Eyelid Lesions and Dry Eye Reasons

Transcription

1 1 Eyelid Lesions and Dry Eye Reasons Blair B Lonsberry, MS, OD, MEd., FAAO Diplomate, American Board of Optometry Clinic Director and Professor of Optometry Pacific University College of Optometry blonsberry@pacificu.edu 2 Agenda Benign vs. Malignant lesions Benign Eyelid Lesions Malignant Eyelid Lesions What is OSD or Ocular Surface Disease What does OSD include? Eyelid Lumps and Bumps 15-20% of periocular skin lesions are malignant Benign vs malignant: Benign lesions are: Well circumscribed and possibly multiple Slow growing Less inflamed Look stuck on instead of invasive and deep Which of the following is the most common benign eyelid lesion? Benign Eyelid Lesions Most common types of benign eyelid lesions include: Squamous papillomas (skin tags)-most common Hordeola/chalazia Epidermal inclusion cysts Seborrheic keratosis 1

2 Seborrheic keratosis Apocrine hidrocystoma Capillary hemangioma (common vascular lesion of childhood) Benign Eyelid Lesions: Squamous Papilloma Most common benign lesion of the eyelid Also known as fibroepithelial polyp or skin tag Single or multiple and commonly involve eyelid margin Benign Eyelid Lesions: Squamous Papilloma Flesh colored and maybe sessile (no stalk) or pedunculated (with a stalk) Differentials: seborrheic keratosis, verruca vulgaris and intradermal nevus Treatment is simple excision at the base of the lesion. Benign Eyelid Lesions: Seborrheic Keratosis Also known as senile verruca Common and may occur on the face, trunk and extremities Usually affect middle-aged and older adults, occurring singly or multiple, greasy, stuck on plaques Benign Eyelid Lesions: Seborrheic Keratosis Color varies from tan to brown and are not considered premalignant lesions Differentials include skin tags, nevus, verruca vulgaris, actinic keratosis and pigmented BCC Simple excision for biopsy or cosmesis or to prevent irritation. Benign Eyelid Lesions: Hordeola Acute purulent inflammation Internal occurs due to obstruction of MG External (stye) from infection of the follicle of a cilium and the adjacent glands of Zeiss or Moll Painful edema and erythema, 2

3 11 Benign Eyelid Lesions: Hordeola Typically caused by Staph and often associated with blepharitis Treatment includes hot compresses, topical antibiotics possibly systemic antibiotics Treat concurrent blepharitis Benign Eyelid Lesions: Chalazia Focal inflammatory lesion resulting from obstruction of a meibomian or Zeis gland Results in a chronic lipogranulomatous inflammation Benign Eyelid Lesions: Chalazia May drain spontaneously or persist as a chronic nodule Recurrent lesions need to exclude a sebaceous gland carcinoma Treatment varies from hot compresses/massage, intralesional steroid injection or surgical drainage. Benign Eyelid Lesions: Epidermal Inclusion Cyst } Appear as slow-growing, round, firm lesions of dermis or subcutaneous tissue } Eyelid lesions are usually solitary, mobile and less than 1 cm } Maybe congenital or may arise from trauma Benign Eyelid Lesions: Epidermal Inclusion Cyst May become infected or may rupture Differentials include dermoid cyst, pillar cyst or neurofibroma Treatment is complete excision to prevent recurrence. Benign Eyelid Lesions: Eccrine Hidrocystoma Sudoriferous or sweat gland cysts Solitary or multiple, small nodules on the eyelids Overlying skin is smooth and shiny and the cyst usually is translucent and fluid filled 3

4 translucent and fluid filled Benign Eyelid Lesions: Eccrine Hidrocystoma Tend to increase in size in hot, humid weather Differential are apocrine hidrocystoma and epidermal inclusion cyst Treatment is complete excision Benign Eyelid Lesions: Apocrine Hidrocystoma } Also known as cystadenoma } Usually appears as a solitary, translucent cyst on the face and sometimes eyelid margin } Usually small and filled with clear or milky fluid with a shiny smooth overlying skin Benign Eyelid Lesions: Apocrine Hidrocystoma Do not increase in size in warm weather Differential is the eccrine and cystic BCC Treatment is complete excision Benign Eyelid Lesions: Capillary Hemangioma } Common vascular lesion in childhood (1-2% of infants) } Females 3:2 } Periorbital may appear as a superficial cutaneous lesion, subcutaneous, deep orbital or combination } 1/3 visible at birth, remainder manifest by 6 months } 75% regress to some extent by 7 years Benign Eyelid Lesions: Capillary Hemangioma } Classic superficial lesion-strawberry lesion, appears as a red, raised, nodular mass which blanches with pressure } Most common ocular complication is amblyopia } Because regression is common, treatment is reserved for patients who have specific ocular, dermatologic or systemic indications for intervention. Benign Eyelid Lesions: Pyogenic Granuloma Most common acquired vascular lesion to involve the eyelids Usually occurs after trauma or surgery as a fast growing, fleshy, red-to-pink mass which readily bleeds with minor 4

