Ophthalmic Review for General Practitioners PDF

Ophthalmic review for General Practitioners Dr. Riyad G. Banayot 1  Eyelids l Applied anatomy l Stye and chalazion l Blepharitis l Madarosis & Poliosis l Diffuse eyelid disease l Benign eyelid lesions l Malignant eyelid tumors...

Ophthalmic review for General Practitioners Dr. Riyad G. Banayot 1  Eyelids l Applied anatomy l Stye and chalazion l Blepharitis l Madarosis & Poliosis l Diffuse eyelid disease l Benign eyelid lesions l Malignant eyelid tumors 2  Applied anatomy Cross section of lower eye lid Skin: Thinnest in body Margins: meibomian glands, lashes in 2-3 irregular rows anteriorly, glands of Zeis (holocrine) and Moll (apocrine) present Subcutaneous tissue: Loose connective tissue, contains no fat Orbicularis oculi: voluntary sphincter, reflex blink and voluntary Levator palpebrae superioris: Tarsus: Dense connective tissue, meibomian glands are modified holocrine sweat glands Conjunctiva: Transparent vascularized membrane 3  Eye Lid Redness External Hordeolum - Stye l Infection of lid gland l Local pain redness and swelling l No need to refer l Treatment: compresses, topical antibiotic An external hordeolum (stye) is a small abscess caused by an acute staphylococcal infection of a lash follicle and is associated gland of Zeis or Moll. It may be associated with chronic staphylococcal blepharitis Treatment: hot compresses and topical antibiotics 4  Eye Lid Redness Chalazion l Granulomatous inflammation of Meibomian gland l Slow course - months l Compresses at onset; antibiotics no benefit l If non-resolving refer electively for transconjunctival incision & curettage A chalazion (meibomian cyst) is a chronic inflammatory lesion caused by blockage of meibomian gland orifices and stagnation of sebaceous secretions. Patients with acne rosacea and seborrhoeic dermatitis are at increased risk of chalazion formation. Treatment consists of hot compresses. Topical antibiotics have NO effect If the condition does not resolve, surgical incision and curettage can be done electively (as seen in the following slide) 5  Treatment of chalazion Injection of local anaesthetic Insertion of clamp Incision and curettage 6  Eye Lid Redness Blepharitis - staphylococcal l Chronic infection with periodic flare-ups l Staphylococcal or seborrheic l Irritation, burning and itching l Scales or crusting on lashes l Treatment: lid hygiene & topical antibiotics Staphylococcal Blepharitis is an inflammation of the lid margins. It is a very common external eye disorder, the exact etiology of which is unclear, although staphylococcal infection and seborrhea play important roles In Staphylococcal inflammation Collarettes at base of lashes can be seen; in severe long standing cases, loss of lashes can be seen 7  Eye Lid Redness Blepharitis - seborrheic l Chronic infection with periodic flare-ups l Staphylococcal or seborrheic l Irritation, burning and itching l Greasy scales or lashes stuck together l Treatment: lid hygiene & topical antibiotics seborrheic Blepharitis is an inflammation of the lid margins. It is a very common external eye disorder, the exact etiology of which is unclear, although staphylococcal infection and seborrhea play important roles In Seborrheic inflammation Greasy lashes which are stuck together is seen; also waxy lid margins with mild telangiectasia can be seen In acute cases; lid hygiene and topical antibiotics is sufficient Treatment of Chronic Blepharitis: 1. Lid hygiene - with 25% baby shampoo 2. Tear substitutes - for associated tear film instability 3. Systemic tetracyclines - for severe posterior blepharitis 4. Warm compresses - to melt solidified sebum in posterior blepharitis 8  Madarosis Decrease in number or complete loss of lashes Local causes Chronic anterior lid margin disease Infiltrating tumours Burns, radiotherapy or cryotherapy Systemic causes Generalized alopecia Myxoedema SLE Syphilis Leprosy Following removal 9  Poliosis Premature localized whitening of hair Ocular associations Chronic anterior blepharitis Sympathetic ophthalmitis Systemic associations Vogt-Koyanagi-Harada syndrome Waardenburg syndrome 10  Diffuse eyelid disease l Acute allergic edema l Contact dermatitis l Atopic dermatitis l Systemic causes of lid edema 11  Acute allergic oedema Causes - insect bites, urticaria and angioedema Unilateral or bilateral Painless, red, pitting oedema Chemosis may be present Self-limiting 12  Contact dermatitis Sensitivity to topical medication Unilateral or bilateral Painless oedema and erythema Vesiculation and crusting Thickening if chronic 13  Atopic dermatitis Associated with asthma and hay fever Chronic itching and scratching Facial - in young children Flexural - knees, elbows, wrists and ankles 14 Ocular associations of atopic dermatitis Thickening, crusting Staph. blepharitis and fissuring Angular blepharitis Vernal disease 15 Ocular associations of atopic dermatitis Keratoconjunctivitis Keratoconus Shield-like cataract Retinal detachment 16 Systemic causes of lid oedema Myxoedema Renal disease Congestive heart failure Obstruction of superior vena cava Fabry's disease 17  Benign eyelid lesions l Xanthelasma l Capillaryhemangioma l Naevus flammeus 18  Xanthelasma Common in elderly or those with hypercholesterolemia Yellowish, subcutaneous plaques containing cholesterol and lipid Usually bilateral and located medially 19  Capillary haemangioma Rare tumour which presents soon May be associated with after birth intraorbital extension Starts as small, red lesion, most frequently on upper lid Grows quickly during first year Blanches with pressure and swells Begins to involute spontaneously on crying during second year 20 Periocular haemangioma Treatment options Steroid injection in most cases Surgical resection in selected cases Occasional systemic associations High-out heart failure Maffuci syndrome - skin haemangiomas, endrochondromas and bowing of long bones Kasabach-Merritt syndrome - thrombocytopenia, anemia and reduced coagulant factors 21 Port-wine stain (naevus flammeus) Rare, congenital subcutaneous lesion Segmental and usually unilateral Does not blanch with pressure Associations Ipsilateral glaucoma in 30% Sturge-Weber or Klippel-Trenaunay-Weber syndrome in 5% 22  Malignant eyelid tumors l Basalcell carcinoma l Squamous cell carcinoma l Meibomian gland carcinoma l Melanoma l Kaposi sarcoma 23  Basal Cell Carcinoma (BCC) 1. Most common human malignancy 2. Usually affects the elderly 3. Slow-growing, locally invasive 4. Does not metastasize 5. 