical steroid
    - Fluorometholone 0.1% eye drops 4x daily (reduce by 1 drop a week to zero)
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37
Q

What is a Pterygium?

A
  • A winged-shaped fibrovascular growth progressing from the bulbar conjunctiva to involve the cornea
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38
Q

Pterygium Predisposing Factors

A
  • Older age
  • Male gender (probably related to occupational exposure)
  • Long term exposure to ultraviolet radiation
  • Sunlight (residence at or near the equator, outdoor work, especially on reflective surfaces e.g. sand, concrete, water, snow)
  • Dry, arid climate
  • Inflammatory and allergic ocular surface disease
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39
Q

Pterygium Symptoms

A
  • Mild irritation, redness, dryness, foreign body sensation which may be exacerbated by episodes of acute inflammation
  • Effect on vision
    o result of astigmatism (with the rule)
    o in severe cases, pterygium may extend over visual axis
  • Cosmetic concern
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40
Q

Pterygium Signs

A
  • Typically bilateral; most common nasally; often asymmetrical.
  • Starts with scarring, thickening and distortion of the bulbar conjunctiva
  • Small grey corneal opacities appear near the limbus later conjunctiva overgrows these opacities
  • Slow insidious growth on to cornea (or may become stable)
  • Destroys Bowman’s membrane and superficial stroma lamellae
  • Epithelial iron deposit (Stocker’s line) ahead of advancing pterygium
  • Relatively rich surface vascularisation
  • Flattening of cornea in horizontal meridian
  • Tear film instability
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41
Q

Pterygium Management

A
  • Advice
    o Advise on UV protection to minimise risk of inflammation
    - Brimmed hat
    - Sunglasses in wrap-around style for side protection
  • If inflamed
    o Cold compress when inflamed
    o Ocular lubricants for symptomatic relief (drops for use during the day, unmedicated ointment for use at bedtime)
    o PoM Acute inflammation of a pterygium usually responds to a brief course of a ‘non-penetrating’ topical steroid
    - Fluorometholone 0.1% eye drops 4x daily (reduce by 1 drop a week to zero)
  • Normally no referral unless
    o Threatens visual axis
    o Induces irregular astigmatism
    o Associated with chronic inflammation
    o Cosmetically unacceptable
  • Possible management by Ophthalmologist
    o Topical steroids if inflamed
    o Excision
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42
Q

What is Acute Bacterial Conjunctivitis?

A
  • Most cases are acute, self-limited, and not a major cause of morbidity
  • because of its high prevalance, it has a large societal impact in terms of missed days of school or work
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43
Q

Organisms which Cause Acute Bacterial Conjunctivitis

A
  • Staphylococcus aureus
  • Streptococcus pneumoniae
  • Haemophilus influenzae.
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44
Q

Acute Bacterial Conjunctivitis Predisposing Factors

A
  • Children and the elderly have an increased risk of infective conjunctivitis
    (NB Bacterial conjunctivitis in the first month of life is a serious condition that must be referred urgently to the ophthalmologist.
  • contamination of the conjunctival surface
  • superficial trauma
  • contact lens wear (particularly poor lens hygiene) (NB infection may be Gram –ve)
  • secondary to viral conjunctivitis
  • diabetes (or other disease compromising the immune system)
  • steroids (systemic or topical, compromising ocular resistance to infection)
  • blepharitis (or other chronic ocular inflammation)
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45
Q

Acute Bacterial Conjunctivitis Symptoms

A
  • Acute onset of:
    o Redness
    o discomfort, usually described as burning or grittiness
    o discharge (may cause temporary blurring of vision)
    o crusting of lids (often stuck together after sleep and may have to be bathed open)
  • Usually bilateral – one eye may be affected before the other (by one or two days)
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46
Q

Acute Bacterial Conjunctivitis Signs

A
  • lid crusting
  • purulent or mucopurulent discharge
  • conjunctival hyperaemia – maximal in fornices
  • tarsal conjunctiva may show mild papillary reaction
  • cornea: usually no involvement
  • pre-auricular lymphadenopathy is usually absent
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47
Q

Acute Bacterial Conjunctivitis Management

A
  • Advice
    o Bathe/clean the eyelids with proprietary sterile wipes, lint or cotton wool dipped in sterile saline or boiled (cooled) water to remove crusting.
    o Advise patient that condition is contagious (do not share towels, etc.)
    o Public health guidance in all UK Nations states that school or nursery exclusion is not required for children with this condition
    o Contact lenses should not be worn during the treatment period. Beware corneal involvement in contact lens wearers
  • Pharmacological Treatment
    o Treatment with topical antibiotic for one week may improve short-term outcome and render patient less infectious to others
    - Ask if allergic to Chloramphenicol
    - If not, supply Chloramphenicol 1% eye ointment 3 times daily for a week
    - If allergic to Chloramphenicol, or pregnant, supply Fusidic acid 1% liquid gel twice a day for a week
  • Refer if:
    o Condition fails to resolve
    o There is corneal involvement
  • Possible management by Ophthalmologist
    o Conjunctival swabs taken for analysis
    o Treatment with other antibiotics, based on culture results
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48
Q

What is Chlamydial Conjunctivitis?

A
  • Chronic follicular conjunctivitis caused by the sexually transmitted microorganism Chlamydia trachomatis
  • Spread by direct contact or fomites
  • Chlamydial infection ranges in severity from mild to severe.
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49
Q

Chlamydial Conjunctivitis Predisposing Factors

A
  • Most common in young adulthood (15-35 years)
  • Sexual activity leading to genital infection (up to 70% of cases of chlamydial conjunctivitis have a concurrent genital infection):
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50
Q

Chlamydial Conjunctivitis Symptoms

A
  • History usually more than two weeks
  • Ocular gritty sensation and sticky discharge
  • Drooping upper lid(s) (often unilateral but may involve both eyes)
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51
Q

Chlamydial Conjunctivitis Signs

A
  • Lid and other features
    o oedema +/- ptosis (‘mechanical’)
    o non-tender pre-auricular lymph node swelling (may or may not be present)
  • Conjunctival features
    o hyperaemia and chemosis
    o mucopurulent conjunctivitis
    o large follicles in upper and lower fornices (double eversion of lid needed to view upper fornix)
    o limbal and/or bulbar follicles may also be present
  • Corneal features
    o epithelial keratitis, usually superior
    o subepithelial infiltrates, similar to those seen in adenovirus KC
    o marginal infiltrates
    o superior pannus
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52
Q

Chlamydial Conjunctivitis Management

A
  • Advice
    o Advise against contact lens wear
    o Advise patient that genitourinary infection commonly associated (70% of cases)
  • Non-Pharmacological Treatment
    o Symptomatic relief with ocular lubricants
  • Referral Urgency
    o Urgent referral to ophthalmologist and GP
  • Ophthalmologist Management
    o Conjunctival swabs and genital swabs for chlamydia
    o Liaison with Sexual Health Clinic
    o Treatment with systemic Azithromycin
    o Topical Azithromycin
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53
Q

Signs on Ophthalmic Exam Which Suggest Viral over Acute Bacterial

A
  • Follicular reaction
  • Pre-auricular lymphadenopathy
  • Watery discharge
  • Itchy eyes
  • Concurrent pharyngitis, fever, and upper respiratory infection
  • A history of prior conjunctivitis
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54
Q

What is Adenoviral Conjunctivitis?