5 Usually occurs after trauma or surgery as a fast growing, fleshy, red-to-pink mass which readily bleeds with minor contact Benign Eyelid Lesions: Pyogenic Granuloma Differential include Kaposi s sarcoma Treatment can include use of steroid to reduce the inflammation or surgical excision at the base of the lesion. Benign Eyelid Lesions: Xanthelasma Typically occurs in middle-aged and older adults as soft, yellow plaques on the medial aspect of the eyelids Hyperlipidemia is reported to occur in approx 50% of patients therefore screening recommended Benign Eyelid Lesions: Xanthelasma Composed of foamy, lipid-laden xanthoma cells clustered around blood vessels and adnexal tissue within the superficial dermis Treatment includes surgical excision, CO2 ablation and topical trichloroacetic acid. Recurrence is common. Benign Eyelid Lesions: Molluscum Contagiosum Common viral skin disease caused by a large DNA pox virus Infection usually from direct contact in children and sexually transmitted in adults Typical lesion appears as a raised, shiny, white-to-pink nodule with a central umbilication filled with cheesy material Benign Eyelid Lesions: Molluscum Contagiosum } Eyelid lesions may produce a follicular conjunctival reaction } Patients with AIDS may have a disseminated presentation (30-40 each eyelid or a confluent mass) } Usually spontaneously resolves 3-12 months but maybe treated to prevent spread by excision, incision and curettage, cryosurgery and electrodesiccation. Benign Eyelid Lesions: Verruca Vulgaris Common cutaneous wart caused by the epidermal infection of the human papillomavirus 5

6 Common cutaneous wart caused by the epidermal infection of the human papillomavirus More common in children and young adults and may occur anywhere on the skin Lesions appear elevated with an irregular, hyperkeratotic papillomatous surface Benign Eyelid Lesions: Verruca Vulgaris Lesions along lid margin may cause papillary conjunctivitis Tend to be self limiting but if treatment required cryoptherapy or surgical excision. Lid Nevi } Lid nevi: } congenital or acquired } occur in the anterior lamella of the eyelid and can be visualized at the eyelid margin. } The congenital eyelid nevus is a special category with implications for malignant transformation. } With time, slow increased pigmentation and slight enlargement can occur. } An acquired nevus generally becomes apparent between the ages of 5 and 10 years as a small, flat, lightly pigmented lesion Congenital Nevus } The nevus is generally well circumscribed and not associated with ulceration. } The congenital nevus of the eyelids may present as a "kissing nevus" in which the melanocytes are present symmetrically on the upper and lower eyelids. } Presumably this nevus was present prior to eyelid separation Congenital Nevus Most nevi of the skin are not considered to be at increased risk of malignancy. 6

7 risk of malignancy. However, the large congenital melanocytic nevus appears to have an increased risk of malignant transformation of 4.6% during a 30 year period Acquired Lid Nevi Acquired nevi are classified as: junctional (involving the basal epidermis/dermis junction), typically flat in appearance intradermal (involving only the dermis), tend to be dome shaped or pedunculated compound (involving both dermis and epidermis) tend to be dome shaped Pre-Malignant Eyelid Lesions: Keratoacanthoma Appears as a solitary, rapidly growing nodule on sun exposed areas of middle-aged and older individuals Nodule is usually umbilicated with a distinctive crater filled with keratin Lesion develops over weeks and undergoes spontaneous involution within 6 mo to leave an atrophic scar Pre-Malignant Eyelid Lesions: Keratoacanthoma Lesion on the eyelids may produce mechanical problems such as ectropion or ptosis. Differential SCC, BCC, verruca vulgaris and molluscum Many pathologists consider it a type of low grade SCC Complete excision is recommended as there are invasive variants Pre-Malignant Eyelid Lesions: Actinic Keratosis Also known as solar or senile keratosis Most common pre-malignant skin lesion Develops on sun-exposed areas and commonly affect the face, hands and scalp (less commonly the eyelids) Predominately white males 7

