Download Problem 26- Red Eye

Red Eye
Index conditions
 Conjunctivitus
 Glaucoma
 Iritis
 Dry eyes
 Local trauma / foreign bodies
 Lid disorders
Clinical Skills
 Able to advise on risk reduction (eg industrial trauma, infections)
 Tale appropriate history to exclude systemic cases
 Rake focussed history with particular reference to discriminating between conjunctivitis,
glaucoma and iritis
 Perform full examinations of the eye
 Perform general exam if systemic cause is likely
 Refers appropriately for specialist investigation (eg pressure testing, slit lamp examination,
imaging)
 Appropriate use of microbiological investigations
 Able to diagnose the main causes of red eye (conjunctivitis)
Interpersonal skills
 Able to discuss with patients fears or risk regarding visual loss
 Deals sensitively with patients / families in relation to sexually transmitted causes (eg
ophthalmia neonatorum, STD’s)
 Able to take appropriate protective measures to prevent transmission of infection
Professional Behaviours
 Appropriately refers patient to specialist care
 Recognises and reports notifiable disease
Practical Skills
 Able to use torch and ophthalmoscope
 Able to take microbiological specimens
 Able to test visual acuity
 Able to explain pressure testing and slit lamp examination
Basic Medical Sciences
 Structure and function of the eye and associated structures (e.g. eyelids, tear ducts)
Clinical Sciences
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Mechanisms underlying glaucoma
Microbiological causes
Local and systemic inflammatory mechanisms and underlying causes
Principles of treatments for conjunctivitus, glaucoma and inflammatory causes
Acute painful red eye
Acute angle closure glaucoma
Sudden blockage around the trabecular meshwork so that aqueous humor fluid cannot drain out of
the eye. With fluid still being made this increases pressure and may damage the optic nerve
NB - Chronic open angle glaucoma does not cause red eye. It is usually asymptomatic at first,
presenting with vision loss
Pathology
Epidemiology
Rapid or sudden increase in intraocular pressure
which can cause loss of vision
>50s. 1/1,000. Most common in 60-70 yrs. Longsighted>short sighted, women>men. Most
common in SE Asian and Eskimo people.
Risk factors
FH, abnormal eye structure
Triggers: eye drops that dilate the pupil, antidepressants (SSRIs or tricyclics), entiemetics,
phenothiazines, ipatropium (used in asthma), topiramate, chlorphernamine, cimetidine and
ranitidine and GA medication
Classification:
Aetiology:
Acute angle – sudden, red eye
Open angle – chronic, usually present with a
reduced visual field
possible stricture of the eye eg if the area at the
base of the iris is narrow or if the lens is thicker
and sits further forward than in normal anatomy
History:
Examination:
severely painful in eye and ache around eye,
haloes around lights, photophobia, watering,
systemically unwell (nausea, vomiting and
headache), red eye, eye may feel hard or tender
decreaded visual acuity, hazy cornea, fixed semi
dilated or oval pupil
Complications:
Investigation:
Vision loss
clinically on the appearance of the eye.
Confirmed by examination by specialist gonioscopy
Management:
refer immediately
Treatement – quick treatment – do not cover the eye as this will dilate the pupil and can worsen the
situation.
Topical betablocker (to reduce fluid) and steroids (to reduce inflammation)
Injection of acetazolamide (carbonic anhrdrase inhibitor – reduces eye pressure)
Topical pilocarpine (constricts pupil moving iris away from the trabecular network)
Topical brimonidine to reduce fluid
IV mannitol to reduce fluid
Laser treatment – peripheral iridotomy or surgical iridotomy
Prognosis
good if treatment is started quickly. Delay in treatment risks permanently reducing vision in the
affected eye
Keratitis
Inflammation of the cornea
Superficial – involves only the superficial layers of the cornea – after healing generally doesn’t leave
a scar
Deep keratitis – deeper layers of the cornea involved. Tends to leave a scar.
Pathology
Epidemiology
Inflammation of the cornea. May effect one or
both eyes
Fairly common
Risk factors
Histology
Any break or disruption of the corneal
epithelium.
Contact lenses
Decrease in quantity or quality of tears.
Disturbances in immune function.
Inflammation may see scarring and ulceration if
severe
Classification:
Aetiology:
Classified by location, severity and cause
Superficial if only involving the epithelial layer of
the cornea.