90% occur on head and neck 6. Of these 10% involve eyelids 7. Accounts for 90% of eyelid malignancies 24 Frequency of location of BCC Lower lid - 70% Medial canthus - 15% Upper lid - 10% Lateral canthus - 5% 25  Nodular BCC Early Advanced Shiny, indurated nodule Slow progression Surface vascularization May destroy large portion of eyelid 26  Ulcerative BCC (rodent ulcer) Early Advanced Chronic ulceration Raised rolled edges and bleeding 27  Sclerosing BCC Early Advanced Indurated plaque with loss of Spreads radially beneath normal lashes epidermis May mimic chronic blepharitis Margins impossible to delineate 28  Squamous cell carcinoma Less common but more aggressive than BCC May arise de novo or from actinic keratosis Predilection for lower lid Nodular Ulcerative Hard, hyperkeratotic nodule Red base May develop crusting fissures Borders sharply defined, No surface vascularization indurated and elevated 29 Meibomian gland carcinoma Very rare aggressive tumour with 10% mortality Predilection for upper lid Nodular Hard nodule; may Very large tumour mimic a chalazion Spreading Diffuse thickening of lid Conjunctival invasion; may margin and loss of lashes mimic chronic conjunctivitis 30  Melanoma Nodular Superficial spreading From lentigo maligna (Hutchinson freckle) Blue-black nodule with Plaque with irregular Affects elderly normal surrounding skin outline Slowly expanding May be non-pigmented Variable pigmentation pigmented macule 31  Kaposi sarcoma Vascular tumour occurring in patients with AIDS Usually associated with advanced disease Very sensitive to radiotherapy Early Advanced Pink, red-violet lesion May ulcerate and bleed 32  Treatment Options 1. Surgical excision Method of choice 2. Radiotherapy Small BCC not involving medial canthus Kaposi sarcoma 3. Cryotherapy Small and superficial BCC irrespective of location Adjunct to surgery in selected cases 33  Applied anatomy Orbital septum which separates the anterior structures from the orbit The orbital septum separates anterior lid structures and infections from the orbit 34  Eye Redness Cellulitis l Preseptal cellulitis – Same as cellulitis anywhere else – No orbital signs – No need to refer Preseptal cellulitis typically affects children and is usually secondary to lid infection such as severe acute hordeolum, skin laceration or an insect bite. The infection does not penetrate the orbital septum which separates the anterior structures from the orbit. Examination shows periorbital swelling and tenderness without proptosis (Top picture). Ocular motility, visual acuity and pupillary reactions are all normal. Treatment is with oral antibiotics on an outpatient basis 35  Eye Redness Cellulitis l Orbital cellulitis – Proptosis, restricted extraocular movements, pain – Urgent referral for IV antibiotics – CT helps differentiate preseptal form Bacterial orbital cellulitis is an infection of the soft tissues behind the orbital septum. It is much less common but potentially more serious than preseptal cellulitis The following are the main types: 1. Sinus-related (ethmoidal sinusitis). It typically affects children 2. From adjacent structures such as dental infection. 3. Post-traumatic most commonly develops within 48-72 hours of an injury that penetrates the orbital septum. PoIymicrobial infection is the rule Presentation is with a rapid onset of unilateral chemosis, proptosis and painful diplopia. Examination shows an unwell and pyrexial patient. The proptosis is most frequently lateral and downwards. The eyelids are swollen, erythematous, warm and tender to palpation. Ocular movements are restricted and painful. Orbital cellulitis is an emergency requiring hospital admission 36  Applied anatomy The lacrimal drainage system consists of the following: puncta, ampullae, canaliculi, lacrimal sac and nasolacrimal duct The nasolacrimal duct is the last portion of the lacrimal drainage system to canalize. At birth the lower end of the nasolacrimal duct is frequently non- canalized, but this is of no clinical significance because it becomes patent spontaneously during the first few weeks of life. 37  Congenital nasolacrimal duct obstruction Epiphora and matting Acute dacryocystitis NLDO presents within a few weeks of birth, with epiphora and mattering of the eye. Examination shows that gentle pressure over the lacrimal sac causes reflux of purulent material from the puncta. 38  Congenital nasolacrimal duct obstruction Treatment 1. Massage of the nasolacrimal duct increases the hydrostatic pressure and thereby ruptures the membranous obstruction. In performing this maneuver, the index finger is placed over the common canaliculus to block the exit of material through the puncta and then stroked downwards firmly to increase the hydrostatic pressure within the lacrimal sac. Ten strokes should be applied four times a day. Chloramphenicol drops are also prescribed four times a day. 2. Probing (GA) should not be performed until the age of 12 months because spontaneous canalization occurs in about 95% of cases. If symptoms persist despite two technically satisfactory probings it may be necessary to perform a DCR between the ages of 3 and 4 years. 