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192 Cards in this Set
- Front
- Back
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Coloboma
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Absence of portion of eyelid
Usually unilateral/upper eyelid/medial to middle third Can occur in eye - lower third Significant corneal staining w/ corneal exposure - which is common if 30% or more missing Cornea could become keratinized Treatment: AT or ung for ALL/mild cases For more severe (corneal infection risk), also use antibiotic ung: bacitracin BID-QID, polysporin(polymixin B and bacitracin zinc) IO at night or BID-QID, erythromycin(macrolide) BID-QID, gentamicin(aminoglycoside) BID-QID...or viscous antiobiotic gtt: azasite(macrolide) 1 gt BID for two days and 1 gt QD for five days, besivance(fluoroquinolone) 1 gt TID for seven days Lid replacement if 75% missing (w/in 48 hrs of birth - if less severe wait 3-6 months b/c anesthesia |
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Distichiasis
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Double row of lashes that originate at Meibomian orifices
Smaller, shorter, more delicate, misdirected usually Possible/likely corneal staining Usually autosomal dominant if inherited Treatment: lubricants of cornea, epilation or electorysis of lashes, cryotherapy or surgical removal if severe, antibiotic prophylactically(same as coloboma) |
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Epicanthal Folds
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Redundant fold from upper to lower lid in medial canthus
Usually bilateral Asian/Caucasian common Seen in patients with flat bridges, may mimic esotropia - don't misdiagnose NO treatment |
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Ptosis
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Drooping lid - 2mm or more of superior corna covered
IF - measure at widest point, in normal patients, upper lid 1mm below superior limbus LC - margin of lid up to the crease(where levator inserts); Epiblepharon = extra lid crease MPD/MRD - pupillary reflex to lid margin Levator Excursion - how well levator works; have patient look down as far as they can, then up as far as they can - measure in mm |
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Aquired Ptosis (Neurogenic)
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Third Nerve Palsy - most commonly vascular in origin, could be hypertension
Eye could be "down and out" b/c same blood supply to superior/medial rectus and inferior oblique (diplopia) Usually resolves w/in 90 days if benign b/c recanalization Complete ptosis - eye shut Neurologic Emergency if pupil involved(dilated) - intracranial aneurysm If pupil not involved, follow patient daily to make sure Horner's Syndrome - sympathetic interruption - ipsilater miosis, anhydrosis LC the same b/c aponeurosis not affected Chest X-ray if patient is smoker - tumor could compress nerve If congenital, often associated with heterochromia |
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Aquired Ptosis (Mechanical)
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Excess weight of lid - swelling, tumors, etc...
Conjunctival Scarring Dermatochalasis - "pseudoptosis," loose lid folds, older patients, loss of elastin, effects of gravity, weak connective tissue...COMMON |
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Aquired Ptosis (Myogenic)
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Aponeurotic - levater insertion pulled back or lost grip, increased LC, MOST COMMON TYPE OF AGE-RELATED PTOSIS
Myasthenia Gravis - loss of ACh receptors, ptosis varies throughout day and may alternate b/w right and left, intermittent VARIABLE diplopia Ice Pack Test - over affected eye for 5-7 mins. and retest, delays AChe |
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Aquired Ptosis Treatment
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Treat underlying condition
Ptosis crutch - attaches to glasses Surgery Phenylephrine - helpful for minor Horner's |
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Congenital Ptosis
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Developmental anomaly of levator
Have to use frontalis to look up "Lid Lag" - in downgaze b/c levator won't stretch either (lack of tissue) Ptotic eye in straight gaze will be higher in downgaze Could develop amblyopia if affected certain gaze Treatment: delay surgery till 4 months unless severe, protect cornea |
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Floppy Eyelid Syndrome (FES)
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Soft, rubbery tarsal plate - loss of elastin
Easily everted during sleep - superior palpebral papillary response and possible PEK Primarily obese males Treatment: bacitracin BID-QID, gentamicin(aminoglycoside) TID, tape lids, eye shield, follow 3-7 days till stable, surgery has variable results |
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Blepharospasm
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Involuntary contractions of orbicular oculi
Bilateral Can be functionally blind Treatment: underlying disease, botox, sugery to remove orbicularis oculi |
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Blepharoclonus
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Seen in mentally retarded/schizophrenic patients and/or with barbiturate abuse
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Lid Myokymia
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Common
Spontaneous fascicular tremor Caused by any type of disease, stress, fatigue Treatmeant: reassuring patient, antihistamines (increase time between APs), quinine - found in tonic water, same as antihistamine |
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Ectropian
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Outward turning of eyelid
Etiology: Involutional/Age-related (senile), CNVII palsy, cicatricial, mechanical - weight (dermoid), allergic, congenital C/O: tearing, irritation, FBS, may see PEK, injection, kertinization Treatment: lubricants, antibiotic ung if area at risk for infection, F/U 1-2 weeks, tape lids, surgery |
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Entropian
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Inward turning
Etiology: senile, cicatricial, spastic, congenital C/O: tearing, irritation, red eyes, may see PEK, injection Treatment: antibiotic ung, tape lids, superglue lids, epilate lashes if trichiasis is mild, surgery, F/U as needed |
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Trichiasis
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Misdirected lashes
C/O: FBS, irritation, tearing, PEK, injection Etiology: chronic bleph, entropian, distichiasis, idiopathic Treatment: removing lashes, antibiotic ung if PEK present |
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Lagophthalmos
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Incomplete lid closure - opens normally