A
  • is the most common form of acute infective conjunctivitis
  • Adenoviruses are highly contagious pathogens (over 50 serotypes)
  • the spectrum of disease varies from mild to severe
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55
Q

Adenoviral Conjunctivitis Risk Factors

A
  • Infection may be preceded by ‘flu-like symptoms
  • Low standards of hygiene
  • Outbreaks can occur in the general population, especially in crowded conditions (schools, camps), in hospital environments (especially ophthalmological units, and neonatal intensive care units) and in nursing homes
  • Eye clinics (transmission by clinicians’ fingers, tonometer prisms, etc.)
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56
Q

Adenoviral Conjunctivitis Symptoms

A
  • Acute onset
  • Redness
  • discomfort, usually described as burning or grittiness
  • watering
  • Symptoms of EKC usually appear within 14 days of exposure and typically last 7 to 21 days
  • Often unilateral at first, becoming bilateral, first eye usually more affected
  • Blurred vision if central cornea involved
  • Systemic malaise
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57
Q

Adenoviral Conjunctivitis Signs

A
  • Watery discharge
  • Conjunctival hyperaemia (may be intense) and chemosis
  • Follicles on palpebral conjunctiva, especially upper and lower fornix (if abundant, follicles can produce folds)
  • Petechial (pin-point) subconjunctival haemorrhages
  • Pseudomembranes on tarsal conjunctival surfaces (severe cases only)
  • Pre-auricular lymphadenopathy which may be tender (not present in every case)
  • Corneal involvement in some cases:
    o punctate epithelial lesions within first two weeks
    o later replaced by sub-epithelial infiltrates which may persist for months
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58
Q

Adenoviral Conjunctivitis

A
  • Advice
    o condition is normally self-limiting, resolving within one to two weeks
    o condition is highly contagious for family, friends and work colleagues (do not share towels, etc)
    o remain infectious for 2 weeks after symptom onset
    o Time off work or school not recommended
    o cold compresses may give symptomatic relief
    o discontinue contact lens wear in acute phase
  • Pharmacological Treatment
    o Current topical and systemic anti-viral agents also ineffective in adenovirus infection
    o Artificial tears and lubricating ointments (drops for use during the day, unmedicated ointment for use at bedtime) may relieve symptoms
    o Topical antihistamines may be used for severe itching
  • Management Category
    o Normally no referral
    o Emergency referral IF:
    - Visual loss
    - Severe pain
    - Significant keratitis
    - Pseudomembrane
  • Possible management by Ophthalmologist
    o Conjunctival swabs for virus isolation and strain identification
    o Topical low dose steroids may be prescribed where sub-epithelial opacities affect vision
    o Topical steroid may also be indicated for conjunctival pseudomembrane formation
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59
Q

The Two Syndromes of Adenoviral Infection

A
  • epidemic conjunctivitis and keratoconjunctivitis (EKC)
    o most cases affect adults aged 20 to 40 years
  • pharyngoconjunctival fever
    o systemic symptoms predominate, with pharyngitis, tender pre-auricular lymphadenopathy, fever and an acute follicular conjunctivitis
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60
Q

What is Molluscum Contagiosum?

A
  • Is a localised skin infection caused by a poxvirus which is mildly contagious and spreads through skin-to-skin contact
  • is particularly common in immunocompromised individuals
  • Lesions on the lid margins may shed viral toxins into the conjunctival sac, causing:
    • follicular conjunctivitis
    • uncommonly, corneal involvement
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61
Q

Molluscum Contagiosum Risk Factors

A
  • attendance at swimming pools
  • eczema
  • Strong association with Human Immunodeficiency Virus (HIV) infection
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62
Q

Molluscum Contagiosum Symptoms

A
  • Presence of skin lesion(s)
  • Ocular symptoms (all mild)
    o Redness
    o Watering
    o Photophobia
    o blurring of vision
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63
Q

Molluscum Contagiosum Signs

A
  • Skin lesion
    o Skin nodule(s) (typically 2-3 mm diameter), often with a central depression (‘umbilicated’)
    o No visible inflammation
    o Central core has cheese-like or waxy material which may discharge spontaneously
    o May be single or multiple on the lid(s) and/or elsewhere on the body
  • Ocular signs (usually unilateral):
    o hyperaemic conjunctiva
    o conjunctival follicles
    o corneal involvement including:
    - punctate keratopathy
    - subepithelial opacities
    - pannus
    o watery discharge
    o No lymphadenopathy
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64
Q

Molluscum Contagiosum Management

A
  • Advice
    o Usually self-limiting (weeks or months) without scarring or other long term sequelae.
    o no reliable evidence-based recommendations can be given for the treatment of molluscum contagiosum at present
    o If lesion is quiet:
    - Leave alone
    - Advise on hygiene to avoid spread
  • Pharmacological Treatment
    o Artificial tears and ointment can reduce symptoms if causing conjunctivitis
  • Management Category
    o Normally no referral
    o Refer if:
    - Multiple peri-ocular lesions
    - Lesions on lid margin
    - Follicular conjunctivitis
65
Q

What is Seasonal and Perennial Allergic Conjunctivitis

A
  • Type I hypersensitivity (IgE-mediated) reaction to specific airborne allergens.
  • Conjunctival mast cell degranulation liberates histamine and other inflammatory mediators into the tissues and tear film, causing dilatation of conjunctival vessels (→red eye), increased permeability of blood vessels (→oedema)
  • Often associated with allergic rhinitis.
66
Q

What is Seasonal Allergic Conjunctivitis?

A
  • caused by seasonal allergens, especially grass pollen
  • onset of symptoms associated with seasonal production of allergens:
    o tree pollen onset is in spring;
    o grasses onset is in early summer
    o weeds and fungal spores onset is in late summer
  • condition not sight-threatening, but reduces quality of life and is associated with a significant economic burden
67
Q

What is Perennial Allergic Conjunctivitis?

A
  • caused by non-seasonal allergens such as house dust mite or animal dander
  • symptoms throughout the year; may be seasonal exacerbations
  • less common and usually less severe than SAC
68
Q

Seasonal and Perennial Allergic Conjunctivitis Predisposing factors

A
  • Atopic disposition (40% of population)
  • Personal history of allergic disease (hay fever, asthma, eczema, food or drug allergy)
  • Family history of allergic disease
  • Exposure to allergens
69
Q

Seasonal and Perennial Allergic Conjunctivitis Symptoms

A
  • Red eye
  • Itching of eye (main symptom)
  • Watering of eye
  • May be associated with sneezing and watery nasal discharge
70
Q

Seasonal and Perennial Allergic Conjunctivitis Signs

A
  • Lids:
    o mild to moderate oedema (peri-orbital oedema in severe cases)
  • Bulbar and tarsal conjunctiva:
    o chemosis (oedema)
    o hyperaemia
    o diffuse papillary reaction
  • Cornea:
    o Uninvolved
71
Q

Seasonal and Perennial Allergic Conjunctivitis Management

A
  • Advice
    o Advise against eye rubbing
    o Advise avoidance of allergen(s)
    o Cool compresses for symptomatic relief
  • Pharmacological Management
    o For acute relief consider PoM topical antihistamine
    - PoM Olopatadine 1 drop twice daily (8 hourly interval) whilst symptomatic. Contraindicated in:
     breastfeeding/pregnancy
     women of childbearing age not using contraception
     Caution in dry eye/compromised ocular surface if prolonged use planned
    o Refer to local Pharmacist for oral antihistamine
    - Effective also for other symptoms of hay fever, e.g. allergic rhinitis
    o Consider anticipatory use of mast cell stabiliser (slow response)
    - Sodium cromoglicate 2% eye drops 4 times daily
72
Q

What is Vernal Keratoconjunctivitis?