39  Eye Redness Nasolacrimal Duct Obstruction l Dacryocystitis (acute/chronic) if infected l Swelling or abscess in lower inner canthus – Depending on severity, may need hospitalization – Referral is required – Initial treatment: IV or PO Antibiotics +/- external drainage In adults NLDO presents as a tender canthal swelling & Mild preseptal cellulitis which may develop into an abscess of the lacrimal sac Treatment consists of systemic antibiotics and warm compresses, and DCR after acute infection is controlled (DCR to create internal fistula from lacrimal sac to nose) 40 Eye Redness l Laceration – Usually requires referral – Assume all lacerations medial to punctum involve lacrimal drainage system – Canalicular lacerations should be repaired within 24 hours Intubation of the lacrimal system following repair of torn upper and lower canaliculi 41  Conjunctivitis l Bacterial l Chlamydial l Adult l Neonatal l Trachoma l Viral l VKC l Atopic Keratoconjunctivitis l Allergic l Ophthalmia neonatorum 42  Conjunctivitis l Irritation l FB sensation l Photophobia l Diffuse redness l Tearing Conjunctivitis is a very common and usually self-limiting condition It presents with acute symptoms of irritation, foreign body sensation, photophobia, diffuse redness and tearing On waking, the eyelids are frequently stuck together and difficult to open. Both eyes are usually involved one more than the other How can we differentiate between types of conjunctivitis 43  Bacterial Conjunctivitis Exudate: Pus Scraping: PMNs Preauricular Lymph nodes: Not palpable Even without treatment, simple conjunctivitis usually resolves within 10-14 days and laboratory tests are not routinely performed. Before initiating treatment, it is important to bathe all discharge away. Initial treatment is broad- spectrum antibiotic drops during the day and ointment at night until the discharge has ceased. 44  Adult chlamydial keratoconjunctivitis Infection with Chlamydia trachomatis serotypes D to K Concomitant genital infection is common Subacute, mucopurulent follicular Variable peripheral keratitis conjunctivitis Treatment - topical tetracycline and oral tetracycline or erythromycin 45 Neonatal chlamydial conjunctivitis Presents between 5 and 19 days after birth May be associated with otitis, rhinitis and pneumonitis Mucopurulent papillary conjunctivitis Treatment - topical tetracycline and oral erythromycin 46  Trachoma Infection with serotypes A, B, Ba and C of Chlamydia trachomatis Fly is major vector in infection & re-infection cycle Progression Acute follicular Conjunctival Herbert pits conjunctivitis scarring (Arlt’s line) Pannus formation Trichiasis Entropion Treatment - systemic azithromycin 47  Viral Conjunctivitis Usually bilateral, acute watery Subconjunctival haemorrhages & discharge and follicles pseudomembranes if severe Exudate: Profuse watery Scraping: Mononuclear Preauricular Lymph nodes: Palpable Viral conjunctivitis presents with acute onset of watering, redness, discomfort and photophobia. Both eyes are affected in about 60% of cases. Examination shows lid edema, a follicular response which is frequently associated with a preauricular adenopathy. In severe cases, subconjunctival hemorrhages, chemosis and pseudomembranes may develop. Treatment is unsatisfactory but spontaneous resolution within 2 weeks is the rule. Topical steroids should be avoided unless the inflammation is very severe and the possibility of herpes simplex infection has been excluded. 48  Vernal Keratoconjunctivitis (VKC) - (spring catarrh) Main symptoms: Intense ocular Itching Exudate: Profuse watery Scraping: Mononuclear Preauricular Lymph nodes: Palpable Vernal keratoconjunctivitis or spring catarrh is a common recurrent, bilateral, external, ocular inflammation affecting children and young adults. It is more common in males than in females. VKC is an allergic disorder. About three- quarters of patients have associated atopy and two-thirds have a close family history of atopy. Atopic patients often develop asthma and eczema in infancy. The onset of VKC is usually after the age of 5 years and the condition eventually resolves around puberty. Main symptoms: Intense ocular Itching, associated with lacrimation, photophobia, foreign body sensation and burning. Thick mucus discharge from the eyes also occurs. The symptoms may occur throughout the year, but are characteristically worse during the spring and summer. Treatment consists of topical steroids for short periods and sodium cromoglycate. 49  Atopic keratoconjunctivitis Typically affects young patients with atopic dermatitis Eyelids are red, thickened, macerated and fissured Infiltration of tarsal conjunctiva causing featureless appearance 50  Allergic Conjunctivitis Exudate: Watery +/- mucoid Scraping: Eosinophil Preauricular Lymph nodes: Not palpable Acute allergic conjunctivitis is an urticarial reaction caused by a large amount of allergen reaching the conjunctival sac. It frequently affects young children after playing outdoors. Clinically, the condition is characterized by a sudden onset of severe chemosis and swelling of the eyelids. Most cases resolve spontaneously within a few hours and, apart from reassurance, require no specific treatment Pictures show; transient eyelid edema and conjunctival chemosis 51  Ophthalmia Neonatorum Neonatal conjunctivitis l Contamination of infant’s eyes when passing through vagina and cervix l Gonococcus: – Rapid blindness, 2ry corneal ulceration – Onset 2-3 days after birth – Broad spectrum topical antibiotics l Chlamydia: – Less destructive, may last months – Onset 5-12 days – topical tetracycline and oral erythromycin Neonatal conjunctivitis is defined as a conjunctival inflammation that occurs during the first month of life Chlamydial infection is the most common cause of neonatal conjunctivitis. Presentation is typically