Deep layers of the cornea (the corneal stroma) it
is called stromal ketatitis or interstilital keratitis.
usually an infection (amoebic infection usually in
contact lens wearers, bacterial – Staph, aureua
and pseudomonas aeruginosa in contact lens
wearers, fungal, viral: HSV and HZV.
Others: exposure keratitis (dry eyes),
photokeratitis (UV exposure), ulcerative keratitis,
CLARE (contact lens acure red eye – gramnegative bacteria on contact lenses), severe
allergic response
History:
Examination:
photophobia, foreign body sensation + history of
contact lens wear + previous episodes (eg HSV
infection)
visual acuity depends of the exact nature of the
problem, peripheral lesions may cause little
change but some decrease is expected. Corneal
defect on staining + hypopyn (pus seen in the
anterior chamber)
Complications:
Investigation:
scaring of the cornea which can affect vision.
With severe ulcerative keratitis the cornea mey
perforate.
Diagnosis by ophthalmology. Culture may be
taken if infection is suspected.
Management:
antofungal / antibiotics, antiviral to treat the infection (eye drops or pills) advisecontact lens wearers
to use glasses
Prognosis
Good outcome expected
Iritis / uveitis
Iritis – inflammation of the iris
Uveitis – inflammation of the uvea (middle layer of the eye)
Pathology
Epidemiology
Inflammation of the iris
accounts for 10% blindness worldwide. Mean
age 20-50 years.
Incidence anterious uveitis 244/100,000.
Risk factors
Histology
Genetic predisposition (HLA-B27), STDs, certain
geographic locations where infectious causes are
more common eg by rivers (fungal infections),
comprised immune system or autoimmune
disease
Signs of inflammation
Classification:
Aetiology:
Acute or chronic
Anterior uveitis – inflammation of the ris
Intermediate uveitis – affects the vitreous and
posterior part of the ciliar body
Posterior uveitis – inflammation of the choroid
Panuveitis – inflammation throughout the uveal
tract (indicates serious disease)
inflammatory (AI disease), infectious (ocular or
systemic pathogens), infiltrative (secondary to
invasive neoplastic processes), injurius (trauma),
iatrogenic (surgery, inadvertent trauma,
mediation eh rifabutin and cidofovir), inherited
(secondary to metabolic or dystrophic disease),
ischaemic (impaired circulation), idiopathic
History:
Examination:
sudden or insidious onset (acute < 3 months <
chronic). Unilateral, painful red eye, blurred
vision and photophobia, excess tear production.
Headache. (less acute presentation in chronic
disease)
reduced visual acuity, abnormal shape and size
of pupil, direct photophobia and consensual
photophobia, cloudy aqueous humour.
Complications:
Investigation and diagnosis
cystoif macular oedema, secondary cataracts,
glaucoma, vitreous opacities, retinal
deteachment, neovascularisation of the retina,
optic nerve or it iris, macular ischaemi, corneal
calcification
fundus fluorescein angiography and optic
coherence tomography
Diagnosis made on location of the inflammation,
anterior chamber cells, anterior chamber flare,
vitreous cells and vitreous haze.
Management:
immediate specialist referral
Prednisolone 1% eye drops (steroid to suppress the inflammatory reaction)
Systemic therapy for severe or posterior disease.
Surgical removal of vitreous
Monitor the disease
Prognosis
self limiting condition, good outcome (91% restore normal vision without treatment)
Relapse is common
Prognosis for chronic depends on whether the underlying condition is effectively managed
Iritis
uveitis
TRAUMA
ACUTE NON-PAINFUL RED EYE
Conjunctivitis
Pathology
Epidemiology
Inflammation of the conjunctiva
Very common
Risk factors
Classification:
Wearing contact lenses, trauma (including
chemical and UV exposure)
associated corneal involvement =
keratoconjunctivitis, eyelid invoilvment =
blepharoconjunctivitis
Aetiology:
Adenoviral (may have fever – very contagious), risks: exposure to affected individual, URTI, recent
ocular exam, Suggesting symptoms – itching, burning, watering, becoming bilateral within days.
Treatmenr – symptomatic, no contact lens use, cool compress, good hygiene./
HSV (I) – young./middle aged men / women. Risks – HSVI infection (previous HSV / cold sores),
physical stess, psycholohical stress, environmental stress. Suggestive symptoms – unilateral pain,
burning, foreign body sensation. Treatment – conservative, no use of contact lenses. Refer if corneal
involvement.
Other viral – HZV and molluscum contagiosum virus.