A
  • is a rare and potentially sight-threatening allergic disorder of children
  • characterised by chronic inflammation of the ocular surface
  • More common in some other parts of the world, e.g. Mediterranean region, parts of Africa, Indian sub-continent
  • Is a complex immune reaction with raised IgE levels in the tears and serum, and mast cells and eosinophils in the conjunctival epithelium. T cells also play a significant role.
73
Q

Vernal Keratoconjunctivitis Predisposing Factors

A
  • Onset usually before 10 years of age
  • More common in male patients
  • typically resolves during puberty
  • Seasonal exacerbations (hence spring catarrh name) but condition may be active year-round if severe
  • Patients usually atopic with a history of eczema and asthma
  • Often a family history of atopic disease
74
Q

Vernal Keratoconjunctivitis Symptoms

A
  • Ocular itching, burning or foreign body sensation
  • Watering
  • Mucoid stringy discharge
  • Blurred vision
  • Pain (if cornea affected)
  • Photophobia (may be intense)
  • Difficulty opening eyes on waking
  • NB: symptoms are typically bilateral but often asymmetrical in the two eyes
75
Q

Vernal Keratoconjunctivitis Signs

A
  • Palpebral
    o hyperaemia and chemosis of conjunctiva when active
    o macro or giant tarsal papillae (1mm or greater in diameter; ‘cobblestone’ appearance)
  • Limbal
    o hyperaemic, oedematous, thickened limbus
    o Trantas’s Dots (discrete white superficial accumulations of eosinophils and degenerating epithelial cells)
    o limbal phenotype may be unilateral
  • Corneal (usually in upper third)
    o punctate epithelial keratopathy
    o macro-erosion (coalescent epithelial loss)
    o plaque (deposited on Bowman’s layer)
    o subepithelial scarring (often ring-shaped)
  • These patients may also have keratoconus and/or atopic cataract
76
Q

Vernal Keratoconjunctivitis Management

A
  • Advice
    o Cold compresses may alleviate acute symptoms
  • Pharmacological Treatment
    o PoM Olopatadine 1 drop twice daily (8 hourly interval) whilst symptomatic
    - Contraindicated in
     breastfeeding/pregnancy
     women of childbearing age not using contraception
     Caution in dry eye/compromised ocular surface if prolonged use planned
    o If persistent, consider use of sodium cromoglicate 2% eye drops 4 times daily
  • Management category
    o Low threshold for referral to ophthalmology as significant corneal involvement common
    o Urgent referral (within one week) if there is active limbal or corneal involvement:
    o Routine referral for PoM for milder cases (without active limbal or corneal involvement)
  • Possible management by Ophthalmologist
    o Topical steroids
    o Mucolytics
    o Topical immunosuppression
    o Systemic immunosuppression
    o Debridement/superficial lamellar keratectomy for corneal plaque/shield ulcer
77
Q

What is Atopic Keratoconjunctivitis?

A
  • Severe and potentially sight-threatening allergic eye disease in adults
  • characterised by chronic inflammation of the ocular surface
  • Is a result of complex immunopathology including T-cell mediated (type 4 hypersensitivity)
  • Symptoms of AKC typically begin in the late teens or early twenties and can persist until the fourth or fifth decade of life
  • It sometimes follows childhood Vernal Keratoconjunctivitis (VKC).
78
Q

Atopic Keratoconjunctivitis Predisposing Factors

A
  • The majority of patients have a personal history of asthma, and eczema
    (atopic dermatitis)
  • There may also be a family history of atopic disease
  • Most patients have eczema affecting the eyelids and periorbital skin
  • There is a strong association with staphylococcal lid margin disease
  • Specific allergens may exacerbate the condition
79
Q

Atopic Keratoconjunctivitis

A
  • Ocular itching, burning, watering, usually bilateral
  • Blurred vision
  • Photophobia
  • White stringy mucoid discharge
  • Onset of ocular symptoms may occur several years after onset of atopy
  • Symptoms are typically bilateral, occur year-round, with exacerbations
80
Q

Atopic Keratoconjunctivitis

A
  • Eyelids may be thickened, crusted and fissured
  • Associated chronic staphylococcal blepharitis
  • Tarsal conjunctiva:
    o giant papillary hypertrophy
    o subepithelial fibrosis
    o scarring
    o shrinkage
  • Entire conjunctiva hyperaemic
  • Limbal inflammation
  • Corneal involvement is common and may be sight-threatening:
    o beginning with punctate epitheliopathy that may progress to macro-erosion
    o plaque formation (usually upper half)
    o progressive corneal subepithelial scarring
    o neovascularisation
    o thinning
    o rarely spontaneous perforation
  • These patients are prone to develop:
    o herpes simplex keratitis (which may
    be bilateral)
    o corneal ectasia such as keratoconus
    o atopic (anterior or posterior polar) cataracts
    o retinal detachment
81
Q

Atopic Keratoconjunctivitis

A
  • Advice
    o Lid hygiene and treatment of associated staphylococcal blepharitis
    o Cool compresses
    o Advise avoidance of specific allergens if known, e.g. elimination of pets and carpeting
  • Pharmacological Treatment
    o For acute relief consider PoM topical antihistamine
    - PoM Olopatadine 1 drop twice daily (8 hourly interval) whilst symptomatic
     Contraindicated in
     breastfeeding/pregnancy
     women of childbearing age not using contraception
     Caution in dry eye/compromised ocular surface if prolonged use planned
    o Refer to local Pharmacist for oral antihistamine
    o If persistent, consider use of sodium cromoglicate 2% eye drops 4 times daily
  • Management Category
    o Urgent referral (within one week) if corneal involvement
    o Routine referral for PoM for milder cases
  • Possible management by Ophthalmologist
    o Topical steroids
    o Topical/systemic antibiotic for lids
    o Topical immunosuppression for eye and or lids
    o Systemic immunosuppression
    o Debridement/superficial lamellar keratectomy for corneal plaque/shield ulcer
82
Q

What is Contact Lens Associated Papillary Conjunctivitis?