between 5 and 14 days after birth with an acute mucopurulent discharge. Treatment is with topical tetracycline and oral erythromycin ethyl succinate 25 mg/kg twice daily for 14 days. Because the infection is transmitted from the mother during delivery it is important that both parents are examined for evidence of genital infection. Gonococcal infection is a rare cause of ophthalmia neonatorum which is transmitted from the mother during delivery. Presentation is usually between 1 and 3 days after birth, with a hyperacute purulent discharge associated with chemosis and sometimes membrane or pseudomembranes formation. Treatment is with topical and systemic penicillin. The dose of systemic benzylpenicillin is 50,000 units/kg in two divided daily doses given for 7 days. Alternative treatment with a single intramuscular injection of cefotaxime 100 52 mg/kg is also effective. Both parents must be examined for evidence of genital infection. 52  Subconjunctival Hemorrhage l Common l Causes: trauma, operation, uncontrolled HTN, valsalva, cough, vomiting, straining maneuvers l No treatment; reassurance A good history is essential to exclude: trauma, operation, uncontrolled HTN, valsalva, coughing, vomiting or straining maneuvers 53  Pingueculum / Pterygium l Pingueculum: – On conjunctiva only l Pterygium: – Invading cornea l Chronic diseases / degeneration l Refer if symptomatic l Treatment: surgical excision – high recurrence rate Pingueculum A common lesion which consists of a yellow-white deposit on the bulbar conjunctiva adjacent to the nasal or temporal aspect of the eye Surgery is not advocated Pterygium A triangular sheet of fibrovascular tissue which invades the cornea. They typically develop in patients who have been living in hot climates and represents a response to chronic dryness and exposure to the sun. Surgical excision is indicated either for cosmetic reasons or in cases of progression towards the visual axis 54  Immuno-bullous diseases l Cicatricial pemphigoid l Stevens-Johnson syndrome 55  Cicatricial pemphigoid Chronic and progressive Typically affects elderly women Increased prevalence of HLA-B12 Oral mucosal lesions in most cases Skin lesions are less common 56 Progression of ocular cicatricial pemphigoid Diffuse hyperemia Pseudomembranes Subepithelial fibrosis and Symblepharon shrinkage 57 Complications of ocular cicatricial pemphigoid Ankyloblepharon Metaplastic lashes Cicatricial entropion Corneal keratinization Obliteration of fornices 2ry bacterial keratitis 58  Stevens-Johnson syndrome Acute, and self-limiting Hypersensitivity to drugs or infection Typically affects young men Lesions of oral mucosa Maculopapules which Vesiculobullous, and lips may develop into target hemorrhagic lesions and necrotic lesions 59 Ocular complications of Stevens-Johnson syndrome Transient conjunctivitis and membranous or pseudo- lid crusting without sequelae membranous conjunctivitis Focal fibrotic patches and Metaplastic lashes occasionally symblepharon 60  Applied anatomy layers of precorneal tear film The precorneal tear film consists of three layers & each has a separate function: 1- Lipid: retard evaporation of the aqueous layer & lubricate the eyelids 2- Aqueous: supply oxygen to cornea, antibacterial function, abolish irregularities of corneal surface, wash away debris 3- Mucin: converts the corneal epithelium a hydrophilic surface 61  Dry Eyes l Chronic redness l Burning l No need to refer l Treatment: artificial tear drops Keratoconjunctivitis sicca refers to a dry eye primarily resulting from aqueous tear deficiency Causes of a dry eye Atrophy and fibrosis of lacrimal tissue of the lacrimal glands alone or in Sjögren's syndrome (autoimmune disease) Other causes include: destruction of lacrimal tissue by tumors, chronic inflammation; Meibomian gland dysfunction; absence of the lacrimal gland by surgery Most common symptoms are irritation, a foreign body sensation, burning, presence of stringy mucus discharge and transient blurring of vision. Symptoms are exacerbated by exposure to conditions associated with increased tear evaporation (e.g. air conditioning, wind) or prolonged reading when the blink reflex is reduced. Treatment includes avoiding warm surroundings, tear substitutes and reduction of tear drainage 62  Applied anatomy The cornea consists of the five layers: 1- epithelium 2- Bowman's layer 3- stroma 4- Descemet's membrane 5- endothelium 63  Keratitis l Bacterial – Contact lens wearers – White infiltrate in cornea – Pain, reduced vision – Should be referred – Treatment: topical antibiotics Predisposing factors include: 1- Contact lens wear is the most common predisposing factor 2- Ocular surface disease post herpetic corneal disease, trauma, corneal exposure and dry eyes Examination reveals acutely painful red eye and a white spot on the cornea. In some cases keratitis can rapidly lead to a corneal ulcer and perforation A bacterial corneal ulcer is a sight-threatening condition which demands urgent identification and eradication of the causative organism. This is best performed with the patient hospitalized 64 Keratitis l Fungal – Frequently preceded by ocular trauma with organic matter – Grayish white infiltrate surrounded by feathery infiltrate in cornea – Pain, reduced vision – Should be referred – Treatment: topical antifungal agents & systemic therapy if severe 65  Keratitis l Acanthamoeba – Contact lens wearers at particular risk – Anterior stromal infiltrates, ulceration, ring abscess & stromal opacification – Pain, reduced vision – Should be referred – Treatment: chlorhexidine or polyhexamethylenebiguanide Predisposing factors include: 1- Contact lens wear is the most common predisposing factor 2- Ocular surface disease post herpetic corneal disease, trauma, corneal exposure and dry eyes Examination reveals acutely painful