Diseases of the External Eye & Cornea PDF

OPHTHALMOLOGY DISEASESOF THE EXTERNAL EYE & CORNEA Dr. C. Quito | August 25, 2022 PRECORNEAL TEAR FILM  Tear Osmolarity  The lipid layer is produced b...

OPHTHALMOLOGY DISEASESOF THE EXTERNAL EYE & CORNEA Dr. C. Quito | August 25, 2022 PRECORNEAL TEAR FILM  Tear Osmolarity  The lipid layer is produced by the Meibomian glands, its primary function is to contribute to the stability of the tear film by retarding the evaporation of the mucoaqueous layer.  The mucoacqueous layer: o The aqueaous layer makes up the bulk of the tear film; primary function is to deliver nutrition to the MANAGEMENT cornea – produced by lacrimal gland.  Environmental modification  Systemic anti-inflammatory o The mucin layer is produced by the goblet cells and surface epithelial  Artificial tears ± preservatives agents (corticosteroids, cells of conjunctiva; primary function is to convert the hydrophobic layer  Secretagogues immuno-suppressants of the ocular surface to hydrophilic  so that aqueous layer will be  Topical anti-inflammatory agents biologics) distributed evenly on the ocular surface. Any problem in the tear film  (corticosteroids, cyclosporine,  Autologous serum drops will give rise to dye eye syndrome.  tacrolimus)  Punctal plugs OCULAR SURFACE DISORDERS  Omega-3 FA supplementation  Moisture chambers/ goggles DRY EYE SYNDROME  Surgery  Eyelid hygiene  “Dry eye is a multifactorial disease of the ocular surface characterized by TYPES a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles.” -- Dry Eye Workshop II (DEWSII), Tear Film and Ocular Surface Society (TFOS), 2017 BLEPHARITIS  Inflammation of the eyelid margins  Location o Anterior – skin, eyelash follicles o Posterior – MG orifices  More than 1 type may be present It starts with the tear film instability which will lead to tear hyperosmolarity that triggers simultaneously cascade of inflammatory reactions  goblet cells and loss of glycocalyx  Chronic eyelid redness, burning, FBS, PEDs over the inferior third of the cornea  Injection and telangiectasia of the eyelid margin SEBORRHEIC BLEPHARITIS  Older patients  Anterior eyelid margin Clinical o Oily or greasy scurfs/ crusts on eyelashes, and scalp; Features increased MG secretions o Eyelid hygiene o Warm compress x 15mins Treatment o Massage with diluted mild shampoo or commercial cleansers x 3-5 minutes o Treat the dermatitis STAPHYLOCOCCAL BLEPHARITIS  Advanced age  Bacterial infection of the anterior eyelid margin by S. aureus and/or S.  Hormonal: OCP use, pregnancy, menopause, ERT, epidermidis (but occasionally by other species) androgen deficiency  Younger patients  Ocular conditions: blepharitis, ocular allergy RISK  Crusting upon waking up; symptoms tend to become worse in the  Ocular surgery FACTORS morning and improve in the afternoon  Systemic conditions: diabetes mellitus, connective tissue diseases, autoimmune diseases o Hard, brittle, fibrinous  Medications: anti-hypertensives, anti-depressants, anti- Clinical scales and matted glaucoma features crusts around the  Others: CTL use, use of video monitors, smoking lashes o Ulcers when crusts are  Redness  Mucoid discharge removed  Eye pain / Foreign body  Photophobia Management o GS/CS sensation  Disturbance of vision SYMPTOMS o Lid hygiene  Tearing  Eyes that are easily o Antibiotic ointment (erythromycin, azithromycin,  Grittiness fatigued bacitracin)  Itchiness  Heaviness o Topical corticosteroids for inflammatory keratitis  Irritation Symptoms are usually more pronounced: in the afternoon, during work, prolonged reading, use of video monitors, low humidity/high wind velocity DIAGNOSIS  Tear Break-up Time (TBUT): normal value is >10 seconds  + dry eye  Schirmer Test  Corneal staining MEIBOMIAN GLAND DYSFUNCTION  Posterior eyelid margin  Older patients, Asian populations  Commonly missed diagnosis  Leading cause of dry eye syndrome throughout the world chismis buddies ☕| OLFU MED 2024|Page 1 of 5  o Pouting MG with white keratin plug extending through o Supportive therapy Clinical the MG orifice o Topical corticosteroids features o Foam in the tear meniscus o Manual removal of membrane GONOCOCCAL CONJUNCTIVITIS  