8 Predominately white males Pre-Malignant Eyelid Lesions: Actinic Keratosis Appear as multiple, flat-topped papules with an adherent white scale. Development of SCC in untreated lesions as high as 20% Management is surgical excision or cryotherapy (following biopsy) Pre-Malignant Eyelid Lesions: Bowen s Disease Marker for development of other skin cancers and internal malignancies Sun exposed skin as a scaly, crusty, well demarcated keratotic plaque Many similar features of SCC and actinic Pre-Malignant Eyelid Lesions: Bowen s Disease Difference from actinic is the epithelium completely replaced with full thickness atypia Treatment is complete excision with possible use of 5-FU or Imiquimod 5% cream Malignant Eyelid Lesions: Basal Cell Carcinoma (BCC) Most common malignant lesion of the lids (85-90% of all malignant epi eyelid tumors) 50-60% of BCC affect the lower lid followed by medial canthus 25-30% and upper lid 15% Malignant Eyelid Lesions: Basal Cell Carcinoma (BCC) Etiology is linked to excessive UV exposure in fair-skinned, ionizing radiation, arsenic exposure and scars Metastases is rare but local invasion is common and can be very destructive Malignant Eyelid Lesions: Basal Cell Carcinoma } Diagnosis is initially made from its clinical appearance, especially with the noduloulcerative type with its raised pearly borders and central ulcerated crater } categorized into two basic types: noduloulcerative and morpheaform 8

9 } categorized into two basic types: noduloulcerative and morpheaform } The morpheaform variant is typically diffuse, relatively flat with indistinct borders. This variant is more aggressive and can be invasive despite showing less obvious features Malignant Eyelid Lesions: Basal Cell Carcinoma Definitive diagnosis made on histopathological examination of biopsy specimens loss of adjacent cilia is strongly suggestive of malignancy and occurs commonly with basal cell carcinoma of the eyelid Surgery is generally accepted as treatment of choice Mohs surgery technique Malignant Eyelid Lesions: Squamous Cell Carcinoma (SCC) Much less common than BCC on the eyelid but has much higher potential for metastatic spread Typically affects elderly, fair-skinned and usually found on the lower lid Malignant Eyelid Lesions: Squamous Cell Carcinoma (SCC) Environmental and intrinsic factors initiate cell growth Many SCC arise from actinic lesions Malignant Eyelid Lesions: Squamous Cell Carcinoma (SCC) Presents as a erythematous, indurated, hyperkeratotic plaque or nodule with irregular margins Lesions have a high tendency towards ulceration and tend to affect lid margin and medial canthus Malignant Eyelid Lesions: Squamous Cell Carcinoma (SCC) Diagnosis requires biopsy Surgical excision is recommended Mohs technique 9

10 Mohs technique Malignant Eyelid Lesions: Sebaceous Gland Carcinoma Highly malignant neoplasm that arises from the meibomian glands, Zeis and the sebaceous glands of the caruncle and eyebrow Aggressive tumor with a high recurrence rate, significant metastatic potential and notable mortality rate rates of misdiagnosis have been reported as high as 50% Malignant Eyelid Lesions: Sebaceous Gland Carcinoma Relatively rare, 1/3 most common eyelid malignancy Uncommon in the Caucasian population and represents only 3% of eyelid malignancies, most common eyelid malignancy in Asian Indian population, where it represents approximately 40% or more of eyelid malignancies Malignant Eyelid Lesions: Sebaceous Gland Carcinoma Upper lid origin in about 2/3 of all cases Typically affects older individuals, women more so than men has also been reported in younger individuals who are immunosuppressed or who have received radiation treatment Malignant Eyelid Lesions: Sebaceous Gland Carcinoma Upper lid origin in about 2/3 of all cases Presents as a firm, yellow nodule that resembles a chalazion. May mimic: chronic blepharoconjunctivitis, meibomianitis or chalazion that does not respond to standard therapies Malignant Eyelid Lesions: Sebaceous Gland Carcinoma Diagnosis is by biopsy Treatment is surgical excision with microscopic monitoring of the margins 10