red eye and a white spot on the cornea. In some cases keratitis can rapidly lead to a corneal ulcer and perforation A bacterial corneal ulcer is a sight-threatening condition which demands urgent identification and eradication of the causative organism. This is best performed with the patient hospitalized 66  Keratitis l Viral Herpes Simplex – Recurrent dendrites, corneal edema, iritis – Refer – Treatment: Acyclovir ointment Infection with HSV is extremely common and about 90% of the population are seropositive for HSV antibodies. In spite of this, most infections are subclinical Primary ocular infection typically occurs in children between the ages of 6 months and 5 years. In most cases it is self-limited Clinical picture Blepharoconjunctivitis is usually benign and self-limited. Skin lesions typically involve the lids and periorbital area. Initially, they consist of vesicles which rapidly form superficial crusts and then heal without scarring. Keratitis develops within a few days in about 50% of patients with blepharoconjunctivitis. A fine epithelial punctate keratitis may be a transient finding. A coarse epithelial punctate keratitis may give rise to a variety of epithelial lesions which subsequently progress to dendritic shapes Treatment: topical antiviral ointment should be applied prophylactically to the eye five times a day for about 21 days to prevent keratitis 67  Keratitis l Viral Herpes Zoster – V1 Dermatome – Dendrites, iritis, other ocular inflammation – Treatment: Oral Acyclovir; start and then refer Chickenpox and zoster are different conditions caused by the same virus. Zoster mainly affects elderly patients 15% of all cases of herpes zoster affect the ophthalmic division of the trigeminal nerve (any branch: frontal, lacrimal and nasociliary) Clinical features: Rash is maculopapular and then becomes pustular. The pustules subsequently burst to form crusting ulcers. Initially, the rash is accompanied by periorbital edema. Ocular lesions include conjunctivitis, episcleritis, keratitis, uveitis Keratitis takes the form of small, fine, dendritic or stellate epithelial lesions with tapered ends without bulbs Treatment: Systemic therapy is with acyclovir 800 mg tablets administered five times daily for 7 days as early as possible. Topical therapy consists of antiviral creams and a steroid-antibiotic preparation used three times daily 68  keratoconus Nipple cone Oval cone Globus cone Small and steep curve Larger and ellipsoidal Largest cone 69  Signs of keratoconus Bilateral in 85% but asymmetrical Oil droplet reflex Vogt striae Prominent corneal nerves Bulging of lower lids on downgaze Fleischer ring & scarring Munson sign Acute hydrops 70  Systemic associations of keratoconus Atopic dermatitis Down syndrome Ehlers-Danlos syndrome Marfan's syndrome Crouzon syndrome Osteogenesis imperfecta 71  Vortex keratopathy Vortex keratopathy is characterized by symmetrical, bilateral, greyish or golden corneal epithelial deposits which appear in a vortex fashion from a point below the pupil and swirl outwards sparing the limbus It occurs in Fabry's disease and in patients being treated with a variety of drugs including: Chloroquine: (reversible). Malaria & rheumatic diseases. Amiodarone: cardiac arrhythmias. Related to the dosage and duration. Indomethacin: Chlorpromazine: Schizophrenia Tamoxifen: Breast cancer 72  Toxic maculopathy Toxic maculopathy is associated with several drugs. Thioridazine: schizophrenia Chloroquine: Malaria & rheumatic diseases Quinine: Malaria Chlorpromazine: Schizophrenia Tamoxifen: Breast cancer 73  Peripheral corneal involvement in rheumatoid arthritis Without inflammation With inflammation Chronic and asymptomatic Acute and painful Circumferential thinning with intact Circumferential ulceration and epithelium (‘contact lens cornea’) infiltration Treatment - systemic steroids and/or cytotoxic drugs 74  Rosacea keratitis Affects 5% of patients with acne rosacea Bilateral and chronic Progression Peripheral inferior Subepithelial infiltration Thinning and perforation vascularization if severe Treatment - topical steroids and systemic tetracycline or doxycycline 75  Metabolic Keratopathy Metabolic keratopathy Mucopolysaccharidoses are a group of storage diseases which result from a deficiency of lysosomal enzymes Clinical manifestations include facial coarseness, skeletal anomalies and heart disease Ocular features include corneal stromal infiltration, retinal pigmentary degeneration and optic nerve atrophy Wilson’s disease is characterized by a widespread deposition of copper in the tissues and becomes manifest in one of three ways: (1) liver disease, (2) neurological involvement of the basal ganglia or (3) psychiatric features. Corneal copper deposition is present in nearly all patients. The classic Kayser- Fleischer ring is located at the peripheral part of Descemet's membrane. The copper is deposited preferentially in the vertical meridian of the cornea and may disappear with penicillamine therapy. Some patients also have a green 'sunflower' cataract. 