Etiology: orbital/proptic, nocturnal, mechanical, paralytic C/O: FBS, morning irritation, dry eyes, PEK in exposed area - middle/lower 1/3 of cornea Treatment: lubricating ung qhs, antibiotic PRN, soft CL as bandage, tape lids, tarsorrhapy |
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Cyst of Moll
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Moll glands are modified sweat glands at eyelash margins (each follicle)
Excise, benign, called sudoriferous cyst |
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Cyst of Zeis
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Zeis glands are sebaceous glands at eyelash margins (each follicle)
Excise, benign, more opaque |
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Sebaceous Cyst
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Yellowish white, usually multiple lumps on skin
Have central punctum which looks like blackhead Multiple lesions known as milia Excise, benign |
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Xanthelasma
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Cholesterol deposits and other lipids w/in skin
Investigate for hyperlipidemia in young patients Tend to recur, benign |
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Molluscum Contangiosum
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Viral wart - frequent in healthy children or immunocompromised adults (worry about HIV)
Small lesions w/umbilicated centers, see cheesy core that often spontaneously drains (clean with alcohol) May be multiple Can puncture and express in office - clean after with alcohol Resolves w/o scars Rule out Basal Cell Carcinoma |
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Papilloma
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Verrucae Papillomata - benign overgrowth of epithelial cells
Verruca Vulgaris - pedunculated Verruca Plana - flat Keratin may build up and cause cutaneous horn Rough surface - cauliflower-like Many have viral etiology and are linked w/various subtypes of HPV |
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Keratoacanthoma
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Rapidly growing epithelial lesion w/central core of keratin
Grows vigorously over 3 months and then spontaneously involutes Excise if no resolution - small portion may progress to squamous cell carcinoma |
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Hemangioma
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Local/generalized mass with vascular changes from capillary system
May involute or can be surgically excised if cosmesis or visual function impaired Worse in children while crying Blanch with pressure - distinguishes from Sturge-Weber syndrome 40% involute by age 4, 80% by age 8 |
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Actinic Keratosis
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Yellowish rough crusty lesions that bleed easily
PRE-MALIGNANT Lesion which may lead to squamous cell carcinoma From overexposure to sun Excise promptly Appears similar to sebaceous keratosis which is benign but looks greasier |
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Squamous Cell Carcinoma
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Deeply ulcerated lesion with elevated edges
May metastisize to lymph nodes VERY dangerous Destroys lashes, lid tissue Radical excision Second most common form of skin cancer after basal |
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Basal Cell Carcinoma
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Most common malignancy of eyelid
Mostly 40-79 years old Highest prevalence in Australia Uncommon in dark-skinned populations Assiociated with UV exposure More prevalent in lower lid "Classic" type - pearly borders, ulcerated center, variably pigmented "Morpheic" type - highly invasive to local tissue DOES NOT METASTASIZE Photodocument, excise, Mohs procedure, 45% of developing again w/in 5 years |
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Nevus
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Dermal - flat/raised, rarely progress
Junctional - flat, may progress to malignant melanoma Hard to distinguish visually - both have distint borders and pigmentation varies |
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Malignant Melanoma
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From pre-existing nevi or de novo
Uncommon but most deadly Pigmentation variability w/in lesion causes suspicion |
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Kaposi's Sarcoma
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At least 1/3 of AIDs patients
Pink to Dark Purple nodules or plaques Surgery, Radiation, Chemotherapy Rarely seen in non-HIV Related to co-infection of HIV patients w/HSV |
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Staphylococcal Blepharitis
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Hard, brittle scales - scurfs/collarettes
Hyperemia of lid margin Chronic - madarosis, trichiasis, poliosis, tylosis ciliaris, may see ulceration when crusts removed if very severe Can cause associated conjunctivitis, evidenced by papillary reaction May see inferior PEK C/O: FBS, crusting of lids especially in morning, itching, tearing, burning, plus any associated conjuncitivitis symptoms Treatment: lid hygiene for almost all forms, azasite(macrolide) gtt BID, antibiotic ung - bacitracin BID-QID, polysporin BID-QID, erythromycin(macrolide) BID - QID, combo - tobradex(tobramycin and dexamethasone alcohol) 1 gt q 3-4 hours or ung at bedtime, if severe add orals - amoxicillin(penicillin) 250 TID, dicloxacillin(penicillin) 250 QID, erythromycin(macrolide) 250mg QID |
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Demodex in Staph Blepharitis
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Thrives in sebaceous glands and hair follicles
Controversial as to what it does/causes Treatment: metronidazole gel(MetroGel) - not FDA approved for ocular use - must inform, sodium sulfacetamide - high allergy rate |
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Seborrheic Blepharitis (MGD)
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Oily flakes (epithelial cells/sebum) on eyelids and lashes
Usually associated with generalized seborrheic disorder such as acne rosacea or seborrheic dermatitis - may have oily skin, eyebrows etc... S/S: much greasier scales/flakes, often associated w/other MGDs, complain of BURNING as primary symptom in all forms of MGD |
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Meibomian Seborrhea (With Seborrheic Blepharitis) (MGD)
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look up
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Meibomianitis (Posterior Blepharitis) (MGD)
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Stagnation/Solidification of Meibomian secretions
Scattered Involvement - "secondary" All Glands - "primary" S/S: Thick creamy material when expressed from capped glands, thickened red lid margins w/oily texture, reduced TBUT, seborrheic bleph inevitebly present |