Other causes
Inflammatory conditions (ocuilar mucous membrane pemphigoid and erythema multiforme)
Trauma
Chronic and severe anterios blepharitis
Drugs – systemic (practolol, penicillamine), topical (timolol, pilocarpine)
Inherited problems – ectodermal dysplasia
Systemic problems – cicatricial conjunctivitis, rosacea, Sjogren’s syndrome, graft-vs-host disease
Neoplasia
History:
Examination:
Red eye, usually generalies, often bilatereal.
Irritation, discomfort (pain suggests somwthing
more serious), discharge from the eye,
photophobia (suggests corneal involvement)
minimal (if any) reduction in visual acuity.
(wear gloves on examination – very contagious)
Conjunctival injection (dilated conjunctival
vessels) conjunctival chemosis (oedema of the
conjunctiva), follicles or papiollae, corneal
involvement.
Complications:
Investigation:
Deterioration of vision
Generally not required following history and
examination (including fundoscopy). Refer for
tests if severe purulent discharge, follicular
conjunctivitis, neonatal conjunctivitis, unclear
aetiology, not responding to treatment)
Management:
Cold compress on the eyes and paracetamol and ibuprofen can ease symptoms.
Eyes can be cleaned with cotton wool soaked in cooled boiled water
Treat the infection
Prognosis
Even left untreated most forms get better after a few weekd on their own, allergic conjunctivitis
continues with exposure to the aggravating agent.
With appropriate treatment the inflammation can be relieved within a few days (some viral
infections may persist for weeks)
Episcleritis
Pathology
Epidemiology
Irritation and inflammation of the episclera, a
thin layer of tissue covering the sclera of the eye
Common condition
Risk factors
Aetiology:
Certain infections
It can occur without infection
May occur with: HZV, RA, Sjogren syndrome,
Syphilis, TB
History:
Examination:
Pink or purple sclera, possible eye pain, eye
tenderness, sensitive to light, tearing of the eye
Complications:
Investigation:
Condition may return, may cause scleritis
(inflammation of the sclera)
No investigations needed, diagnosis on
examination
Management:
Usually disappears without treatment in 1-2 weeks
Corticosteroid eyedrops may relieve symptoms faster
Prognosis
Full recovery expected
Subconjunctival haemorrhage
Small bleed behind the conjunctiva, looks alarming but there are usually no symptoms and it is
usually harmless
Pathology
Epidemiology
One of the tiny blood vessels running between
the conjunctiva and the sclera burst
Tends to occur in older people
Aetiology:
No apparent cause
Occasionally head trauma or after a bout of coughing or vomiting
History:
Examination:
Usually no symptoms – noticed in the mirror or
by someone else
Inspect for injuries if thought to be the main
cause
Complications:
Investigation:
None
BP if not done recently.
Management:
No treatment required, fades and disappears within a couple of weeks (turns yellow/brown first, like
a normal bruise)
Prognosis
Full recovery
NON-ACUTE CASES OF RED EYE
Blepharitis
Pathology
Inflammation of the eyelids – usually affects to
edges of the eyelids
History
Aetiology:
Sore eyelids, normally both, eyelids appear
inflamed or greasy, ‘sticky’ discharge (eyelids
may stick together in the morning), scales may
appear on the eyelids
Symptoms come and go
Staphylococcal blephritis, seborrhoeic blephritis,
meibomian blepharitis (aka meibomian gland
dysfunction)
Complications:
Chalazoin (meibomian cyst), stye, loss of eyelashes (madarosis), misdirection of eyelashes towards
the eyes (trichiasis), depigmentation of the eyelashes (poliosis), eyelid ulceration and scarring,
conjunctivitis, conjunctival phlyctenules, corneal inflammation
Management:
No cure. Regular eyelid hygiene. Antibiotics. Treatment of complications. Rubbing eye can make
condition worse.
Prognosis
Will re-occur
Trichiasis / Distichiasis
Abnormally positioned eyelashes
Pathology
Epidemiology
Eyelashes grow in an abnormal way and can
cause irritation and harm to the eye
Rare, in all ethnicities, no gender discrimination,
all ages (trichiasis seen more commonlu in
adults)
Risk factors
Histology
Family history
Previous history including Stevens-Johnson
syndrome, ocular cicatricial pemphigoid (OCP),
trauma, previous surgery
Abnormal position of eyelashes which can be
fully formed or very fine, pigmented or
nonpigmented, properly orientated or
misdirected
Classification:
Aetiology:
Distichiasis – growth of lashes from the orifices
of the meibomian glands on the posterios
lamella of the tarsal plate.