76  Corneal Foreign Body l Ifmetal striking-metal is the mechanism of injury always get an X-Ray/CT scan of skull (This is mandatory if there is an open globe injury or suspicion of entry wound) l Superficial corneal FB can be removed with Q-tip or needle tip, otherwise refer l Rust rings develop after initial removal Treatment consists of: - Removal of FB ASAP - Topical antibiotic ointment - Patching the eye 77  UV burn Treatment consists of: - Removal of FB ASAP - Topical antibiotic ointment - Patching the eye 78  Applied anatomy The scleral stroma is composed of collagen bundles of varying size and shape that are not uniformly oriented There three vascular layers that cover the anterior sclera: conjunctival, superficial episcleral and deep vascular plexus 79  Applied anatomy of vascular coats Normal Episcleritis Scleritis Radial superficial Maximal congestion Maximal congestion of episcleral vessels of episcleral vessels deep vascular plexus Deep vascular plexus Slight congestion of adjacent to sclera episcleral vessels 80  Episcleritis / Scleritis l Episcleritis: – Common – Localized inflammation, lasts 2 wks. – Treatment with topical steroids or oral NSAIDs l Scleritis: – Rare – Granulomatous or necrotizing, Vision threatening. – Treatment with immunosuppression Episcleritis is a common, benign, self-limiting and frequently recurrent disorder which typically affects young adults. It is seldom associated with a systemic disorder and never progresses to scleritis Presentation is with unilateral mild discomfort and tenderness to touch Examination shows sectoral or, rarely, diffuse redness Simple episcleritis usually resolves spontaneously within 1-2 weeks. Mild cases may need topical steroids and/or topical non-steroidal anti-inflammatory drugs (NSAIDs) Scleritis is a granulomatous inflammation of the scleral coat of the eye. It is much less common than episcleritis. About 45% of patients with scleritis, particularly of the necrotizing type, may have one of the following systemic diseases: 1. Rheumatoid arthritis (the most frequent) 2. Connective tissue vascular disorders Presentation is with a gradual onset of pain and localized redness Early cases show distortion of blood vessels in the affected area, this is followed by the development of scleral necrosis. Eventually, the sclera becomes transparent and the underlying uvea visible Treatment is with oral steroids, Immunosuppressive drugs or combined therapy 81  Uveitis l Pain, reduced vision, ciliary flush l Systemic association: Sarcoid, HLA B-27, inflammatory bowel disease, TB, syphilis l Refer l Treatment: topical steroids, dilating drops By strict definition, uveitis is an inflammation of the uveal tract ( iris, ciliary body and retina) The main symptoms of acute anterior uveitis are photophobia, pain, redness, decreased vision and lacrimation The main symptoms of posterior segment inflammation are floaters and impaired vision Uveitis is associated with arthritis: Ankylosing spondylitis, Reiter's syndrome, Psoriatic arthritis, Juvenile chronic arthritis Uveitis is also associated with chronic systemic infections: AIDS, Acquired syphilis, Tuberculosis, Leprosy Uveitis is also associated with parasitic infections: Toxoplasmosis, Toxocariasis Treatment of uveitis includes: Mydriatics (To give comfort & prevent formation of posterior synechiae); Steroids administered topically in the form of drops or ointment, by periocular injection or systemically. Cytotoxic drugs are used in blinding (usually bilateral), reversible, uveitis which has failed to respond to adequate steroid therapy and intolerance side effects from systemic steroid therapy 82  Applied anatomy The aqueous is secreted by the non-pigmented ciliary epithelium. It travels from the posterior chamber, in front of the lens, through the pupil into the anterior chamber reaching the trabecular meshwork through which aqueous humor leaves the eye 83  Acute Angle Closure Glaucoma l Sudden severe pain, loss vision, N & V l Red eye with ciliary flush, pupil fixed & mid dilated, cornea steamy, increased IOP l Emergency referral l Treatment: drops to lower IOP, constrict pupil, diuretics, laser iridotomy Presentation is with rapidly progressive impairment of vision associated with periocular pain and congestion. Nausea and vomiting may occur in severe cases. Examination shows injection of the limbal and conjunctival blood vessels. The IOP is severely elevated and the cornea is edematous. The anterior chamber is shallow with peripheral iridocorneal contact. The pupil is vertically oval, fixed in the semidilated position and unreactive to both light and accommodation Initial treatment is aimed primarily at lowering IOP through systemic medication. Subsequent treatment is aimed at re-establishing the communication between the posterior and anterior chambers 84  Eye chemical injuries l Chemical burns – irrigate immediately – NEVER give acid for alkali or vice versa l For all but least severe trauma – refer l Always protect the eye from further injury during transfer A chemical burn is therefore the only type of ocular injury that requires immediate treatment without first taking a history and performing a careful examination. Acid burns are usually less serious than alkalis because acids tend to precipitate tissue proteins which coagulate and form a barrier preventing deep penetration. Alkaline burns are more serious because alkalis saponify lipids in the corneal epithelium, and bind to the mucoproteins and collagen in the corneal stroma. Alkali therefore disrupt the normal barriers of the cornea and rapidly increase the pH of the anterior chamber, with resultant damage to the lens and anterior uvea Copious irrigation with fluids and removal of all particulate matter IMMEDIATELY. Then refer 85  Acquired cataract l Age related l Diabetes l Myotonic dystrophy l Atopic dermatitis l Trauma l Drugs l Complicated (secondary) 86 Age related cataract Nuclear Cortical Subcapsular Christmas 87  Diabetic cataract Juvenile Adult White punctate or snowflake Cortical and subcapsular posterior or anterior opacities opacities May progress more quickly than May mature within few days in non-diabetics 88  Myotonic dystrophy cataract Myotonic facies Stellate posterior subcapsular opacity Frontal balding 90% of patients after age 20 years No visual problem until age 40 years 89  Atopic dermatitis cataract Cataract develops in 10% Anterior subcapsular plaque of cases between 15-30 years (shield cataract) Bilateral in 70% Wrinkles in anterior capsule Frequently becomes mature 90  Traumatic cataract Concussion ‘Vossius’ ring from imprinting of iris