A
  • is an inflammatory condition of the upper tarsal conjunctiva, presenting with hyperaemia and roughness of the conjunctival surface in response to contact lens wear
  • Its multifactoral aetiology is not fully understood.
  • CLAPC is thought to be immunological in origin but mechanical factors may also play a role
83
Q

Contact Lens Associated Papillary Conjunctivitis Mechanism of Allergic Response

A

Type I immediate hypersensitivity mediated by IgE
- Possible antigens:
o altered host protein on lens surface
o bacterial cell wall constituents
o other lens contaminants
- Reaction causes degranulation of mast cells and the products of degranulation stimulate recruitment of basophils and eosinophils to conjunctival epithelium
- Type IV delayed hypersensitivity mediated by T-cells which amplifies the inflammatory response

84
Q

Contact Lens Associated Papillary Conjunctivitis Predisposing Factors

A
  • Risk of CLAPC increases with duration of contact lens wear.
  • More common in reusable soft lens wear compared to disposable soft or rigid lens wear.
  • High modulus silicone hydrogel (SiHy) lenses may contribute to the mechanical aspect of the disease due to increased frictional irritation of the tarsal conjunctival surface.
  • Overnight contact lens wear
  • Lens deposits
  • Thick or poorly designed or manufactured lens edges
  • Preservatives in contact lens care products
  • Meibomian gland dysfunction
  • Atopy
85
Q

Contact Lens Associated Papillary Conjunctivitis Symptoms

A
  • Itching and non-specific irritation e.g. burning, foreign body sensation.
  • may increase after lens removal (manipulation of lids mechanically stimulates mast cell degranulation)
  • Mucus discharge
  • Increased lens movement
  • Loss of lens tolerance
  • Decreasing comfort (may abandon wear)
  • Blurred vision
  • (NB: poor correlation of severity with symptoms and signs)
86
Q

Contact Lens Associated Papillary Conjunctivitis Signs

A
  • Almost always bilateral
  • Upper tarsal conjunctiva (lower usually not affected)
  • Papillae
    o may be localised or generalised
    - in the localised form (more common in SiHy wearers) the papillae are confined to one or two areas of the tarsal conjunctiva.
    - In the generalised form, papillae are present over the entire tarsal conjunctiva
    o macropapillae (diameter between 0.3 and 1 mm) or giant papillae (diameter > 1 mm)
    o apices of papillae may stain with fluorescein when inflammation active
    o apices may be whitish due to scarring in chronic cases
  • hyperaemia
  • stringy mucus in tear film and on conjunctival surfaces
  • conjunctival oedema
87
Q

Contact Lens Associated Papillary Conjunctivitis Non-Pharmacological Management

A

o Initial management of CLAPC should focus on addressing predisposing factors relating to contact lenses or their care products.
o Removal of lens deposits
- replace soft lenses more frequently
- improve hygiene – more rigorous surfactant cleaning, more frequent enzyme use
- polish or replace rigid lenses
o Reduce exposure time
- abandon extended wear
- reduce daily wearing time to minimum possible
- cease wear for a period in some cases
o Optimise lens fit, material and wearing regime
- rigid lens: alter overall diameter (repositions lens edge relative to tarsus), reduce edge clearance and edge thickness
- soft lens: change material to one with improved deposit resistance, and/or lower modulus
- change to daily disposable soft lenses
o Ocular prostheses
- polish, adjust or replace prosthesis

88
Q

Contact Lens Associated Papillary Conjunctivitis Pharmacological Management

A

o Where recurrent and continued contact lens use is required consider
- Preservative free sodium cromoglicate 2% eye drops 4 times daily
- Do not use preserved drops with CL in situ
o If very symptomatic consider
- PoM Olopatadine 1 drop twice daily (8 hourly interval) if very symptomatic
 Contraindicated in
 breastfeeding/pregnancy
 women of childbearing age not using contraception
- then PoM Fluorometholone 0.1% eye drops 4x daily (reduce by 1 drop a week to zero)

Management Category
- Normally no referral

89
Q

What is Episcleritis?

A
  • Inflammation of the episclera which is the vascular connective tissue layer that lies between the sclera and conjunctiva.
  • Generally idiopathic, but up to one third of cases (especially nodular variety and in bilateral cases) associated with systemic disorders
90
Q

Systemic disorders which can be associated with Episcleritis

A
  • systemic lupus erythematosus
  • rheumatoid arthritis (5% develop episcleritis)
  • inflammatory bowel disease
  • seronegative spondyloarthropathies, e.g. ankylosing spondylitis
  • Sjogrens syndrome
91
Q

Episcleritis Predisposing Factors

A
  • Associated systemic disorders
  • Previous history of episcleritis
  • Infections e.g. HZO
  • Commonest in 4th or 5th decade of life
92
Q

Episcleritis Symptoms

A
  • Typically unilateral red eye, but bilateral in 25-50% of cases. Also has an acute onset
    o Mild ache or burning sensation
    o Sometimes tender on palpation
    o Occasionally watery
    o Condition commonly recurrent
93
Q

Episcleritis Signs

A
  • General Signs
    o Hyperaemia from dilated episcleral vessels in one or more quadrants of one or both eyes. (Bilateral involvement suggests underlying systemic disease).
    o Hyperaemia blanches with vasoconstrictors (e.g. gutt. phenylephrine 2.5%)
    o Typically no anterior chamber reaction
    o Usually no corneal or palpebral conjunctival involvement
    o No effect on visual acuity
  • Simple episcleritis (80%)
    o sectoral or diffuse redness
    o dilated episcleral vessels follow a regular radiating pattern and are largely immovable, unlike the finer overlying conjunctival vessels which move freely with the conjunctiva
  • Nodular episcleritis (20%)
    o nodule (mild elevation of the conjunctiva) with injection
    o in most cases, nodule within palpebral aperture
    o dilated episcleral vessels are moveable as the lesion is elevated
94
Q

Episcleritis Management

A
  • Advice
    o Usually self-limiting in 7-10 days; nodular form may persist for longer
    o Reassurance: condition does not generally progress to more serious ocular disorder
    o Cold compresses
    o Advise patient to return/seek further help if symptoms persist
  • Pharmacological Treatment
    o If symptomatic: refrigerator cooled artificial tears as necessary for 1-2 weeks and/or oral NSAIDs e.g. Flurbiprofen.
    - Inconsistent evident for use of topical NSAID (off label use)
    o If particularly symptomatic but no signs to suggest scleritis:
    - Prednisolone 0.5% 4x daily (reduce by 1 drop a week to zero)
    - or Fluorometholone 0.1% eye drops 4x daily (reduce by 1 drop a week to zero)
    - patients on topical steroids should be re-examined after 7-10 days
  • Management Category
    Refer if:
    o Pain on eye movement
    o Scleral tenderness
    o Deeper vessel involvement (redness remains despite Phenylephrine 1%)
    o If underlying systemic disease suspected
    - episcleritis with symptoms suggestive of systemic disease, or at second recurrence (third episode), refer for investigation
95
Q

What is Scleritis?