Sexually-transmitted or through vaginal delivery, urine*  N. gonorrheae  Explosive onset and rapid progression of severe purulent conjunctivitis o Adults: Hyperacute o Neonates: 3-5 days after birth o Lid hygiene o Pre-auricular lymphadenopathy o Artificial tear drops andgels Clinical o Conjunctival membranes Management o Topical corticosteroids features o Superior corneal thinning  perforation o Omega-3 FA(controversial) o Adults o Systemic tetracycline  Ceftriaxone 1g IM single dose DEMODEX BLEPHARITIS  Azithromycin 1g PO single dose o Neonates Management  Ceftriaxone 25-50mg/kg IM or IV single dose  Topical erythromycin  Frequent irrigation of purulent discharge with saline  Treat parents and all sexual partners  Older patients  Anterior and posterior blepharitis o D. folliculorum – Hair follicles o D. brevis – Sebaceous glands  Lid itchiness and irritation in the morning  Unresponsive to conventional treatment BACTERIAL CONJUNCTIVITIS Clinical o cylindrical dandruff – pathognomonic features o In-office treatment with diluted Tea Tree Oil Management o Home regimen with diluted Tea Tree Shampoo lid hygiene CHALAZION  Painless, sterile lipogranulomatous inflammation of MG or glands of Zeiss  May develop from a hordeolum o May resolve spontaneously o Warm compress INCLUSION CONJUNCTIVITIS Management o Antibiotic-steroid ointment o Intralesional triamcinolone o Incision and curettage HORDEOLUM  Painful, red , tender nodular mass near the eyelid margin  Sexually-transmitted, through vaginal delivery, or shared cosmetics  Location  C. trachomatis o Extenal – Glands of Zeiss or hair follicles  Late onset of chronic conjunctivitis o Internal – Meibomian glands o Adults: > 2 weeks o May resolve spontaneously o Neonates: 5-14 days after birth o Warm compress o Adults : follicular conjunctivitis with scant Management o Antibiotic-steroid ointment Clinical mucopurulent discharge o Incision and drainage Features o Neonates: beefy red conjunctiva ± bleeding o Systemic antibiotics o Pre-auricular lymphadenopathy CONJUNCTIVITIS o Adults: Oral Azithromycin 1g PO single dose OR o Redness Topical erythromycin Management o Discharge (watery, mucoid, purulent) o Neonates: Systemic and topical erythromycin 5 Signs of Conjunctivitis o Conjunctival reaction o Treat parents and all sexual partners o Membrane/pseudomembrane ALLERGIC CONJUNCTIVITIS o Pre-auricular lymphadenopathy  IgE-mediated hypersensitivity reaction  Hallmark: itchiness  Recurrent episodes on the same month every year  Triggered by exposure to air-borne allergens  (+) personal and family history of atopy o Pale, boggy mucosa Clinical o Papillary conjunctivitis features o Ropy/ stringy mucoid discharge o Allergen avoidance o Cold compress Management o Artificial tear drops and gels o Topical corticosteroids o Anti-histamine and mast cell stabilizers VERNAL KERATOCONJUNCTIVITIS  Type I and IV hypersensitivity reaction  Young males  (+) personal and family history of atopy  Seasonal or year-round exacerbations  Limbal or Palpebral or Mixed type o Cobblestone papillae Clinical o Diffuse punctate corneal erosions, superior pannus, features ADENOVIRAL CONJUNCTIVITIS shield ulcer  Highly contagious, transmitted via direct contact and fomites o Environmental modification  Follicular, mucoid discharge, pre-auricular lymphadenopathy o Artificial tear drops and gels o Topical corticosteroids Management o Topical anti-histamine and mast cell stabilizers o Topical immunomodulatory agents (cyclosporine, tacrolimus) o Supratarsal corticosteroid injection Management o Frequent handwashing chismis buddies ☕| OLFU MED 2024|Page 2 of 5  GIANT PAPILLARY CONJUNCTIVITIS  Immune-mediated response to CTL, sutures, FB, ocular prosthesis Clinical o Hyperemia, discharge itchiness, large papillae presentation (>0.3mm) on the superior tarsal conjunctiva o Removal of offending agent Management o Short course of topical corticosteroid STEVENS-JOHNSON SYNDROME/ TOXIC EPIDERMAL NECROLYSIS  Acute inflammatory vesiculobullous reactions involving the skin and at least 2 mucous membranes  Nomenclature (based on the skin involvement) o SJS: 30%  Incidence increases with advancing age and diagnosis of HIV  