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All MGD Treatment
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Lid Hygiene
AT Liberally after hygiene procedures orals - doxycycline(tetracycline) 100mg BID first day then 50-100 QD for 21 days), use azasite(macrolide)(off-label) for pregnant women 1 gt BID could use smaller dose for maintenance of oil secretion, tetracycline 250mg QID Co-managed with PCP for systemic disease (acne rosacea) - need topical and/or oral steroids in addition Shampoo for seborrhea Topical - Restasis (cyclosporine A) to treat chronic MGD as option to steroids in rosacea |
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Mixed Seborrheic-Staph Blepharitis
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Most cases
Lid hygiene Azasite(macrolide) gtt 1 gt BID, or ung |
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Angular Blepharitis
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Usually caused by Moraxella or Staph
S/S: chronic hyperemia, desquamation, ulceration of lateral/medial canthal regions C/O: redness, tenderness Treatment: zinc sulfate ung, erythromycin(macrolide) ung BID-QID |
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Phthiriasis Palpebrarum
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Pubic lice causing chronic bleph
Treatment: stye ung, yellow murcuric oxide, bland ointment, clean lids/head/genitalia with RID(OTC) or KWELL(Rx, avoid eyes) Smother lice Remove cilia with nits(waxy eggs) Complains of same symptoms as bleph |
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Internal Hordeolum
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Bacterial infection of meibomian glands
Almost always staph Hurts b/c rigic tarsal plate has to conform May be associated with preceptal cellulitis More common in upper lid C/O: pain, warm sensation, may have PAN Treatment: hot compress alone BID - QID for mild - watch for spread b/c of heat, orals - dicloxacillin(penicillin) 250mg QID, amoxicillin(penicillin) 250mg TID, or erythromycin(macrolide) 250 QID (topicals don't reach lesion), surgery for resistant cases (done after lesion is quiet) |
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External Hordeolum (Stye)
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Acute staph infection of Zeis or Moll glands, at lid margin, may have yellow point on it
C/O: acute and recent onset Treatment: usually drain w/o assistance within 3-4 days of "pointing," hot compress may hasten, can punture and drain then apply gentamicin(aminoglycoside), plucking infected lash could clear it out |
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Chalazion
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Sterile, chronic, lipogranulomatous inflammation of meibomiam gland due to abnormal retention of normal secretions, spontaneous or after internal hordeolum infection
Hard, immobile, nontender lump, can point to external lid surface or inwards Treatment: 25% resolve over 6 months, for new small lesions hot compress QID for 4-6 weeks, steroid injection - Kenalog-10(injected on inner lid b/c of scarring and discoloration), resistant lanced and drained, antibiotics dont work Recurrent could be sebaceous cell carcinoma |
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Preseptal Cellulitis
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Anterior eyelid infection, in front of orbital septum
Usually Strep or H.Flu (especially kids) Staph more common in adults Arises from pre-existing infection such as dacryocystitis, conjunctivitis, internal/external hordeolum Penetrating lid injury is another route S/S: lid is red, swollen, painful, warm, may have PAN, fever with H.flu Treatment: staph - amoxicillin(penicillin) 250mg to 500mg TID, dicloxacillin(penicillin) 125mg to 250mg QID, H.flu - 3rd gen. cephalosporin, warm compress once antibiotics start, hospitalized if meningitis suspected(high fever, stiff neck), blood cultures **MUST differentiate from orbital cellulitis - life threatening and arises from sinusitis...orbital ALSO has proptosis, limited EOM, extreme pain, obliteration of LC, decreased VA, APD |
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Acute Bacterial Conjunctivitis
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Red eye, tearing, FBS, mucopurulent discharge in lower fornix, papillae, usually one eye first then spreads to other
Usually diffuse injection, chemosis present but not profound, usually uncomfortable (NOT painful) Lids may be "matted shut" in morning(single-most accurate predictor) Most infectious material drains through nasolacrimal duct so PAN usually not present (too big for blood/lymph system) Acute bacterial keratoconjunctivitis more painful Treatment: if mild combo, tobradex gt q 3-4 hours or zylet gt q 4-6 hours, w/significant corneal staining use broad spectrum QID, polytrim(trimethroprim and polymixin B) 1 gt q 3 hours, ciloxan(fluoroquinolone), ocuflox(fluorquinolone), zymar(fluorquinolone), vigamox(fluoroquinolone) TID, azasite(macrolide) BID for 2 days then QD for 5 days, If cornea at risk, DO NOT use steroid on first day, wait and see if antibiotic improves |
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Chronic Bacterial Conjunctivitis
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Four or more weeks
Staph Aureus most common May have additional chronic infectious/inflammatory signs(phylctenules usually at 4 and 8 or 10 and 2, infiltrates, bleph) If significant corneal involvement - chronic bacterial keratoconjunctivitis (causes more discomfort/pain) Treatment: treat associated disorders (especially bleph), antibiotic with good gram+ coverage, polytrim(trimethoprim and polymixin B) 1 gt q 3 hours, bacitracin ung q BID-QID |
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Hyperacute Conjunctivitis
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Almost always caused by Neisseria
Gonorrheae (gram-diplococcus) Genital-hand-eye contact SEVERE copious mucopurulent discharge, lid edema, A/C reaction, PAN, HOT eye Treatment: 1 dose IM ceftriaxone 125mg(cephalosporin), 1 dose IM 1g Spectinomycin, co-treat for chlamydia(zithromax - macrolide - 1g), topical prophylaxis (good opportunity for fungal infection) |
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Neonatal Conjunctivitis
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Treatment: erythromycin oral(macrolide) BID-QID, bacitracin BID-QID, polysporin BID-QID, polytrim 1 gt q 3 hours
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Bacterial Keratitis w/Ulceration
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Most of all cases are bacterial