11 Treatment is surgical excision with microscopic monitoring of the margins Malignant Eyelid Lesions: Malignant Melanoma MM of the eyelid accounts for about 1% of all eyelid malignancies Incidence been increasing and it causes about 2/3 of all tumor related deaths from cutaneous cancers Incidence increases with age Malignant Eyelid Lesions: Malignant Melanoma Risk factors include congenital and dysplastic nevi, changing cutaneous moles, excessive sun exposure and sun sensitivity, family history, age greater than 20 and white. History of severe sunburns rather than cumulative actinic exposure thought to be a major risk factor Malignant Eyelid Lesions: Malignant Melanoma Flat lesion with irregular borders and variable pigmentation typically occurring in sun exposed areas Confirmed diagnosis by biopsy Malignant Eyelid Lesions: Malignant Melanoma Prognosis and metastatic potential are linked to the depth of invasion and thickness of the tumor Treatment is wide surgical excision confirmed with histological monitoring What s Up with OSD? OSD presents a significant challenge to physicians Differentiation Diagnosis Treatment OSDs are Difficult to Tell Apart: Overlapping Signs/ Symptoms Case 11

12 27 year old pharmacy student presents to the clinic on emergent basis complains about red/painful eyes for the past 2 days started OD then transferred to OS reports a watery discharge, no itching, and is not a contact lens wearer reports that others in his class have had a similar red eye no seasonal, food or drug allergies has taken Visine 4-5 times/day since eyes became red but hasn t helped much Conjunctivitis Bacterial Conjunctivitis Signs and Symptoms of Bacterial Conjunctivitis Clinical presentation uni- / bi-lateral Signs: Bulbar conjunctival injection Purulent discharge Morning matting of eyelashes Chemosis 2 Symptoms: Photophobia Blurred vision Tearing 63 Treatment/Management Topical antibiotic therapy Vigamox TID for 7-10 days Moxeza BID for 7 days Category C 12

13 Category C Zymaxid q 2 hours for Day 1, then BID-QID Days 2-7 Category C Azasite BID for 2 days then qd for next 7-10 days Category B Besivance TID for 7-10 days Category C Tobramycin/Gentamicin QID for 7-10 days Category B Polytrim q3hrs (max 6x/day) for 7-10 days approved to age of 2 months Category C Allergic Conjunctivitis Prevalence of Allergic Conjunctivitis Allergies affect as many as 40 to 50 million Americans 66 1 Incidence and prevalence of allergic conjunctivitis has been rising over the last 40 years Signs and Symptoms of Allergic Conjunctivitis Clinical presentation bilateral 2 Signs: Conjunctival edema Conjunctival hyperemia Chemosis Lid edema Watery discharge Symptoms: Itching Burning Photophobia Foreign body sensation Blurred vision 13

14 Blurred vision Mast Cell Cascade Treatment Ocular allergy sufferers need; fast relief of signs and symptoms, long-lasting therapeutic effects, comfortable and safe topical drugs, convenient treatment regimen Therapeutic focus is mostly confined to the suppression of mast cells, their degranulation and the effects of histamine and other mast-cell derived mediators. Treatment of Ocular Allergy Medications: Topical OTC drops Oral antihistamines (prescription and OTC) Topical NSAID drops Topical antihistamines Topical mast cell stabilizers Topical steroid drops Topical dual-action drugs (antihistamine/mast cell stabilizers) Viral Conjunctivitis Most common infectious keratitis presenting on emergent basis 62% caused by adenovirus Two major types: Pharyngoconjunctival fever Epidemic keratoconjunctivitis Viral Conjunctivitis PCF: history of recent/current upper respiratory infection EKC: highly contagious with a history of coming in contact with someone having a red eye. 14

15 EKC: highly contagious with a history of coming in contact with someone having a red eye. Adenovirus 8 common variant leading to rule of 8 s First 8 days red eye with fine SPK Next 8 days deeper focal epithelial lesions Following 8 potential development of infiltrates Resolution RPS AdenoPlus available to use for adenoviral confirmation. Marketed by NiCox AdenoPlus Have you heard about this? Interpreting the Results NEGATIVE RESULT Only a BLUE line appears in the control zone. A negative result is indicative of an absence of Adenovirus Antigens. POSITIVE RESULT The presence of both a BLUE line in the control zone and a RED line in the result zone indicates a positive result. Even if the RED line is faint in color, incomplete over the width of the test strip, or uneven in color, it must be interpreted as positive. A positive result indicates the presence of Adenovirus antigens. 75 Interpreting the results Invalid Result If a BLUE line does not appear, the test may be invalid. Reimmerse the absorbent tip into the buffer vial for an additional 10 seconds. If a BLUE line still does not appear after 10 minutes, the test must be discarded and the subject retested by 15