Mortality rates of 1-5% for SJS and 25-30% for TEN VIRAL KERATITIS o Sudden onset of fever, malaise, arthralgia, URTI/LRTI o Skin eruptions (“target” lesions) Clinical o Maculopapular and bullous lesions presentation o Bullous lesions in the MM of the eyes, skin and genitalia with pseudo/membrane formation o Mucopurulent conjunctivitis and episcleritis, bullae and necrosis o Complications caused by cicatrization – conjunctival Ocular shrinkage, eyelid margin keratinization, trichiasis, tear findings PSEUDOMONAS KERATITIS FUNGAL KERATITIS deficiency, LSCD o More prone to infection due to lack of epithelium and DED Acute phase o Mainstay of therapy is aggressive lubrication (non- preserved AT) and prevention of infection o Topical corticosteroids o Lysis of symblephara Management o Early amnion grafting of ocular surface including the eyelid margins Chronic phase PERIPHERAL ULCERATIVE KERATITIS o Address dry eye, cicatrization, and LSCD  Appear in patients with systemic immune-mediated or rheumatic disease o Ocular surface reconstruction  Associations MUCUS MEMBRANE PEMPHIGOID Rheumatoid arthritis Polyarteritis nodosa  Idiopathic autoimmune bilateral chronic cicatrizing conjunctivitis Wegener granulomatosis Ulcerative colitis  Type II hypersensitivity reaction – autoantibodies directed against a cell SLE Relapsing polychondritis surface antigen in the basement membrane zone  Peripheral thinning of a sector of the cornea accompanied by vaso-  60 y/o at initial diagnosis occlusion of the adjacent limbal networks and inflammation of the  Chronic vesicobullous disease of the conjunctiva but may affect other MM adjacent conjunctiva (mouth, oropharynx, genitalia, anus)  Unilateral  Recurrent attacks of mild and nonspecific conjunctival inflammation  Adjacent sclera may be  Complications due to cicatrization involved o Mainstay of therapy: systemic  Systemic work-up immunosuppression o Goal: To prevent progression of corneal melting by o Methotrexate, azathioprine, cyclophosphamide improving lubrication, promoting re-epithelialization, and Management o Intravenous immunoglobulin, anti-TNFα, rituximab – suppressing local and systemic inflammation Treatment for unresponsive cases o Topical lubricants o Nonpreserved AT, corticosteroids, cyclosporine, o Topical and systemic immunosuppressants tacrolimus o Surgery MOOREN ULCER  Chronic, progressive, painful idiopathic ulceration of the peripheral corneal stroma and epithelium  “Overhanging lip”  Mounting evidence of autoimmunity KERATITIS  Precipitating Infectious o viral, bacterial, fungal, parasitic factors: Trauma, surgery, parasitic infection o Hypersensitivity reaction to microbial toxins or  Types Immune- manifestation of a systemic disease o I: unilateral, older population, slowly progressive mediated o Marginal keratitis, phlyctenulosis, interstitial keratitis, o II: bilateral, common in Africa (parasitemia), rapid progressive, peripheral ulcerative keratitis, Mooren ulcer unresponsive to treatment  Systemic work-up o Topical lubricants Treatment o Topical and systemic immunosuppressants o Surgery PINGUECULA  Bilateral, yellow-white elevated mass seen on the nasal limbus Risk o UV light exposure factors o Aging chismis buddies ☕| OLFU MED 2024|Page 3 of 5  o Usually left alone o Cogan-Reese/ Iris nevus o Lubricant drops  Multiple pigmented iris nodules (caused Management o Topical corticosteroids by contracting endothelial membranes) o Excision DEPOSITS AND DEGENERATIONS o Glaucoma PTERYGIUM  ~50% of patients  Fibrovascular wing-shaped growth of the limbal  Essential iris atrophy & Cogan-Reese > conjunctiva and superficial cornea Chandler o UV light exposure o Corneal edema o Wind, dust, irritants  5% NaCl drops  Management  Surgery – PKP/ EK o Lubricant drops Management o Glaucoma o Indications for excision o Progressive growth towards the visual axis  Topical IOP lowering drops o Irregular astigmatism  Surgery – trabeculectomy/ shunt/ valve o Persistent discomfort CONJUNCTIVAL TUMORS o Cosmetically unacceptable PAPILLOMA o Restricted ocular motility SESSILE o Caused by HPV 16, 18, or 33 o May represent a dysplastic or carcinomatous lesion o Found at the limbus and has a