Epithelial defect over thick stromal infiltrate w/edema surrounding, A/C reaction, pain, photophobia, blurred vision, tearing, PLUS all other keratoconjunctivitis findings Mostly CL wearers, predominantly extended wear (hypoxia -> infiltrates -> epithelial breakdown -> opportunity for bacteria - pseudomonas usually) Cornea swells more overnight in CL wearers Contaminated CL solutions/medications, decreased immune response from other diseases, dry eye syndrome, recurrent eye disease(HSV), chronic desease(dacryocystitis, canaliculitis, bleph), prior surgery/trauma, trichiasis, corneal exposure, corneal edema/bullous keratopathy, collagen-vascular disease, other mucous membrane disorders, VITAMIN A DEFICIENCY, hospitals can all be risk factors Treatment: remove CL till cleared, lavage purulent material, broad-spectrum, 4th gen. fluoroquinolones - vigamox LOADING DOSE - 1 gt q 5 mins. for one hour, then 1 gt q hr for 24 hours then q 2 hours, same for zymar, besivance LOADING DOSE 1 gt q15min. for 1 hr, 1 gt q hour hour, 2 gtt overnight (NOT FDA approved for ulcers but approved for conjunctivitis - must inform), 2nd gen. fluoroquinolones (FDA approved for ulcers) - ciloxan, 2 gtt q 15 min for 6 hours then 2 gtt q 30 min for 18 hours, ocuflox 1 gt q 30 min while awake and twice overnight, can alternate; tobramycin 1 gt q hour and cefazolin 1 gt q hour (drop every 30 min around the clock), reduce inflammation w/COLD compress BID-QID no more than 15 min at a time, cycloplege to reduce pain and seal up leaky vessels and also reduce potential for iris-lens adherence(posterior synechiae), doxycycline (use azasite for females on birth control) optional - reduces collagenase, could use corticosteroids if improvement DEFINITE, NEVER used first day Could taper treatment given the right signs...blunting of perimeter etc.. Stain every day and do VA and pupils first(vision often worse next day but will feel better) |
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Fungal Eye Infections
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Higher in southeast, vegetative debris, CL wear, topical steroid use, immunosupression, corneal surgery, chronic keratitis
Most worldwide: Aspergillis, southern US: Fusarium, Northern: Candida, Aspergillis C/O: FBS, pain, reduced vision, photophobia, injection, chemosis (INDOLENT presentation so get worse gradually - 5 to 7 days) Signs: epi defect, purulent discharge, dense stromal infiltrate, A/C reaction, hypopyon, FEATHERY BORDERS, SATELLITE LESIONS, rough textured, brown pigmentation, "dry" infiltrate Treatment: Polyenes; natamycin 1 gt q 1-2 hours (drug of choice - otc), amphotericin B(must be prepared), and/or Azoles; oral intraconazole - candida and aspergillis, oral ketoconazole 200mg QD - fusarium, miconazole and/or Pyrimidines; topical/oral voriconazole - fusarium, flucytosine - adjunctive with other agents, can add antibiotic; neomycin, vigamox TID (kill bacteria that fungi feed off of), sub-conj injections, cold compress, cycloplege, topical steroids ONLY if vision threatened and ONLY after two weeks of care(b/c antifungals aren't strong and indolence of fungi)...require about 12 weeks of treatment Mechanical debridement of lesion allows better penetration of topical drugs 1/3 require PKP to be done within 4 weeks of infection when no response |
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Acanthamoeba Keratitis
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Free living, ubiquitous in soil, water, air, dust
Can be trophozite or double-walled cyst(can't penetrate, hard to treat) Severe, painful, sight threatening, 80% ASSOCIATED WITH CL USE, encephalitis, disseminated disease, keratitis, DON'T HAVE THICK INFILTRATE, purulent discharge, symptoms may seem out of proportion to appearance, pain(goes to corneal nerves - show up on SL), photophobia, tearing, injection, PEK, PSEUDODENDRITIC EPITHELIAOPATHY(ROSE BENGAL WON'T STAIN), PAN possible, later findings - dense infiltrate, RING INFILTRATE, perineuritis, intense injection, keratouveitis possible Confocal microscopy confirms diagnosis Treatment: epithelial debridement, topical - chlorohexidine hourly for 3 days then q 3 hours with PHMB, brolene, oral - ketoconazole or itraconazole (to kill food source), cycloplege, avoid steroids till resolution, could required PKP(topical therapy continued long-term afterwards), treat for several weeks |
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Adenovirus
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Most frequent cause of infectious conjunctivitis
Serotype 19 most common 1-11, 19 primary cause of NON-SPECIFIC follicular conjunctivitis S/S: Follicles in lower fornix, serous discharge, conjunctival chemosis, acute onset of pink eye, starts with one eye then spreads to other, swollen red lid possible, PAN expected, often history of URTI or close contact with URTI |
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Simple Adenovirus
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S/S: Follicles in lower fornix, serous discharge, conjunctival chemosis, acute onset of pink eye, starts with one eye then spreads to other, swollen red lid possible, PAN expected, often history of URTI or close contact with URTI
Treatment: LIMIT SPREAD - wash hands (preferred to gels b/c they kill normal flora also), don't share bedding or towels, discard tissues cloths, discard CLs, discard cosmetics SUPPORTIVE - AT, vasoconstrictors, NSAIDs, Betadine (non-selective - toxic), cool compress |
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Epidemic Keratoconjunctivitis (EKC)
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Caused by serotypes 8,19,37
HIGHLY CONTAGIOUS More extreme S/S Rule of 8's: Days 1-7 = incubation Days 8-16 = active infection, PAN VISIBLE, huge follicles, severe chemosis Day 16+ = SEIs, no longer contagious Acute onset (one eye then both), significant discomfort - PAIN, follicles, petechial hemorrhages, chemosis, PAN, pseudomembranes probable, PEK, SEIs late (lots centrally - lymphocytes, not PMNs because not bacterial) Treatment: Supportive, prophylactic gtt when PEK present (almost always) - Polytrim q3h (ONLY USE PROPHYLACTIC DOSE REGARDLESS OF SEVERITY), combo discouraged because SEIs will resolve then rebound aggressively, if steroid necessary because of severe symptoms and reduced VA, use combo first, then steroid ONLY and taper for 8-12 weeks - if SEIs, could use betadine also with steroid (no longer than 4 days) |
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Pharyngoconjunctival Fever (PCF)
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Caused by serotypes 3,4,5,7
"Swimming pool conjunctivitis" Looks same as simple adenovirus Follicular conjunctivitis with sore throat, fever, IF there is corneal involvement, usually mild/transient Short incubation (1-2 days) and duration, usually starts unilateral then bilateral after 2-5 days SELF-LIMITING Treat supportively |
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Acute Hemorrhagic Conjunctivitis
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BLOODY
Follicular and caused by enterovirus, coxsackievirus Prominent subconjunctival hemorrhages (DOES NOT ALWAYS MEAN VIRAL-BACTERIAL POSSIBLE) with follicles, BILATERAL ONSET Incubation is less than a day, symptoms 3-5 days No corneal or systemic involvement HIGHLY CONTAGIOUS Self-limiting Treat supportively |