16 If a BLUE line still does not appear after 10 minutes, the test must be discarded and the subject retested by resampling the eye using a new AdenoPlus test kit 76 JOURNEY OF THE RED EYE Viral Conjunctivitis: Signs and Symptoms Gritty sensation Watery discharge Sticky in mornings Follicular response Chemosis Injection SPK Infiltrates possible Positive lymph nodes n Pseudomembranes in severe cases n Subconjunctival hemes Management Consider the use of anti-inflammatory treatment to relieve patient symptoms and improve comfort FML QID OU Lotemax QID OU (there is a new Lotemax gel that has a higher viscosity and increases contact time) EKC patients are typically very uncomfortable and would benefit from anti-inflammatory treatment especially if infiltrates or pseudomembrane present Management Betadine (Melton-Thomas Protocol): 16

17 Betadine (Melton-Thomas Protocol): Proparacaine 4-5 drops of Betadine 5% Get patient to close eye and gently roll them around After one minute, lavage the eye Lotemax 4 times a day for 4 days Alternative: Betadine swabsticks. 5% Betadine solution only comes in 30 ml bottles cost $ Case of 200 Betadine swabsticks apprx. 45 dollars. Management Antivirals used in HSV keratitis are ineffective in treatment of viral conjunctivitis New Update: in conversation with several colleagues, Zirgan 4-5 times/day has shown significant improvement in patients over a 7-10 time period. Important to stress limited contact with others, frequent hand washing, not sharing of towels, etc. Dry Eye Prevalence of Dry Eye Disease (DED) Prevalence estimated from 7.4% to 33.7% depending on study quoted, how DED is defined and patient population studied Prevalence in Canada is reported at approximately 25% Affects women more than men Increases as patient population ages 14.4% of patients self-report history of dry eye 7.8% of women aged 45 to 84 were clinically diagnosed with DED (Beaver Dam Study) Affect on quality of life (QOL): Mild DED = psoriasis Moderate DED = moderate angina Severe DED = class III/IV angina or diabling hip fracture 17

18 Case 55 yr white female complains of fluctuating vision Worse at near Spends 8-10 hours/day on the computer Medical Hx: Hypertension for 10 years Joint pain Medications: HCTZ for HTN Celebrex for her joint pain Exam Data VA (corrected): OD: 20/25, OS: 20/25 PERRL EOM s: FROM CVF: FTFC SLE: TBUT 5 sec OD, OS Positive NaFl staining and Lissamine green staining of conj and cornea Decreased tear prism Additional Testing/Questions Schirmer: < 5 mm of wetting in 5 minutes OD, OS RF and ANA: normal for patients age SS-A: 2.0 (normal < 1.0), SS-B: 1.9 (normal <1.0) Additional symptoms reported: Patient experiences dry mouth and taking Salagen Diagnosis: Sjogren s Syndrome 87 Differential Diagnosis of Dry Eye 18

19 Signs and Symptoms of Dry Eye Signs: Ocular Surface Damage Corneal Staining (Fluorescein and/or Rose Bengal) Conjunctival Staining (Lissamine Green ) Decreased Tear Quantity Schirmer Score Phenol Red Thread Test Tear Meniscus Height Decreased Tear Quality Tear Break Up Time (TBUT) Tear Osmolarity Symptoms: Grittiness Burning Irritation Stringy discharge Blurring of vision Ocular Surface Disease Index (OSDI) Treatment We initiated: Omega-3 supplements (3-4 grams per day) Recommended warm compresses and lid washes qhs Testosterone cream 3% applied to upper lid bid Patient had significant improvement in symptoms with the use of the topical testosterone cream. However, she was still symptomatic at the end of the day and she still had significant staining on her cornea and conjunctiva Initiated FML tid for 1 month, restasis bid after 2 weeks 2 months later patient reported further improvement in her symptoms 19