pigment Flower-shaped Penetration Other causes Ionizing radiation Electric shock Lightning 91  Drugs Systemic or topical steroids Chlorpromazine - initially posterior subcapsular - central, anterior capsular granules Other drugs Long-acting miotics Amiodarone Busulphan 92  Complicated cataract Posterior subcapsular Glaukomflecken Chronic anterior uveitis Follows acute angle closure glaucoma High myopia Central, anterior subcapsular Hereditary fundus dystrophies opacities 93  Congenital cataract 33% - idiopathic - may be unilateral or bilateral 33% - inherited - usually bilateral 33% - associated with systemic disease - usually bilateral Other ocular anomalies present in 50% Congenital cataract The mother complains that the infant has an abnormal white eye OR the referring doctor sends the infant for consultation for abnormal white red reflex (seen on direct ophthalmoscopic examination) Treatment: Lensectomy and IOL implant as soon as possible 94  Classification of congenital cataract Anterior polar Posterior polar Coronary Cortical spoke-like Lamellar Central pulverulent Sutural Focal dots 95 Causes of cataract in healthy neonate Hereditary (usually dominant) Idiopathic With ocular anomalies PHPV Aniridia Coloboma Microphthalmos Buphthalmos 96  Causes of cataract in unwell neonate Intrauterine infections Rubella Toxoplasmosis Cytomegalovirus Varicella Metabolic disorders Galactosaemia Hypoglycaemia Hypocalcaemia Lowe syndrome Intrauterine causes Congenital rubella is associated with cataract in 15% of cases Toxoplasmosis, CMV inclusion disease, and maternal drug ingestion during pregnancy (thalidomide and steroids) 97  Ectopia lentis - Acquired Trauma Stretched zonules Buphthalmos Megalocornea Anterior uveal tumours Degenerate eye Ectopia lentis refers to a displacement of the lens from its normal position. The lens may be completely dislocated (luxated) from the pupillary space or partially displaced (subluxated), but still remain in the pupillary space. Ectopia lentis may be heredofamilial or acquired. Acquired causes include trauma, a very large eye (i.e. high myopia, buphthalmos) and anterior uveal tumors Associations of ectopia lentis: Marfan's syndrome Weill-marchesani syndrome Homocystinuria Hyperlysinaemia, Stickler's syndrome, Ehlers-Danlos syndrome and aniridia 98  Ectopia lentis - AD Systemic features of Marfan's syndrome Limb-trunk disproportion Arachnodactyly Pectus excavatum Aortic dilatation, dissection and regurgitation High-arched palate Mitral valve prolapse 99  Ocular features of Marfan syndrome Lens Retinal detachment Upward subluxation Lattice Axial myopia Zonule usually intact degeneration Angle anomaly and Cornea plana Blue sclera glaucoma 100  Ectopia lentis - AR Weill-Marchesani syndrome Systemic features Ocular features Short stature Microspherophakia Short stubby fingers (brachydactyly) Anterior lens subluxation Mental handicap Angle anomaly and glaucoma 101  Ectopia lentis - AR Homocystinuria (Defect in cystathionine synthetase) Systemic features Ocular features Malar flush and fine, fair hair Downward lens subluxation Marfanoid habaitus Disintegration of zonule Increased platelet stickiness Mental handicap 102  Congenital glaucoma Buphthalmos Corneal edema associated with lacrimation and photophobia Congenital glaucoma affects 1 in 10,000 births, with 65% of patients being boys The mother complains of lacrimation, photophobia and blepharospasm Examination the following: Corneal haze resulting from epithelial edema and corneal clouding; Buphthalmos (large eye). Note that as the sclera enlarges, it also becomes thinner and takes on a blue appearance as a result of enhanced visualization of the underlying choroid Treatment: Surgical. Goniotomy and Trabeculectomy to establish a communication between the anterior chamber and Schlemm's canal 103  Dysthyroid Ophthalmopathy l Bilateral autoimmune swelling of extraocular muscles +/- orbital inflammation l Findings: – Proptosis (exophthalmos) – Restricted EOM – Inflammation – Optic nerve compression – Corneal exposure l Treatment: steroids / radiotherapy when active surgery when “burnt out” Graves' disease is an autoimmune disorder most commonly presenting in the fourth to fifth decades of life and affecting women more frequently by a ratio of 8:1. It is the most common cause of thyrotoxicosis. In 10-25% of cases, thyroid ophthalmopathy occurs in the absence of both clinical and biochemical evidence of thyroid dysfunction There are 5 main clinical manifestations of dysthyroid ophthalmopathy: 1- Eyelid retraction 2- Soft tissue involvement: Conjunctival injection, chemosis and edema & fullness of the eyelids 3- Proptosis: Permanent in about 70% of patients. Severe proptosis prevents adequate lid closure and leads to severe exposure keratopathy and corneal ulceration 4- Optic neuropathy: It is caused mainly through direct compression of the optic or its blood supply at the orbital apex by the congested and enlarged recti muscles 5- Restrictive myopathy: Between 30% - 50% of hyperthyroid patients develop ophthalmoplegia. The diplopia may be transient but, in 50% of patients, it is permanent. Ocular motility is restricted by edema (infiltrative) and by fibrosis (fibrotic) phase 104  Diabetic Retinopathy l Background / Non- proliferative – Leaking vessels cause edema & exudates – Treatment: referral for laser if VA less than 6/9 l Proliferative – Ischemic retina secretes vascular growth factor – fragile new vessels rupture & bleeding may lead to scar and retinal damage / detachment – Treatment: referral for PRP DR is the most common cause of blindness in individuals between the ages of 20 and 65 years Risk factors for diabetic retinopathy Duration of diabetes: Good metabolic control: of diabetes will not prevent DR, BUT poorly controlled patients may develop DR sooner. Miscellaneous