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Molluscum Contangiosum
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Follicular (secondary) conjunctivitis in association with lid lesion (primary)
Conjunctival reaction is immune response to pox-virus particles contained in lid lesion If lesion removed, conjunctivitis will resolve on its own Treat supportively in meantime Check for immunocompetence |
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Newcastle Disease
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Can cause follicular conjunctivitis
From paramyxovirus group, seen in poultry workers Treat supportively |
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Moraxella
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BACTERIA - Can cause FOLLICULAR conjunctivitis
Young girls sharing eye makeup Topical erythromycin, tetracycline, ZINCFRIN |
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Parinaud's Oculoglandular Conjunctivitis
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TREAT SYSTEMIC CONDITION
Can cause follicular conjunctivitis Ipsilateral lymphadenopathy, fever, granulomas, CAT SCRATCH disease Hot compress nodes, gentamicin ung. or bacitracin ung. q2h, analgesics PRN TARGETED LAB WORK |
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Axenfeld's
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Upper palpebral follicles
Can cause follicular conjunctivitis Mild, asymptomatic, UPPER, no treatment |
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MMR
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Can cause follicular conjunctivitis
Mild Supportive treatment |
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Chronic Folliculosis
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Can cause follicular conjunctivitis
Pre-adolescent children, marked inferior conjunctival follicular response which is asymptomatic - from chronic viral or lymphoid hyperplasia No treatment |
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Herpes Simplex (Overview)
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Double stranded DNA virus
MOST COMMON CAUSE OF CORNEAL OPACIFICATION/CORNEAL BLINDNESS IN DEVELOPED COUNTRIES HSV-1 and HSV-2 Enters body through mucosal surfaces, replicates in cell nucleus, then kills host cell Primary (first) Infection: between 6 months and 5 years old (systemic), infects peripheral end organ (eyelid), then the virus travels to ganglia (especially trigeminal and cervical) where it may become latent, self-limited and not destroyed by immune system - transmission via resp. droplets (1) or direct transmission (1 & 2) Reactivation: latent virus reactivates due to immunocompromise, steroids, UV, stress, fatigue, irradiation, trauma, surgery, fever - reaccurs in 25-50% of patients, usually within 5 years of primary infection(WHERE OUR CLINICAL OCULAR DISEASE IS SEEN) Genital and Gingivostomatitis disease Most adults have the antibodies (80%) but only 20-25% manifest disease 70-90% adults seropositive for HIV-1 (DELAYED ONSET NOT A GOOD THING) 22-25% adults seropositive for HSV-2 HSV-1 highest incidence in kids 6 months - 3 years HSV-2 highest 18-25 years old HSV-1 genital infection rapidly rising HSV-2 antibodies present in 20% Caucasians vs. 65% African Americans HSV-2 more likely in females HSV-2 recurrence 20% more likely in males Only small % of seropositive people report a hx of genital lesions Fastest rise in infection in young white patients Blepharitis, Canaliculitis, Conjunctivitis, Keratitis, Uveitis, Retinitis, Encephalitis |
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Herpes Simplex Blepharitis
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Most likely at time of primary infection
VESICULAR LESIONS later become PUSTULAR LESIONS Pustules eventually break and ulcerate Usually resolves in a week without scarring Usually first manifestation of disease but patients don't seek care Self-limiting, not always perceived as "eye-problem" If close to lid margin could prophylax w/Viroptic QID, could possibly prophylax over pustules but not necessary |
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Herpes Simplex Conjunctivitis
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Follicular (indistinguishable from simple adenoviral and other viral disease in absence of corneal involvement)
Moderate to severe May have pseudomembrane formation May stand alone or accompany blepharitis, keratitis, uveitis etc... Any case of recurrent follicular conjunctivitis, even without a history of prior herpes infection, should be regarded with suspicion for HSV |
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Herpes Simplex Keratitis (Epithelial)
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Most common INITIAL eye manifestation seen in office (although blepharitis may have preceded but gone undiagnosed)
Epithelial lesions represent active HSV replication within epithelial cells - tiny vesicles form within the epithelium Usually unilateral Redness, pain, photophobia, tearing, FBS, reduced VA, hypoesthesia Dendritic, branches/linear stain with NaFl (b/c these cells are gone) - percolation of fluorescein in the area surrounding the dendrite is common "end bulbs" stain vividly with Rose Bengal (these cells are dead/dying) Lissamine green does not seem to posses similar staining patterns for HSV DON'T USE PROPARACAINE FIRST BECAUSE COULD CAUSE SPK - PARADOXICAL FINDING MAY PRESENT AS PEK - must distinguish bacterial from viral (follicles, serous discharge, PAN etc...) Geographic ulcers are larger areas of epithelial loss: May generally follow original dendrite pattern Postinfectious/Metaherpetic Ulcers - persist after active herpetic infection and represent non-healing epithelium in the absence of viral replication |
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Herpes Simplex Keratitis (Neurotrophic Keratopathy)
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Arises from impaired corneal innervation, combined with decreased tear formation, toxic effects of meds, and possibly trace amounts of HSV virus replication w/in the persistent epithelial defect
Oval-shaped corneal ulcer in presence of decreased corneal sensitivity - hemidesmosomes and desmosomes need innervation to stay connected No infiltrate, no discharge, treat prophylactically - "STERILE ULCER" |
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Herpes Simplex Keratitis (Stromal Disease - Interstitial Keratitis)
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IK = Immune stromal keratitis
Often from chronic, recurrent ocular HSV Antibody-complement cascade reaction to retained viral antigen within stroma Infiltration, immune rings, ghost vessels, AC reaction common - may be significant, associated with other ocular inflammation (uveitis, trabeculitis, secondary glaucoma), could present as dense edema, could be disciform Necrotizing Stromal Keratitis Dense stromal infiltrate, ulceration (DEEP - epithelium intact), AC, necrosis, thinning or perforation, inflammatory response to viral antigen and viral replication within stromal keratocytes, could be associated with other ocular inflammation - uveitis, trabeculitis, secondary glaucoma COULD HAVE REDUCED VA DON'T USE AMINOGLYCOSIDES |