20 her symptoms No conjunctival staining was noted and only slight SPK Schirmer values improved to OD: 9 mm, OS: 10 mm Transdermal Testosterone Cream Recent studies have suggested that androgen deficiency may be the main cause of the meibomian gland dysfunction, tear-film instability and evaporative dry eye seen in Sjogren patients Transdermal testosterone promotes increased tear production and meibomian gland secretion, thereby reducing dry eye symptoms (Dr. Charles Connor). argentis and Allergan have conducted trials to see if topical androgens are effective in treating dry eye SJOGREN S SYNDROME: OLD/NEW CLASSIFICATION Old: 1 o Sjogrens: occurs when sicca complex manifests by itself no systemic disease present 2 o Sjogrens: occurs in association with collagen vascular disease such as RA and SLE significant ocular/systemic manifestations New: The diagnosis of SS should be given to all who fulfill the new criteria while also diagnosing any concurrent organspecific or multiorgan autoimmune diseases, without distinguishing as primary or secondary. Diagnosis: New Criteria Sjogren s International Collaborative Clinical Alliance (SICCA) was funded by the National Institutes of Health to develop new classification criteria for SS New diagnostic criteria requires at least 2 of the following 3: 1) positive serum anti-ssa and/or anti-ssb or (positive rheumatoid factor and antinuclear antibody titer >1:320), 20

21 rheumatoid factor and antinuclear antibody titer >1:320), 2) ocular staining score >3, or 3) presence of focal lymphocytic sialadenitis with a focus score >1 focus/4 mm2 in labial salivary gland biopsy samples Ocular Surface Score (OSS) The ocular surface score (OSS) is the sum of: 0-6 score for fluorescein staining of the cornea and 0-3 score for lissamine green staining of both the nasal and temporal bulbar conjunctiva, yielding a total score ranging from Antibodies to SS-A and SS-B Sjogren s syndrome A and B Typically tested by ELISA and immunoblot Associated Conditions: Uncommon in the normal population and in patients with rheumatic diseases other than Sjogren s syndrome and SLE Present in 75% of patients with primart Sjogren s but only 10-15% of patients with RA and secondary Sjogren s syndrome Antibodies to SS-A and SS-B Indications: Should be measured in patients with a clinical suspicion of Sjogren s or SLE Interpretation: Presence of AB s is a strong argument for the diagnosis of Sjogren s Syndrome in a patient with sicca syndrome Sjo: new diagnostic test for Sjogrens SP-1 (salivary gland protein-1), CA-6 (carbonic anhydrase-6) and PSP (parotid secretory protein). Traditional tests use ANA, SS-A and SS-B and RF antibodies which have significant limitations of sensitivity and/or specificity and are associated with later-stage disease. 21

22 and/or specificity and are associated with later-stage disease. During studies, these novel antibodies were found in 45% of patients meeting the criteria for Sjögren s Syndrome who lacked the traditional antibodies for SS-A and SS-B. 97 Dry Eye and Lid Disease? It is estimated that 67-75% of patients who have dry eye have some form of lid disease it is often the most overlooked cause for dry eye symptoms Important to address the lids in any treatment plans for patients with dry eye Treatment/Management Case 20 year old male presents with a red painful eye complains about red/painful right eye Started that morning when he woke up reports a watery discharge, no itching, and is not a contact lens wearer SLE: See attached image with NaFl stain 100 Herpes Simplex Keratitis: Clinical Features Characterized by primary outbreak and subsequent reactivation Primary outbreak is typically mild or subclinical After primary infection, the virus becomes latent in the trigeminal ganglion or cornea Stress, UV radiation, and hormonal changes can reactivate the virus Lesions are common in the immunocompromised (i.e. recent organ transplant or HIV patients) 22

23 101 Dendritic Ulcers Herpes Simplex Keratitis Topical: Viroptic (trifluridine) q 2h until epi healed then taper down for days. Viroptic is toxic to the cornea. Zirgan (ganciclovir) available, use 5 times a day until epi healed then 3 times for a week Oral acyclovir (2 g/day) has been reported to be as effective as topical antivirals without the toxicity Valtrex (valcyclovir)) 500 mg TID for 7-10 days Famvir (famciclovir) 250 mg TID for 7-10 days If stomal keratitis present, after epi defect has healed, add Pred Forte QID until inflammation reduced and then slowly taper Prophylaxis?? Prophylaxis of 400 mg acyclovir BID vs placebo for 1 year resulted in a lower recurrence in the treatment arm (19% vs 32%) Valtrex 500 mg qd was found to be equivalent to acyclovir BID Pitfalls to Prophylaxis: Reduction of recurrence does not persist once drug stopped Resistance???? van Velzen, et. al., (2013) demonstrated that long-term ACV prophylaxis predisposes to ACV-refractory disease due to the emergence of corneal ACVR HSV