A
  • is a rare but potentially severe sight-threatening inflammatory disease of the sclera
  • Scleritis can be broadly divided into anterior and posterior sub-types, based on the location of the inflammation relative to the ora serrata
  • Scleritis is often associated with systemic inflammatory disorders however 4-10% of scleritis is infectious in origin
96
Q

Scleritis Predisposing Factors

A
  • Patients are usually in the middle age group (40-60 years)
  • M:F = 2:3
  • May be idiopathic
  • often associated with autoimmune disease, of which, scleritis may be the first presentation
97
Q

Scleritis Symptoms

A
  • Typically, severe pain
    o eye ‘ache’ may be referred to brow or jaw, which is often exacerbated by eye movement.
    o Pain may radiate to the face/scalp/ear and may be worse at night (possibly disturbing sleep).
    o Usually gradual onset over several days
    o Tenderness of globe
  • Photophobia
  • Epiphora
  • Visual loss
  • Possible history of previous episodes
98
Q

Scleritis

A
99
Q

Anterior Scleritis Signs

A

o Non-necrotising (75% of all cases of anterior scleritis)
- usually unilateral
- hyperaemia of superficial and deep episcleral vessels; does not blanch with vasoconstrictors and deep episcleral vessels do not move with a cotton bud
- anterior uveitis may be present (in approx. 30%)
- corneal infiltrates/thinning may be present
- When inflammation resolved, choroidal pigment may show through thinned sclera as a blue/black colouration
- approximately 60% are diffuse and 40% nodular (scleral nodule cannot be moved over underlying tissue)
o Necrotising (15% of cases)
- the most severe form
- may occur in the absence of pain or clinical signs of inflammation
- 75% will eventually have visual impairment
- more common in older patients
- avascular patches leading to scleral melting with ectasia and choroidal herniation

100
Q

Posterior Scleritis Signs

A

o Involves sclera posterior to the ora serrata.
o Eye may be white.
o Ophthalmoscopy may show:
- exudative retinal detachment
- macular oedema
- optic disc oedema
- but may also show no abnormality

101
Q

Scleritis Management

A
  • Advice
    o Sunglasses for photophobia
  • Pharmacological Treatment
    o Usually requires oral steroids
    o Discuss with ophthalmology. If they agree prescribe or co-prescribe:
    - Omeprazole 20mg daily for gastric protection
    - Prednisolone 30mg daily for one week, 20mg daily one week, 15mg daily one week, 10mg daily one week
    - Will need reassessment when on 10mg daily and decision made in conjunction with ophthalmology about subsequent tapering.
    - 10mg of prednisolone unlikely to immunocompromise a patient.
  • Management Category
    o Urgent referral to ophthalmology
102
Q

Anterior Uveitis Classification

A

Uveitis can be classified as follows:
- Onset: sudden or insidious
- Duration: limited, if it is ≤3 months, or persistent, i.e. >3 months in duration
- Recurrent: describes repeated episodes of uveitis separated by periods of inactivity without treatment of ≥3 months in duration
- Chronic: describes persistent uveitis characterized by prompt relapse (in <3 months) after discontinuation of therapy

103
Q

Granulomatous or Non-Granulomatous Anterior Uveitis

A

is traditionally classified as ‘non-granulomatous’ or ‘granulomatous’, based on the nature of the keratic precipitates
- non-granulomatous uveitis:
o acute onset
o fine KP
o more likely to be idiopathic
- granulomatous uveitis:
o as a chronic condition
o Large ‘mutton fat’ KP
o iris nodules
o more likely to be associated with systemic conditions

104
Q

Anterior Uveitis Predisposing Factors

A
  • Age over 20 years in 90% of cases (mean age at onset = 40 years)
  • Genetic link
  • Systemic disease as above.
105
Q

Anterior Uveitis Symptoms

A
  • Onset usually sudden at first episode, gradual at subsequent episodes
  • If condition recurrent, eye may be asymptomatic and white despite presence of inflammation
  • Usually unilateral (if bilateral, more likely to be associated with systemic disease and more likely to become chronic)
    o pain (dull/ache)
    - exacerbated on induced pupillary constriction (direct, near or consensual)
    o photophobia
    o redness
    o decreased vision
    o lacrimation
106
Q

Anterior Uveitis Signs

A
  • hyperaemia:
    o circumcorneal (‘ciliary injection’)
  • keratic precipitates (KP)
    o fine,
    o stellate (mutton fat)
  • aqueous cells
  • aqueous flare
  • hypopyon/fibrin (severe cases)
  • intraocular pressure commonly normal but raised in some cases
  • posterior synechiae possibly causing pupil block and iris bombé
  • iris nodules: Koeppe (small, near pupil), Bussaca (large, far from pupil)
107
Q

Anterior Uveitis Management

A
  • Advice
    o Advise sunglasses for photophobia

-Pharmacological Management
o If no reason to refer to the Ophthalmology department, and if there are no contraindications, prescribe
- PoM Prednisolone 1% eye drops every waking hour
- Cyclopentolate 1% eye drops 3 times daily
- Instruct the patient to re-attend for review next day
o Day Two
- Re-examine the patient
- Check the IOP (looking for steroid response)
o If no better
- Phone ophthalmology to discuss next steps
- At the request of Ophthalmology, you may be asked to prescribe or co-prescribe
 Omeprazole 20mg daily for gastric protection
 POM Prednisolone 30mg daily for one week, 20mg daily one week, 15mg daily one week, 10mg daily one week, 5mg daily then stop
o If better
- Continue Cyclopentolate 1% eye drops 3 times daily for 7 days and then stop
- Reduce POM Prednisolone 1% eye drops as follows:
 Every second waking hour for 1 week
 Then 6 times a day for the next 1 week
 Then 4 times a day for the next 1 week
 Then 3 times a day for the next 1 week
 Then 2 times a day for the next 1 week
 Then 1 times a day for the next 1 week
 Then stop
- One week after stopping Prednisolone 1% eye drops
 Re-examine the patient
 Check the IOP
 If no better, phone ophthalmology to arrange for an urgent appointment

108
Q

Anterior Uveitis Management Category

A

o Refer same day if:
- Patient is a child
- Patient is already on systemic treatment for uveitis (oral steroids, immunosuppressants, biologics or similar)
- Patients on systemic treatment for non-ocular reasons do not need to be referred
- Bilateral involvement
- New posterior synechiae or non-dilating pupil
- IOP > 30 mmHg
- Hypopyon or vitritis
- Macular oedema
- Choroiditis
- Vasculitis
- You cannot see anterior chamber cells, but symptoms or other signs point to anterior uveitis

109
Q

What is Bacterial Keratitis?

A
  • Microbial keratitis is a sight-threatening infection of the cornea
  • Severe contact lens-related infections tend to be Gram -ve, particularly Pseudomonas species
110
Q

Bacterial Keratitis Predisposing Factors

A
  • contact lens wear (incidence 4–5 times higher in CL wearers than non-wearers). The risk of MK with overnight corneal reshaping contact lenses (ortho-K) is similar to rates associated with use of daily wear soft contact lenses. The main risk factors for CL-related MK are:
    o increased days of wear
    o poor hand, lens and storage case hygiene
    o youth
    o male gender
    o smoking
    o internet purchase of lenses, particularly cosmetic lenses
  • ocular surface disease, including:
    o corneal exposure
    o corneal decompensation
    o chronic epithelial defect
    o neurotrophic keratopathy, e.g. secondary to HSK or diabetes
  • ocular trauma or surgery, including loose or broken sutures
  • immune compromise
  • topical steroid use
  • lid margin infection (usually Staphyloccocal)
111
Q

Bacterial Keratitis Symptoms

A
  • Pain, moderate to severe (usually acute onset, rapid progression)
  • Redness
  • photophobia (may be severe)
  • Discharge
  • blurred vision (especially if lesion on visual axis)
  • Awareness of white or yellow spot on cornea
  • Usually unilateral
112
Q

Bacterial Keratitis Signs

A
  • Lid oedema
  • Epiphora
  • Discharge (mucopurulent or purulent)
  • Conjunctival hyperaemia and infiltration
  • Corneal lesion usually single (central or mid-peripheral)
    o excavation of epithelium, Bowman’s layer, stroma (tissue necrosis)
    o stromal infiltration beneath lesion
    o stromal oedema with folds in Descemet’s membrane
    o endothelial fibrin plaque beneath lesion
    o optical coherence tomography (OCT) may be helpful in determining depth of involvement
  • Anterior chamber activity (flare, cells, hypopyon or coagulum if severe)
113
Q