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Herpes Simplex Keratitis (Endotheliitis)
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KP's (keratic/keratitic precipitates WBCs from iris that land on back of cornea) with epithelial and stromal edema overlying (DISCIFORM AREA COMMON)
NO INFILTRATE Uveitis usually present Immune reaction to viral antigens - active viral replication? DIFFUSE, DISCIFORM, LINEAR |
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Herpes Simplex Uveitis
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Can be profound, cells and flare in anterior chamber, with or without hypopyon, cells and flare can persist long after the active infectious process occurs
DIFFICULT TO TREAT BECAUSE CONTRAINDICATION OF STEROID USE IN PRESENCE OF ACTIVE EPITHELIAL INFECTION |
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Herpes Simplex Encephalitis
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MRI is diagnostic
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Herpes Simplex Virus Treatment
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Treatment for active epithelial disease: Debridement (start in good area and move into bad area) with semi-sharp instrument using topical anesthesia, then follow with Viroptic (works 80-85% of time - highly toxic) 1% q2h up to 9 times per day, then taper as condition responds, continue QID for 3-5 days after COMPLETE re-epithelialization occurs - generally recommended not to continue treatment longer than 21 days due to kerato-toxicity of Viroptic drops, can use Acyclovir adjunctively (especially for stromal involvement) follow patient daily till re-epithelialization - if Viroptic not an option, Vidarabine ung, oral antivirals, NO STEROID ON ACTIVE INFECTION, can use NSAIDs, could use antibiotic prophylactically, supportive, can cycloplege if significant stain/AC
Conjunctivitis treatment: prophylax against corneal involvement Viroptic QID, supportive - AT, cool compress, vasoconstrictors, NSAIDs if severe, could use Vidarabine ung and follow up every 2-3 days to check for corneal involvement (if there is, use Viroptic), can use Vidarabine adjunctively with Viroptic for overnight coverage, can use Acyclovir Blepharitis treatment: prophylax on lid lesions against secondary bacterial infection of conjunctiva and cornea - ung, antiviral optional - if lid lesions are close to margin and conjunctivitis is suspected or expected, use Viroptic QID, could use oral Acyclovir in severe or complicated cases, follow up depending on suspicion |
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HSV Immune Disease Treatment
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Includes stromal disease, uveitis - NON-ACTIVE EPITHELIAL INFECTION
Antiviral therapy PLUS STEROIDS - Pred Forte (prednisolone acetate 1%) - use in same dosing frequency as topical Viroptic 1% (q3h or q4h) No dosing schedule established for steroid plus Zirgan (but probably 5xday w/steroid) Use a steroid with less frequent dosing requirements (Durezol) Must prophylax with anti-viral while using steroid Restasis - immunosuppressant (Cyclosporine-A 0.05%, 1 gt BID 12 hours apart, AT 15 min. after) may be emerging as a viable and safer alternative to steroids in HSV stromal keratitis - good response in patients who didn't respond to topical steroids |
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Herpes Zoster Virus (Overview)
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Same virus as chickenpox
Primary infection is vesicular rash over face, trunk, extremities (1 side usually) Incomplete immunity results in virus establishing latency in sensory ganglia and reactivating periodically - due to fatigue, trauma, immunosuppression, NOT SURGERY Herpes Zoster Ophthalmicus if V1 affected - incidence and severity increase with age Blepharitis, Conjunctivitis, Keratitis, Episcleritis/Scleritis, Uveitis, Glaucoma, Retinitis/Choroiditis, Neurological complications (could look like stroke - must differentiate), POST-HERPETIC NEURALGIA IS POTENTIAL SERIOUS COMPLICATION Prodromes: pain, itching, paresthesias along future site of eruption, diminished sensation despite exquisite tenderness, precedes skin eruptions (bleph) by 2-3 days, may have flu-like symptoms |
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HZ Blepharitis
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Dermatologic manifestation - PRIMARY IDENTIFYING SIGNS OF ZOSTER OPHTHALMICUS, may experience tingling in this area prior, then active phase involved pustules which eventually break/ulcerate - look like open sores or scabs on face on one side, this phase can last days to weeks
Well-circumscribed, erythematous, maculopapular skin eruptions following dermatomes Prophylax with antibiotic ung (don't have to) Small, tense, painful vesicles develop within 12 to 24 hours which break, crust, and heal (scar) Lasts between 7-10 days May become disseminated All S/S follow specific dermatome V1 will effect tip of nose (Hutchinson's Sign - nasociliary branch of V1) - this suggests high probability of ocular involvement and poorer prognosis for complications - called Herpes Zoster Ophthalmicus |
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HZ Conjunctivitis
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Follicular, indistinguishable from other types of viral/follicular disease Chemosis and hyperemia may be profound
Usually not most impressive feature of illness |
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HZ Uveitis
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Extremely difficult to treat
IOP increases common Can result in significant iris atrophy and scarring - directly dependent upon viral load in AC at time of acute infection |
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HZ Keratitis
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look up
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Neurotrophic Keratitis
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Possible sequela to HZV infection, result of damage to corneal nerves, which are critical for epithelial integrity Treated with aggressive lubricant therapy at a minimum – may require surgical intervention
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Post-Herpetic Neuralgia (PHN)
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Pain that persists beyond the course of active infection (1-3 months after symptoms first appear) Potentially most serious/common manifestation of HZ Caused by scarring of nerve endings as a result of skin eruptions Incidence increases with age – common cause of suicide in elderly?
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More Varicella Complications...