24 Herpes Zoster Ophthalmicus Herpes Zoster Presents with: pain and tingling in region of skin supplied by V few days before lesions, malaise and fever, papulomacular then pustular rash, mucopurulent conjunctivitis, uveitis, glaucoma, episcleritis, keratitis, and retinitis can all occur. neurological complications include cranial nerve palsies and optic neuritis. Herpes Zoster Associated factors include increasing age, immune deficiency and stress. Management includes: oral antivirals (800mg acyclovir 5x/day, valacyclovir (Valtrex) 1g TID, famciclovir (Famvir) 500 mg TID effectiveness of therapy is best started within 72 hours oral steroids, and management of pain (tricyclic antidepressants, gabapentin). If ocular complications, consider topical steroids (Pred Forte QID) Corneal Ulcers Infective bacterial and fungal corneal lesions cause severe pain and loss of vision Signs and Symptoms: Pain, photophobia, tearing 24

25 Pain, photophobia, tearing Mucopurulent discharge with generalized conjunctival injection Decreased VA (esp if on visual axis) Possible AC reaction and hypopyon Dense infiltrate Satellite lesions around main lesion may indicate fungal infection Sterile vs Infectious Infiltrates Peripheral (Sterile) Corneal Ulcer Infectious Corneal Ulcer Corneal Ulcers Infective bacterial and fungal corneal lesions cause severe pain and loss of vision S and S: Pain, photophobia, tearing Mucopurulent discharge with generalized conjunctival injection Decreased VA (esp if on visual axis) Possible AC reaction and hypopyon Dense infiltrate Satellite lesions around main lesion may indicate fungal infection Associated Factors Contact lens wear, especially soft and extended wear lens Recent history of corneal trauma Topical steroid use History of exposure to vegetative matter (fungal etiology)

26 Tetracyclines: Acne Rosacea Acne rosacea: affects females>males after 30 with peak incidence 4-7th decade of Celtic/Northern European descent. Males more disfigured. 4 subtypes with classic signs of flushing, papules or pustules usually in crops, telangiectasia. secondary ocular complications (85% of patients) and often precede other skin manifestations include erythema, itching and burning. Mainstay oral Tx is Oracea (40 mg in morning) or tetracycline 500 mg po BID or doxycycline 100 mg po BID or minocycline 100 mg po BID for 4-12 wks. NOTE: Oracea is subantimicrobial therapy Acne Rosacea Treatments Blepharitis Current Prevalence of Blepharitis Although blepharitis may be a frequently overlooked condition in the United States, ophthalmologists and optometrists report that blepharitis is commonly seen in 37% and 47% of their patients, respectively 1,2 Differential Diagnosis of Blepharitis Signs and Symptoms of Blepharitis Symptoms Burning Irritation Foreign body sensation (FBS) Itching Tired eyes

27 Tired eyes Photophobia Contact lens intolerance Most Common Clinical Presentations Reported by Practitioners Pathophysiology of Blepharitis Inflammatory condition of the anterior lid margin and eyelashes bacterial exotoxins and/or delayed hypersensitivity to antigens Tends to be staphylococcal and/or seborrheic in nature Staphylococcal infection can be purulent or ulcerative and often causes angular blepharitis Pathophysiology of MGD (previously Posterior Blepharitis) Altered meibomian gland (MG) secretions Thickened secretion (rich in keratin) Cicatricial obstructive disease with duct exposure and retroplacement of orifices Epithelial hyperplasia/ hyperkeratinization Cystic dilatation of ducts and acini Atopy, psoriasis Inflammation Hyperemia of the lid margin Lid swelling Bacterial Secretion of toxins, enzymes (lipases, esterases) Hypersecretory Meibomian seborrhea Acne rosacea Physicochemical Differences in Normal vs MGD Patients 27

28 Treatment Goals for Blepharitis Long-term control of underlying pathophysiology: bacteria, inflammation and meibomian gland secretions Improvement of signs and symptoms Improve health of tear film lipid layer Reduce risk of fluctuating visual acuity Reduce possible risk of progression to other conditions such as dry eye disease or chalazion Improve outcomes in surgical procedures and comfortable contact lens wear time Treatment/Management Lid hygiene Oral doxycycline 50 mg bid for 7-14 days then qd for next 6-8 weeks Topical azythromycin (AzaSite) 1 gtt BID for 2 days then qhs for next 28 days Omega 3 supplements 28