factors: pregnancy, systemic hypertension, renal disease and anemia. DR is classified into Non-Proliferative and Proliferative retinopathy Signs of Non-Proliferative DR include: Microaneurysms, Hemorrhages, Hard exudates, Retinal edema, Vascular changes and cotton-wool spots Signs of Proliferative DR include: Neovascularization, Vitreous detachment, Hemorrhage (vitreous & preretinal) 105  Exposure keratopathy Exposure keratopathy is caused by improper wetting of the corneal surface by the precorneal tear film because of the inability of the lids to resurface the cornea with each blink. This occurs despite the presence of normal tear production. Important causes include facial nerve palsy and severe proptosis. Occasionally, corneal exposure during sleep may occur in normal individuals in the absence of any of these factors. Examination shows a spectrum of clinical findings which ranges from minimal inferior punctate epitheliopathy to severe ulceration, neovascularization, infection and even perforation. Treatment is with frequent use of artificial tears during the day and, instillation of ointment at night and taping shut of the eyelids. If the underlying condition is likely to be permanent, lid surgery is usually required 106  Rosacea keratitis Acne rosacea is a common skin disease of unknown etiology which typically affects women aged between 30 and 50 years Skin lesions include chronic hyperemia of the face, usually involving the nose, central forehead and upper cheeks. Flushing of these areas may be precipitated by ingestion of alcohol or spicy foods. Other features include variable degrees of telangiectasia, papules, pustules (Figure top left and right) and hypertrophic sebaceous glands (Figure bottom left), leading to increased sebum production. Rhinophyma is the most advanced form of the disease (Figure bottom right). Keratitis may take several forms: Punctate epitheliopathy involving the inferior two thirds of the cornea, Peripheral vascularization, followed by subepithelial infiltrates central to the vessels (Figure top). In severe cases pannus formation may obscure the visual axis (Figure middle). Thinning also occurs. 107  Keratitis in systemic collagen vascular disorders Keratitis in systemic collagen vascular disorders Presence of severe, persistent, peripheral, corneal infiltration, ulceration or thinning unexplained by coexistent ocular disease should prompt a search for an associated systemic collagen vascular disease Four main diseases should be considered are: Rheumatoid arthritis, Systemic lupus erythematosus, Polyarteritis nodosa and Wegener's granulomatosis. The ocular lesions may occasionally precede the clinical manifestation of the systemic disease 108  Applied anatomy The sella turcica is a bony cavity in the sphenoid bone in which the pituitary gland lies. The roof of the sella is formed by a fold of dura matter which stretches from the anterior to the posterior clinoids (diaphragma sellae). The optic nerves and the chiasm lie above the diaphragma sellae. 109  Pituitary adenoma Visual field defects caused by compression of chiasm from below by pituitary adenoma Axial CT scan of right pituitary adenoma invading right cavernous sinus Chromophobe adenoma is the most common primary intracranial tumor to produce neuro-ophthalmological features Presentation is typically during early adult life or middle age with the following: Headache may be the prominent feature as a result of involvement of pain-sensitive fibers in the diaphragma sellae. As the tumor expands upwards and breaks through the diaphragma the headaches may stop. Visual symptoms of bitemporal visual field defects usually have a very gradual onset and may not be noticed by the patient until well established. It is therefore essential to examine the visual fields in all patients with non specific headaches or endocrine disturbance 110  Optic Neuritis l Mostly unilateral sudden loss of vision, disturbance in color vision and pain with EOM l 50% go on to develop MS l Findings: poor vision, poor color vision, afferent pupillary defect, optic nerve usually normal, visual field defect l Treatment: usually refer to neurologist, IV not oral steroids Axial MRI scan showing periventricular plaques of demyelination (left: T1; right: T2) Optic neuritis is an inflammatory or demyelinating disorder of the optic nerve Multiple sclerosis Is a common idiopathic demyelinating disorder of the CNS characterized by intermittent disturbances of neurological function. It does not affect the peripheral nervous system and is characterized by the following clinical features: Spinal cord lesions which give rise to weakness, stiffness, muscle spasms, fatigue, sensory disturbances in the limbs, and disturbance of bladder, sexual and bowel function. Brain-stem lesions which may produce diplopia. nystagmus, ataxia, dysarthria and dysphagia. Hemisphere lesions which may cause intellectual decline, depression, euphoria and even dementia. Large plaques may produce sudden hemiparesis, hemianopia and dysphasia. Transient phenomena include: epilepsy, Lhermitte's sign (electrical sensation on neck flexion), the transient dysarthria - dysequilibrium - diplopia syndrome, tonic spasms, trigeminal neuralgia and Uhthoff's phenomenon (sudden, temporary worsening of visual or other symptoms brought on by physical exercise or increase in body temperature). 111 Ocular presentation is with an acute onset of monocular visual loss which is frequently associated with periocular discomfort made worse on moving the eye. There may also be frontal headache and tenderness of the globe. The following close association exists between optic neuritis and multiple sclerosis: 74% of women and 34%, of men with ON may ultimately develop MS (when followed up for 15 years) Evidence of ON may be found in 70% of established MS cases. 111