Bacterial Keratitis Management

A
  • Advice
    o Cease contact lens wear
    o Do NOT discard lens or cases as useful for culture
  • Pharmacological Treatment
    o None, unless rapid access to ophthalmology impossible or advised by ophthalmology
    - PoM Ofloxacin 0.3% hourly, titrate as per response, minimum final frequency 4 times a day
    - Cyclopentolate 1% three times a day for one week, if in pain
  • Management Category
    o Emergency (same day) referral is indicted if any of the following signs are present:
    - infiltrate >1mm
    - 2 or more adjacent lesions
    - location 3mm or less from corneal centre
    - AC reaction (≥10 cells in a 1mm beam (≥ 1+ on the SUN scale)
    - signs suggestive or fungal or acanthamoeba keratitis
    - high likelihood of poor patient compliance to treatment
  • Management by Ophthalmologist
    o Intensive topical antibacterial therapy
114
Q

What is Fungal Keratitis?

A
  • Fungal infection causes a small proportion of infectious keratitis cases in temperate regions; however, in tropical climates it can cause up to 50% of cases
  • The most common fungal corneal pathogens are:
    • Candida sp. (yeast-like)
    • Fusarium sp. (filamentous)
    • Aspergillus sp (filamentous)
115
Q

Fungal Keratitis Predisposing Factors

A
  • Fungal keratitis (filamentous)
    o usually secondary to trauma involving organic material
    o it can also be contact lens or solution related
  • Fungal keratitis (yeast-like)
    o most usually complicates ocular surface disease or in immunocompromised patients
116
Q

Fungal Keratitis Symptoms

A
  • Pain, moderate to severe (usually acute onset, rapid progression)
  • Redness
  • photophobia (may be severe)
  • discharge
  • blurred vision (especially if lesion on visual axis)
  • Awareness of white or yellow spot on cornea
  • Usually unilateral
117
Q

Fungal Keratitis Signs (vs Bacterial Keratitis)

A
  • Fungal keratitis produces similar signs to bacterial keratitis. Some differences could include:
    o deep lesions
    o lesion with a feathery edge
    o raised profile
    o presence of satellite lesions
    o the presence of endothelial plaque
    o may develop more slowly
118
Q

Fungal Keratitis Management

A
  • Advice
    o Warn contact lens wearers not to discard their lenses or lens cases, but to retain them for culture
  • Management Category
    o Emergency referral to an ophthalmologist
  • Ophthalmologist Management
    o Intensive topical anti-fungal therapy
119
Q

What is Acanthamoeba Keratitis?

A
  • Acanthamoeba keratitis (AK) is a severe sight-threatening corneal infection
  • Early detection is very important
  • most people have Acanthamoeba antibodies, suggesting that exposure is commonplace
  • much more common in contact lens wearers, accounting for approximately 90% of UK cases.
  • In 10% of cases there is associated scleritis
120
Q

Where are Acanthamoeba Found?

A
  • well water, drains, soil, dust
  • ponds, swimming pools, hot tubs
  • often present in domestic tap water (especially from storage tanks)
121
Q

What are the two Forms of Acanthamoeba

A
  • motile, feeding and replicating form: trophozoite (most common form found in water and easily destroyed)
  • dormant form: cyst (highly resistant to disinfection, can survive for long periods in hostile environments)
122
Q

Acanthamoeba Keratitis Symptoms

A
  • Can be bilateral
  • Pain (may be severe and out of proportion to degree of ocular inflammation; may also be painless in the early stages)
  • Visual disturbance/loss
  • Redness
  • Watery eye
  • Photophobia
123
Q

Acanthamoeba Keratitis

A
  • General Signs
    o Reduced visual acuity in later stages
    o Conjunctival and limbal hyperaemia
    o Epiphora
    o Corneal lesions
  • Early signs
    o punctate epitheliopathy
    o epithelial or subepithelial infiltrates
    o pseudodendrites
    o radial keratoneuritis (infiltrates along corneal nerves)
    o recurrent breakdown of the corneal epithelium
  • Later signs
    o deep inflammation of the cornea consisting of a central or paracentral ring-shaped or disciform stromal infiltrate or abscess
    o stromal thinning
    o extension of inflammation into sclera
    o anterior chamber cells and flare
    o hypopyon
124
Q

Acanthamoeba Keratitis Management

A
  • Advice
    o Cease contact lens wear immediately
  • Management category
    o Emergency referral to ophthalmology
  • Ophthalmologist Management
    o Prolongued and intensive course of anti-infective agents
125
Q

What is Herpes Simplex Keratitis?

A
  • The infection can manifest as blepharoconjunctivitis, keratitis, anterior uveitis or acute retinal necrosis
  • Infections are most commonly caused by the HSV-1 subtype, which primarily infects mucous membranes of the body ‘above the waist’, including the lips, face and eyes.
  • HSV-2 generally infects ‘below the waist’ and is usually sexually acquired but may rarely cause keratitis
  • The most common form of HSK is epithelial keratitis, accounting for 50% to 80% of cases.
126
Q

Herpes Simplex Keratitis Predisposing Factors

A
  • Poor general health
    o Immunodeficiency
    o fatigue
  • Systemic or topical steroids, or other immunosuppressive drugs
  • History of previous attacks of ocular herpes simplex infection (key diagnostic feature)
  • Severe atopic disease
  • Possible aggravating factors
    o sunlight (UV)
    o fever
    o extreme heat or cold,
    o Infection (systemic or ocular)
    o trauma (ocular)
127
Q

Herpes Simplex Keratitis Symptoms

A
  • Usually affects one eye; may be bilateral, especially in severely atopic patients
  • Severity of symptoms can be very variable and may include:
    o Pain
    o Burning
    o Irritation
    o Photophobia
    o blurred vision
    o redness
128
Q

Herpes Simplex Keratitis Signs

A
  • Epithelial
    o Initially punctate lesions, coalescing into dendriform pattern
    - dendritic ulcer, single or multiple opaque cells arranged in a stellate pattern progressing to a linear branching ulcer; terminal bulbs may be visible
    - dendritic lesions stain with fluorescein, edges of lesion, containing dead cells, stain with lissamine green
    o associated with reduced corneal sensitivity
    o continued enlargement may result in an ‘amoebic’ or ‘geographic’ ulcer (especially following inappropriate use of topical steroids)
  • Stromal
    o Stromal infiltrates
    o Vascularisation
    o oedema and opacification
    o Stromal HSK can be either necrotising or non-necrotising.
    - In non-necrotising stromal HSK, the oedema is localised, and mostly self-limiting.
    - In necrotising keratitis, the stromal inflammation is widespread and the infection progresses to ulceration, necrosis and possible perforation
129
Q

Herpes Simplex Keratitis Pharmacological Management

A

o PoM in non-contact lens wearing adults and where HSK is confined to the epithelium (dendritic), commence antiviral therapy with the following:
- Ganciclovir 0.15% ophthalmic gel 5x daily for one week
o Instruct the patient to return in one week
- If the dendritic ulcer has not healed
 Instruct the patient to continue using the treatment five times a day and phone the Ophthalmology department to arrange an appointment (or follow local HB protocols where in place)
- If the dendritic ulcer has healed
 Instruct the patient to reduce the treatment to three times a day for another seven days and then STOP