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Increased IOP – trabeculitis, uveitic glaucoma Protective Ptosis Secondary infections Sclerouveitis (from ischemic vasculitis) Optic Neuritis Acute Retinal Necrosis Contralateral Hemiplegia Puntal occlusion
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HZV Palliative Treatments
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Cool Compress, cover with ung (warm will dry out lesions)
Cover lesions with loose gauze or cloth Narcotics, TCAs for PHN, neurontin Oral/Topical steroids (required if ocular involvement) - don't use oral right away Topical Lidocaine - anesthetic Topical Voltaren - NSAID Supportive: AT, vasoconstrictors Anticonvulsants can be used for PHN (neurontin) Oral opiates (analgesics) for PHN - can add steroids after 3 days if this didn't work |
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HZV Antiviral Therapy
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Oral Acyclovir 800mg 5xday x 7-10days (most effective if skin lesions are less than 72 hours old)
Oral Famvir 500mg TID x 7 days Oral Valtrex 1g TID (supposedly better at preventing PHN than other two) Ung Acyclovir Immunocompromised my require hospitalization with IV acyclovir to prevent retinal necrosis Prophylaxis - antibiotic ung over skin lesions , ung for conjunctivitis with keratitis IF cornea at risk (significant staining) MUST INDICATE WHERE UNG IS PUT ON Steroid also mandatory |
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CMV
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Opportunistic, far more common in immunocompromised
Very significant retinopathy Prior to HAART, approximately 30% of HIV patients developed CMV |
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Simple Allergic Conjunctivitis
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Papillae in upper palpebral conjuntiva (have central blood vessel), chemosis, ITCHING (MOST IMPORTANT COMPONENT), injection which is usually less intense than with infectious disease, dishcharge may be watery with mucin strands (ROPY/STRINGY), can have eczema on lids
SIMPLE/SEASONAL USUALLY DOESN'T CAUSE CORNEAL EFFECTS - don't use antibiotic, even in combo (overtreating) |
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Vernal Keratoconjunctivitis
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HORNER-TRANTAS DOTS (limbal papillae made of up degenerated eosinophils), GIANT COBBLESTONE papillae, INTENSE ITCHING, protective ptosis, SHIELD ULCER possible (b/c of rubbing) - in this case use prophylactic antibiotic and MUST use steroid - special case, ulceration can become bacterially infected and have discharge - NOW SWITCH TO KERATITIS TREATMENT, seasonal (warm months), young males
Vernal w/o ulcer - steroid (pulse - alrex), antihistamine/mast cell (Pataday - DON'T HAVE TO) Vernal w/ulcer w/o discharge (non-infected) - steroid (pulse), antihistamine/mast cell (Pataday), prophylax, cycloplege Vernal w/ulcer w/discharge - steroid (pulse) (NOT Tobradex), antihistamine/mast cell (Pataday), antibiotic, cycloplege, cold compress (don't rub) IN ALL CASES REMOVE CL, no bandage contact lens |
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Atopic Conjunctivitis
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Identical presentation to vernal
Year-round Males > Females |
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Giant Papillary Conjunctivitis
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a.k.a CL-related conjunctivitis - usually soft, not rigid
Itching worse with CL than without Switch brands, wear less, remove, switch to peroxide-based solution, switch to RGPs Poor lens fit, transient vision blur, mucin strands in tear film, injection, chemosis, large papillae on upper palpebral conjunctiva If severe use pulse and antihistamine/mast cell |
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Allergic Conjunctivitis Treatment
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Eliminate allergen
Desensitization Cool compress AT Vasoconstrictors - Naphcon (be cautious of patients with narrow angle glaucoma), Visine - usually a poor choice, warn patients about rebound effect Vasoconstrictors/antihistamine combo - Naphcon-A QID, many OTCs Antihistamines - Emadine (also used for lid myokymia) (emedastine 0.05%) QID, 3+, very powerful and fast acting Antihistamines/Mast cell stabilizers (MOST COMMONLY USED - 3+) - Patanol (olopatadine .1%) BID, Pataday (olopatadine .2%) QD, Bepreve (2+) (bepotastine besilate 1.5%) BID, Elestat (epinastine .05%) BID, Optivar (azelastine .05%) BID OTCs (good for patients w/o insurance)= Ketotifen fumarate .025% BID (3+), Alaway (MOST COMMONLY USED TO TREAT ALLERGIC CONJUNCTIVITIS), Refresh, Zaditor, Claritin Eye Topical NSAIDs - Acular QID, 3+, not used because it burns Oral antihistamines - MAY EXACERBATE DRY EYE Mast cell stabilizers - POOR CHOICE, AVOID - Alomide (lodoxamide tromethamine .1%) QID, Alocril (nedocromil 2%) BID - BEST CHOICE, Crolom (cromolyn 4%) QID, Opticrom (cromolyn 4%) QID, Alamast (pemirolast .1%) QID for a week then BID For more serious cases (vernal), "PULSE" of steroid along with mild tx like antihistamine - Alrex q hour today, q2h tomorrow, q4h for two weeks, Pataday QD today continue long term |
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Simple Episcleritis
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Normal episclera - radiating vascular pattern, susceptible to any collagen-vascular or connective tissue-based disease
More common (80%), acute, wedge-shaped sectoral involvement, mild to moderate discomfort - NOT PAINFUL, interpalpebral area, causes overlying conjunctival injection and chemosis, deep episcleral vessels won't blanch with vasoconstrictors but superficial will (still can't use to distinguish between conjunctivitis and episcleritis/scleritis), VA not affected, palpebral conjunctiva looks normal More common in women b/c of associated system conditions, usually unilateral, no discharge, no AC reaction, no corneal involvement, often no cause found - could be fatigue, stress, sleep deprivation Associated diseases: rheumatoid arthritis (MOST COMMON), lupus, HZV, lupus, giant cel arteritis, TB, syphilis, gout, lyme disease, sarcoidosis, polyarteritis nodosa, thyrotoxicosis |
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Nodular Episcleritis
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Inflamed yellow/clear nodules near limbus - inflammatory cellular infiltrate (usually more mediators) - may be multiple, less common, symptoms more severe but similar in nature, longer course, longer treatment, no corneal involvement, sometimes mild AC, same systemic associations
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Episcleritis Treatment (Both forms)
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Optional and based on symptoms - start small
Vasoconstrictors - just appearance NSAIDs - discomfort Mild steroids - appearance/discomfort Strong steroids - people with low discomfort tolerance Oral NSAIDs If more than 3 recurrences, systemic workup |
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Scleritis
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More common in women, more commonly bilateral, higher association with systemic disease than episcleritis, SEVERE PAIN (could be only indicator to differentiate from episcleritis)