flat base o Resembles a strawberry PEDUNCULATED o Caused by HPV 6 or 11 EPITHELIAL INCLUSION CYST o Fleshy, exophytic mass with fibrovascular core  Bulbar or forniceal conjunctiva o Inferior fornix, tarsal, bulbar conjunctiva,  Asymptomatic semilunarfold  Risk factors o Pedunculated o Chronic inflammation  May be observed small o Trauma Management  Excision with cautery to the base o Surgery o Sessile  Management  Excision with adjuvant cryotherapy or MMC o May be left alone OCULAR SURFACE SQUAMOUS NEOPLASIA o Complete excision  Epithelial in origin ARCUS SENILIS  Risk Factors  Related to advancing age o Ultraviolet light exposure  Indicative of hyperlipoproteinemia if 40y/o; slight male preponderance  Thinning begins superonasally and spreads o Large feeder vessels circumferentially, rarely involving the inferior Management o Topical chemotherapy limbus o INF-α2b, MMC (with punctal occlusion), 5-FU  Epithelium is intact o Wide excision (2-4mm margin) biopsy with adjuvant  Management: lubrication, surgery Surgery o cryotherapy or MMC IRIDOCORNEAL ENDOTHELIAL SYNDROME o “No touch technique”  ICE syndrome PIGMENTED LESIONS  Unilateral MALIGNANT MELANOMA (Malignant)  Idiopathic Poor prognostic indicators (metastasis/ extension)  20-50 y/o, F>M o Caruncular, forniceal, or palpebral location  Involves an abnormal clone of endothelial cells that take on the o Invasion into deeper tissues ultrastructural characteristics of epithelial cells o Thickness >1.8 mm  Variants: o Involvement of the eyelid margin o Pagetoid or full-thickness intraepithelial spread o Chandler – most common o Lymphatic invasion  Pathology is confined to the inner o Mixed cell type corneal surface  corneal edema o Essential iris atrophy o Wide excision (4mm margin) biopsy with adjuvant  Abnormal endothelium spreads to the Management cryotherapy and MMC iris surface  contractile membranes o Topical chemotherapy as adjuvant therapy  Iris atrophy, correctopia, polycoria o Lifetime monitoring: 50% recurrence rate chismis buddies ☕| OLFU MED 2024|Page 4 of 5  LYMPHOID TUMORS LYMPHOID HYPERPLASIA (Benign) May represent a low-grade B-cell lymphoma Most patients are >40 years old Minimally elevated, salmon-colored subepithelial tumor wit h a pebbly appearance o Incision or excision biopsy with Management immunohistochemical studies o WOF development of systemic lymphoma LYMPHOMA (Malignant) Monoclonal proliferation of B lymphocytes Majority are monoclonal B-cell mucosa-associated lymphoid tissue (MALT) lymphomas Salmon-pink mobile conjunctival mass Unilateral, bilateral in 20% Most patients are older than 50 y/o or are immunosuppressed o Referral to Oncology – 31% develop systemic lymphoma o Incisional/ Excisional biopsy with immunohistochemical staining Management o Local radiothery for conjunctival lymphoma, Systemic chemotherapy for systemic lymphoma o Intralesional interferon-α2b o Intralesional or systemic Rituximab OCULAR SURFACE TRAUMA FOREIGN BODY  Industrial or household injury  Conjunctiva or cornea  Metallic, glass SUBCONJUNCTIVAL HEMORRHAGE  Collection of blood under the conjunctiva  Trauma, hypertension, Valsalva maneuver  Assess underlying structures if due to trauma Management o Reassurance – will resolve in 7-12 days o Systemic work-up if other sites of bleeding are identified CHEMICAL INJURY Alkali o Raise the pH of tissues and cause saponification of FA in cell membranes, and cell death  penetrate the corneal stroma, into the AC  tissue damage and intense inflammation Acid o Denature and precipitate proteins in tissues  act as barrier to penetration of the acid to the stroma and AC Clinical o Mild – conjunctival hyperemia, epithelial defect Presentation o Severe – limbal ischemia, cataract formation, high IOP, intense inflammation o Most important: immediate and copious irrigation with any nontoxic, unpolluted fluid at the site of the incident o Conjunctival sweeping o Goals of treatment: promote re-epithelialization and control of inflammation Management  Topical corticosteroid within the first 2 weeks (acute phase)  Frequent application of nonpreserved lubricant drops or gels  High dose vitamin C chismis buddies ☕| OLFU MED 2024|Page 5 of 5