Trichiasis – eyelashes grow back towards the
eye, touching the cornea or conjunctiva
Distichiasis – acquired, congenital
Trichiasis - Infection, inflammation, autoimmune,
congenital defects, eyelid agenesis and trauma
(eg burns or eyelid injury)
History:
Examination:
Abnormal eyelash growth, corneal irritation,
epiphora, corneal abrasion and possible corneal
ulcers
Include fundoscopy
Complications:
Investigation:
Eye scarring and ulceration
Surgery has complications including
haemorrhage and infection.
None specific. Can check for signs of infection
Management:
Eye lubricants, bandage contact lenses, mechanical apilation of lashes, however they regrow in 4-6
weeks.
Surgery – lid splitting and cryotherapy, direct surgical excision by wedge resection, tarsoconjunctival
approach.
diatichiasis
Trichiasis
Floppy Eyelid Syndrome
Frequently an unrecognised syndrome
Pathology
Epidemiology
Reduced eyelid control, may interfere with vision
Reasonably common but unrecognised, no
known racial predilection, men > women, middle
aged (40-50)
Risk factors
Histology
Contact lens use, seasonal symptoms, acne,
psoriasis, hypertension, congestive heart failure,
obstructive sleep apnoea
Tarsal collagen appears normal, decrease in
tarsal elastin
Meibomian gland dysfunction and atrophy
Classification:
Aetiology:
unknown
History:
Examination:
Unilateral or bilater chronic eye irritation and
burning, tearing, ropy mucoid discharge usually
worse in the morning, decreased vision if there is
associated keratopathy, daytime somnolence,
morning headaches, sleeps facedown with
frequent waking,
Floppy, rubbery, easily upverted eyelids
associated with chronic papillary conjunctivitis of
the upper palpebral conjunctiva and keratoconus
Complications:
Investigation:
Complications if surgical intervention (poor
wound healing, unacceptable eyelid height or
contour)
Slip lamp examination
Conjunctibal scrapings – polymorhonuclear
leukocytes, papillary conjunctival hypertrophy
Management:
Topical lubrication
Antibiotics
Tape eyes closed when asleep
Surgical tightening of eyelids
Encouraged to lose weight
Prognosis
Management above often successful in improving patients symptoms
Dacryocystitis
Lacrimal excretory system is prone to infection and inflammation. The mucous membrane lined tract
is contiguous with 2 surfaces that are normally colonised with bacteria. Stagnation of tears results in
dacrycystitis
Pathology
Epidemiology
Inflammation of the lacrimal sac, may be
congenital with abnormal formation of the
lacrimal drainage system.
Higher incidence in people with crachycephalic
heads.
Rare in black people as their noses are generally
larger.
More common in females (70-83%, congenital is
equal)
Occurs in infants and over 40s.
Risk factors
Histology
Congenital malformation
Changes in the lacrimal drainage system, related
to the primary cause. May see focal ulceration
and loss of goblet cells, abscesses and granuloma
formation.
Classification:
Aetiology:
Acute, chronic and congenital
Congenital – incomplete canalization.
Bacterial infection – aerobic and anaerobic
(commonly staphs, streps and E. Coli)
Nasal disease: sinusitis (maxillary, ethmoidal),
rhinitis (hypertrophic, vasomotor, syphilitic,
ozaenosa), adenoids, etc.
Osteroprosis, lupus, scleroma, leukaemia, GVH
disease etc.
History:
Examination:
Acute – tenderness un medial canthal region,
may radiate to nose cheek, teeth and face.
Tearing, mattering, orbital cellulitis, decreased
visual acuity, periorbital oedema.
Fever, leukocytosis, altered visual acuity, altered
papillary reaction, diplopia, loss of peripheral
vision, conjunctivitis, medial canthal fullness and
tenderness, tearing
Complications:
Investigation:
Infections with CSF leakage, rarely papilloma
Usually clinical diagnosis
FBC – leukocytosis
Blood cultures
ANA testing
Imaging – x-ray, CT (MRI not as useful),
dacryocystography.
Management:
Acute – IV antibiotics.
Patients may benefit from topical steroid drops and lacrimal sac massage
Surgery – probing in an attempt to widen the lacrimal duct. dacryocystorhinostomy
Prognosis
Acute – severe morbidity, rarely mortality. High spread of infection
Chronic – rarely severe morbidity unless associated with a chronic disease
Congenital – very serious disease, significant morbidity and mortality. Can cause orbital cellulitis,
brain abscess, meningitis, sepsis and death.
