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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 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