130
Q

Herpes Simplex Keratitis Management Category

A

o Refer urgently (within one week) to ophthalmologist if
- Epithelium has not healed after seven days
o Emergency (same day) referral if
- Stroma involved
- Anterior uveitis
- Raised intraocular pressure
- Children
- Contact lens wearer
- Bilateral cases

131
Q

Contact lens-associated Infiltrative Events

A
  • contact lens-associated peripheral ulcer (CLPU)
  • contact lens-associated infiltrative keratitis
  • contact lens-associated red eye (CLARE)
131
Q

Contact Lens Peripheral Ulcer Predisposing Factors

A
  • Demographic and person related:
    o bioburden of eyelid margins (i.e blepharitis)
    o male sex
    o younger age (<25 years)
    o smoking
    o previous history of CIE
  • Contact lens–related:
    o long-term lens wear
    o extended (overnight) wear
    o silicon hydrogel material
    o tight lens fit
    o multipurpose contact lens solutions
    o poor lens hygiene
    o bioburden of lenses and lens case
132
Q

Contact Lens Peripheral Ulcer Symptoms

A
  • Red and watery eye
  • Foreign body sensation
  • Photophobia
  • some may be asymptomatic
133
Q

Contact Lens Peripheral Ulcer Signs

A
  • Peripheral anterior stromal infiltrate, single or multiple (multiple infiltrates more likely in CLARE)
    o Usually small (generally less than 1.0mm in diameter)
    o Overlying epithelium may stain with fluorescein (ulcer formation in CLPU)
  • Conjunctival hyperaemia
  • Adjacent limbal hyperaemia
  • Epiphora, mild (or absent)
  • Anterior chamber quiet or mildly inflamed
  • No lid oedema
  • Usually unilateral
134
Q

Contact Lens Peripheral Ulcer Management

A
  • Advice
    o Temporarily discontinue lens wear
    o Most signs and symptoms resolve within 48 hours
  • Infiltrates resolve over 2-3 weeks
    o Advise against extended wear
    o Warn about possibility of recurrence
    - If condition recurs, switch to disposable contact lenses
  • Non-Pharmacological Treatment
    o Treat any associated blepharitis
135
Q

What is Marginal Keratitis?

A
  • Marginal keratitis is an inflammatory response of the peripheral cornea to bacterial (e.g. Staphylococcal) exotoxins rather than direct inoculation.
136
Q

Marginal Keratitis Predisposing Factors

A
  • Bacterial (e.g. Staphylococcal) blepharitis or meibomitis
  • Condition tends to be recurrent
137
Q

Marginal Keratitis Symptoms

A
  • Ocular discomfort (foreign body sensation, increasing to pain)
  • Lacrimation
  • Red eye
  • Photophobia
138
Q

Marginal Keratitis Signs

A
  • Stromal infiltrate, which may be:
    o round or arcuate
    o single or multiple
    o unilateral or bilateral
    o Infiltrates are typically adjacent to the limbus and separated by an interval of clear cornea.
  • Overlying epithelial loss may occur resulting in ulcer formation which stains with fluorescein
  • Hyperaemia of adjacent limbus
  • Hyperaemia and oedema of adjacent bulbar conjunctiva
139
Q

Marginal Keratitis Management

A
  • Advice
    o Sunglasses to ease photophobia
    o Refer to local Pharmacist for analgesia for pain relief (Paracetamol or Ibuprofen; dose depends on age)
    o Marginal keratitis is a self-limiting condition which may recur
    - Offer to review patient, if symptoms recur
    o Regular lid hygiene for associated blepharitis will help limit recurrence
  • Pharmacological Treatment
    o Treat infection with antibiotic
    - Ask if allergic to Chloramphenicol
    - If not, supply Chloramphenicol 1% eye ointment 3 times daily for a week
    - If allergic to Chloramphenicol, or pregnant, supply Fusidic acid 1% liquid gel twice a day for a week
    o If no suspicion of herpes simplex keratitis, treat inflammation with
    - PoM Prednisolone sodium phosphate 0.5% 2 times daily for a week
    o Ask patient to return in one week for review, or sooner if symptoms worsen. Re-examine the patient
    - If healed: Discharge
    - If not healed, phone ophthalmology department to arrange an urgent appointment
  • Management Category
    o Management to resolution. Normally no referral
    o Refer to ophthalmologist if:
    - Anterior chamber cells present
    - Contact lens wearer
    - Children should always be referred
140
Q

Features of General Herpes Zoster

A
  • previous systemic infection, typically in childhood (varicella, i.e. chickenpox)
    o virus lies dormant (sometimes for decades) in dorsal root and cranial nerve sensory ganglia
    o reactivation leads to herpes zoster (shingles)

the NHS offers routine herpes zoster vaccination for people aged 70-79 years. Vaccination has been shown to reduce the incidence rate of shingles and post-herpetic neuralgia.

141
Q

What is Herpes Zoster Ophthalmicus?

A
  • is caused by a localized reactivation of the varicella zoster virus (VZV) in the ophthalmic division of the trigeminal nerve
  • the most common sites of ocular involvement include conjunctivitis, followed by keratitis and uveitis.
  • most cases of ocular involvement develop within three to four weeks of the initial primary care diagnosis
  • HZO can result in moderate-to-severe loss of vision in a significant proportion of patients with ocular involvement, even with timely and appropriate management.
142
Q

Herpes Zoster Ophthalmicus Predisposing Factors

A

Age:
o the peak incidence in healthy individuals is in the 5th to 7th decades
o one in three cases occur in people under the age of 50
- Immune compromise:
o HIV infection
o medical immunosuppression e.g. corticosteroids/chemotherapy

143
Q

Herpes Zoster Ophthalmicus Symptoms

A
  • Pain and altered sensation (often described as “tingling“, “burning” or “shooting”) of the forehead on one side
  • Rash affecting forehead and upper eyelid appears a day to a week later
  • General malaise, headache, fever
  • Ocular symptoms in acute phase:
    o Discomfort
    o Discharge
    o Redness
    o Pain
    o photophobia
144
Q

Herpes Zoster Ophthalmicus Skin Signs

A

o unilateral painful, red, vesicular rash on the forehead and upper eyelid, progressing to crusting after 2-3 weeks; resolution often involves scarring
o involvement of the skin supplied by the ophthalmic division of the trigeminal nerve. Does not cross the midline
o skin lesions on the side of the tip of the nose (Hutchinson’s sign) makes ocular involvement more likely.
o Zoster sine herpete is a rare variant which has no cutaneous manifestations
o periorbital oedema (may close the eyelids and spread to opposite side)
o lymphadenopathy (swollen regional lymph nodes)