95% dacryocystorhinostomy rate.
Acne Rosacea
Pathology
Epidemiology
Defined: persistent erythema of the central
portion of the face lasting for at least 3 months.
Accurate incidence not available. In Sweden 1/10
middle-class workers. More common in people
of Asian and African origin.
Risk factors
Histology
Climatic exposures, chemicals and ingested
agents (spicy foods, alcohol, hot beverages),
demodex species,
Increase in facial vasculature
Classification:
Aetiology:
Erythematotelangiectatic type, papulopustular,
phymatous, ocular
Unknown
History:
Examination:
Facial flushing
Other symptoms intermittent: high colour,
permanent telangiectasia, gritty quality in eyes
and facial oedema
Spectrum disease. Rhinoplyma, lymphoedema,
conjunctival injection, episcleritis, abscesses
Complications:
Investigation:
Rosacea keratitis, keratoconjunctivitis sicca. Rare
complication – rosacea fulminans. Scarring
generally doesn’t occur.
Clinical diagnosis – skin biopsy may be necessary
to exclude other disease states.
Management:
Sunscreen, laser, moderately high dose prednisolone (30-60 mg/d) followed by oral isotertinoin.
Pulsed dye laser, cosmetic improvement with mechanical dermabrasion, carbon dioxide laser peel,
surgical shave techniques.
Dietary – avoid triggers
Prognosis
Those who receive treatment, a stable state is reached with variable residual symptomatology. The
disease takes a chronic relapsing or pregressibe course for some patients.
Dry Eyes syndrome
Multifactorical disease of the tears and ocular surface resulting in discomfort, visual disturbance and
tear film instability with potential damage to the ocular surface
Pathology
Epidemiology
Chronic inflammatory state with production of
10-30% of the population, particularly affecting
autoantibodies (including antinuclear
the over 40s.
antibodies, rheumatoid factor), inflammatory Slightly more commone in women.
cytokine release, focal lymphocytic infiltration More common in Hispanic and Asian populations
of the lacrimal and salivary gland with
than Caucasians.
glandular degeneration and induction of
apoptosis of the conjunctive and lacrimal
gland.
Risk factors
Histology
Genetic predisposition (HLA-B8)
Normal tear film:
1.
A superficial thin lipid layer (0.11 µm) is
produced by the meibomian glands, and its
principal function is to retard tear evaporation
and to assist in uniform tear spreading.
2.
A middle thick aqueous layer (7 µm) is
produced by the main lacrimal glands (reflex
tearing), as well as the accessory lacrimal glands
of Krause and Wolfring (basic tearing).
3.
An innermost hydrophilic mucin layer
(0.02-0.05 µm) is produced by both the
conjunctiva goblet cells and the ocular surface
epithelium and associates itself with the ocular
surface via its loose attachments to the
glycocalyx of the microplicae of the epithelium.
It is the hydrophilic quality of the mucin that
allows the aqueous to spread over the corneal
epithelium.
Aetiology:
Deficient aqueous production: Sjogrens syndrome (primary and secondary), lacrimal gland deficiency
or obstruction, reflex hyposecretion, systemic drugs
Evaporative: meibomian gland dysfunction, disorders of lid aperture, low blink rate, drug action, Vit
A deficience, topical drugs, contact lens wear, allergy
History:
Examination:
Ocular irritation, dry sensation, burning, itching,
pair, foreign body sensation, photophobia,
blurred vision.
Symptoms exacerbated by smoky or dry
environments, indoor heating, excessive
reading, computer use.
Bulbar conjunctival vascular dilation, decreased
ear meniscus, irregular corneal surface,
decreased tear break-up time, punctuate
epithelial keratopathy, corneal filaments,
increased debris in the tear film, conjunctival
pleating, mucous dischares, corneal ulcers in
severe cases.
Complications:
Investigation:
Sterile or infectious corneal ulceration
Decreased visual acuity
Blindness
Labs: conjunctival impression cytology, serology
for autoantibodies.
Tear break-up test
Management:
Artificial tears
Anti-inflammatory agents
Surgery – lid, tarsorrhaphy, mucous membrane/salivary gland/ amniotic membrane transplantation
Antibiotics
Corticosteroids
Prognosis
Very good prognosis