145
Q

Herpes Zoster Ophthalmicus Ocular Signs

A

o mucopurulent conjunctivitis (common), associated with vesicles on the lid margin; usually resolves within 1 week
o keratitis (more than half of all cases)
- punctate epithelial – early sign, within 2 days (50% of cases)
- pseudodendrites – fine, multiple stellate lesions (around 4-6 days)
- nummular – fine granular deposits under Bowman’s layer
- disciform – 3 weeks after the rash (occurs in 5% of cases)
- reduced corneal sensation
- endothelial changes and KP
o episcleritis: occurs in around one third of cases
o scleritis: less common; usually develops after 1 week
o anterior uveitis
o secondary glaucoma (check IOP)
o rarely, posterior segment involvement: retinitis, acute retinal necrosis, choroiditis, optic neuritis, optic atrophy
o rarely, neurological complications: cranial nerve palsies, encephalitis
o post-herpetic neuralgia is defined as pain and/or itch lasting beyond 90 days after the onset of zoster. This affects around 25% of patients and is chronic and severe in about 7%

146
Q

Herpes Zoster Ophthalmicus

A
  • Advice
    o Refer all patients to General Practitioner for a course of oral anti-viral therapy
    o Rest and general supportive measures (reassurance, support at home, good diet, plenty of fluids)
    o Advise avoidance of contact with
    - Elderly or pregnant individuals
    - Babies and children not previously exposed to varicella zoster virus (chicken pox)
    - Immunodeficient/immunosuppressed patients
    o Stronger analgesics (e.g. opiates) may be indicated (co-manage with GP)
    o Review patient at one week to check for development of uveitis
  • Pharmacological Treatment
    o PoM Early treatment with oral Aciclovir (within 72 hours after rash onset) reduces the risk of ocular involvement and lessens acute pain
    o Topical lubricants for relief of ocular symptoms
    o Refer to local Pharmacist for analgesia for pain relief (Paracetamol or Ibuprofen; dose depends on age)
  • Management Category
    o Emergency referral (same day) to GP for systemic anti-viral treatment
    o Management to resolution if co-managed with GP and keratitis limited to epithelium
    o Urgent referral to ophthalmologist if
    - Uveitis
    - Scleritis
    - Keratitis (deeper than epithelial)
    - Retinitis
147
Q

What is Blepharitis?

A
  • Blepharitis is a chronic inflammation with possible acute exacerbations that primarily affects the eyelid margins
  • is one of the most common presentations in primary eye care
148
Q

Blepharitis and Dry Eye

A
  • 50% of people with staphylococcal blepharitis
  • 25-40% of people with seborrhoeic blepharitis.
  • Posterior blepharitis is a leading cause of evaporative dry eye.
149
Q

Blepharitis Classification

A
  • Anterior blepharitis (also known as Anterior Lid Margin Disease)
    o bacterial (usually staphylococcal)
    - caused by direct infection, reaction to staphylococcal exotoxin or allergic response to staphylococcal antigen
    o seborrhoeic
    - disorder of the ciliary sebaceous glands of Zeis.
    o Demodex folliculorum infestation of the lash follicles
  • Posterior blepharitis
    o meibomian gland dysfunction (MGD)
    - bacterial lipases break down meibomian lipids
    - meibomian secretion becomes abnormal both chemically and physically
    - plugging of duct orifices with abnormal lipid leading to dilatation of glands and potential formation of microliths and chalazia
    - tear film becomes unstable.
150
Q

Blepharitis Predisposing Factors

A
  • Seborrhoeic dermatitis (for example, of the face and/or scalp).
  • Ocular rosacea (a cause of posterior blepharitis).
  • Demidicosis
  • Demodex folliculorum found in the lash follicles
  • Demodex brevis found in meibomian glands.
  • Long-term contact lens wear.
151
Q

Staphylococcal Anterior Blepharitis Signs

A

o crusting of anterior lid margin
o lid margin swelling and hyperaemia
o secondary signs include:
- misdirection of lashes
- loss of lashes (madarosis)
- recurrent hordeola and chalazia
- punctate epithelial erosion over lower third of cornea
- marginal keratitis
- neovascularisation and pannus
- mild papillary conjunctivitis.

152
Q

Seborrhoeic Anterior Blepharitis Signs

A

o lid margin hyperaemia
o oily or greasy deposits on lashes and/or lid margins

153
Q

Demodex Anterior Blepharitis Signs

A

o lid margin hyperaemia
o collarettes (cylindrical dandruff)
- extending further up lash than flat staphylococcal rosettes
o persistent infestation of the lash follicles may lead to misalignment, trichiasis or madarosis.

154
Q

Posterior Blepharitis Signs

A

o thick and/or opaque secretion at meibomian gland orifices, making it difficult or impossible to express oil by finger pressure
o foam in the lower tear film meniscus
o plugging of duct orifices
o lid margin and conjunctival hyperaemia
o evaporative tear deficiency, unstable pre-corneal tear film
o secondary signs include:
- punctate epithelial erosion over lower third of cornea
- marginal keratitis
- scarring; neovascularisation and pannus
- mild papillary conjunctivitis
- chalazia
- meibomian gland dropout

155
Q

Blepharitis Non-Pharmacological Management

A
  • Advice
    o Explain it is a long-term condition that may flare intermittently
    o Explain lid hygiene needs to be performed indefinitely
    o Advise the avoidance of cosmetics, especially eye liner and mascara
    o Advise patient to return/seek further help if symptoms persist
  • Non-Pharmacological Management
    o Lid hygiene consisting of warm compresses, lid massage and lid scrubs is the first line of management regardless of type of blepharitis
    - Apply microwaveable reusable warm compresses two to four times daily for 5 to 10 minute intervals
    - Clean lid margins (but not beyond the muco-cutaneous junction)
     Diluted baby shampoo (1:10) solution with a swab or cotton bud or commercial products e.g. dedicated lid cleaning solutions or impregnated wipes
    - Twice daily at first; reduce to once daily as condition improves
156
Q

Blepharitis Pharmacological Management

A

o Treat any aqueous tear deficiency with lubricants
o Consider topical antibiotics to the anterior lid for resistant cases
- Ask if allergic to Chloramphenicol
 If not, supply Chloramphenicol 1% eye ointment 3 times daily for a week
 If allergic to Chloramphenicol, or pregnant, supply Fusidic acid 1% liquid gel twice a day for a week
- Long term intermittent maintenance may be required
o If topical antibiotics ineffective consider treatment as for Rosacea
- PoM Antibiotics as for Rosacea require co-management with GP
o Treat associated seborrhoeic dermatitis or dandruff
- Refer to local Pharmacist
o Consider Demodex blepharitis
- weekly lid scrub with 50% tea tree oil (experienced practitioners only)
- or OTC pre-prepared demodex-specific lid wipes

157
Q

What are Corneal Infiltrates?

A
  • is a single or group of inflammatory cells in the normally clear cornea
  • results from an infection, decreased oxygen supply or injury to the cornea
  • visible under high magnification as round, gray spots surrounded by areas of swelling
  • Sterile corneal infiltrates rarely lead to mucus discharge. They also tend to be less painful and don’t lead to sensitivity to light like infectious corneal infiltrates. They are, in general, more common in the peripheral cornea.
158
Q

What are Corneal Dellen?

A
  • Dellen are shallow, saucer-like excavations at the margin of the cornea
  • are thought to occur due to localized tear film instability especially the mucin layer and dehydration
  • Cornea epithelium is hydrophobic and in absence of mucin will repel water causing a dry spot and eventually localized dehydration.
  • This is followed by thinning of cornea in that area forming a dellen.
  • usually last for 24-48 hours and disappear spontaneously
  • If left untreated, the underlying corneal stroma may undergo secondary degeneration, leading to corneal scarring and/or vascularisation with accompanying loss of vision