Pain may radiate to jaw and sinuses and temple, can cause overlying episcleritis and conjunctival injection, vasculature has reddish-purple-blue coloration, many recurrences Palpebral conjunctiva looks normal Complications: uveitis, glaucome, keratitis, vision loss, retinal detachment, ONH involvement |
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Diffuse Anterior Scleritis
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Most common form, may be wedge-shaped, diffusely distributed, may affect entire anterior sclera, only 9% of patients have VA affected (least), deep and superficial vessel engorgement, PAIN, no nodules, no necrosis
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Nodular Anterior Scleritis
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Second most common, one or more immovable nodules (b/c in sclera) with adjacent edema and injection, sclera may transparent below nodule, no necrosis, 25% have associated VA loss
Could see choroid after resolution |
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Necrotizing Anterior Scleritis
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LOCAL, very painful, acute congestion of vessels which become distorted or occluded (walls touch), underlying sclera becomes transparent and necrotic, may perforate, MOST SERIOUS FORM BECAUSE OF VISION LOSS AND NECROSIS, 50% have associated vision loss, high association with rheumatoid arthritis
Could see choroid after resolution |
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Scleromalacia Perforans (sub-type of Necrotizing Anterior)
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Really a sub-type of necrotizing anterior scleritis
Least common form of anterior scleritis MINIMAL TO NO SYMPTOMS - NO PAIN Melting of episclera and sclera from necrotic vascular occlusive process Underlying uvea could be totally exposed Nerves could be involved |
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Posterior Scleritis
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Usually unilateral
Difficult diagnosis - posterior sclera is inflamed but hidden from direct view Quite painful - 10 MRI, ultrasound to diagnose Retina could be misshaped |
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Scleritis Treatment
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Targeted workup mandatory if not diagnosed already
Topical steroids - Pred Forte q1h, then taper AND Oral NSAIDs/ oral steroids/ oral immunosuppressives Co-manage Sclera can regenerate itself, do grafts if large involved AFTER inflammation controlled |
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Congenital Disorders
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Discovered at birth
NOT NECESSARILY HEREDITARY Can be chromosomal, teratogenic, environmental Some may not be discovered until adulthood MOST IMPORTANT ASPECT IS WHICH LAYER IS AFFECTED |
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Megalocornea
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Larger than normal cornea (normal width is 10-12.8 mm in newborn)
Usually BILATERAL NONPROGRESSIVE Cornea clear unless tears in Descemet's, then small opacities form Sharply delineated limbal region X-linked recessive (more common males) Patients frequently have high myopia and astigmatism - less commonly associated with cataract and lens dislocation, iridodonesis, phacodonesis, iris and pupillary abnormalities Association with MARFAN'S SYNDROME Could have larger than normal optic cup? Collagen abnormality? NO TREATMENT - DISTINGUISH FROM CONGENITAL GLAUCOMA (Distinct borders) |
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Microcornea
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Normal globe size with corneal diameter less than 10mm - MUST DISTINGUISH FROM BLEPHARIMOSIS, WHICH IS ABNORMALLY SMALL IF
BILATERAL = UNILATERAL MALES = FEMALES Autosomal dominant Normal VA, steeper than normal cornea Associated systemic conditions - MESODERMAL SYNDROMES, CRANIOFACIAL SYNDROMES, NEUROLOGIC, CHROMOSOMAL DISORDERS MORE SUSCEPTIBLE TO ANGLE CLOSURE GLAUCOMA AS LENS GETS LARGER |
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Oval Cornea
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Vertically = Reiger's anomaly, Turner's syndrome, Microcornea
Horizontally = Sclerocornea - sclera more prominent at inferior and superior limbus |
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Corneal Astigmatism
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Variation of normal shape
IF EXTREMELY HIGH, MAY BE AUTOSOMAL DOMINANT |
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Keratoconus
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PROGRESSIVE, non inflammatory ectasia and thinning of central and paracentral cornea which assumes conical configuration
Results from increase in laxity of corneal stroma USUALLY BILATERAL, FEMALES > MALES? No strict hereditary pattern Usually manifests in adolescence, bilateral but asymmetrical and highly variable progression Cone may be small or large, round or oval, near or adjacent to visual axis SCISSORING on Ret IRREGULAR ASTIGMATISM on K's (egg-shaped mires) Often high myopia, might not get corrected VA to 20/20 with spectacles because of irregular astigmatism Fleisher's ring - ferritin (iron) deposition around the base of the cone - seen in moderately advanced cases with cobalt filter Vogt's striae - fine vertical folds in the stroma and Descemet's (disappear with digital pressure) Bowman's breaks - cause fine scars in anterior stroma from repair (DON'T DISAPPEAR WITH DIGITAL PRESSURE) Prominent Corneal Nerves Munson's sign - V-shaped configuration of the lower lid in downgaze from the cone Rizzuti's sign - sharply focused beam of light near the nasal limbus produced by lateral illumination of cornea Associated with - Atopic conditions, Down's syndrome, Retinal disease (Leber's congenintal amaurosis), Mitral valve prolapse Treatment - rigid contact lenses, corneal collagen crosslinking - requires anesthesia and induced corneal abrasion to allow better riboflavin diffusion into the stroma (5-9mm) and topical riboflavin drops are exposed to UVA light for 30 minutes which excites riboflavin into a triplet state with reactive oxygen species and new collagen bonds are formed between amino acids of neighboring collagen fibers HYDROPS - breaks in Descemet's membrane which results in acute stromal swelling in the area and extreme photophobia and severe pain (oral analgesics, narcotics, 800mg ibuprofin); usually resolves within 4 months - leaves a scar, IOP increase, could blister and if blister bursts then need corneal transplant (PKP), BSCL to help with blistering (prophylax with drops over lens), PP better if a lot of cornea is missing (antibiotic ung first), atropine in office |
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Pellucid Marginal Degeneration
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Variation/similar to keratoconus
BILATERAL, NONINFLAMMATORY UNCOMMON cause of corneal ectasia Corneal protrusion occurs inferiorly, above a narrow band of clear, nonvascular corneal stromal thinning from 4-8, thin zone usually 1-2mm wide HYDROPS MAY OCCUR Usually presents in patients 20-40 years old with slow progression Females = Males, no specific hereditary pattern Treatment - surgical correction, collagen crosslinking (GOOD CANDIDATES FOR THIS) |
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Keratoglobus
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EXTREMELY RARE
Bilateral corneal ectasia Globoid protrusion of clear, diffusely thin (1/3 to 1/5 normal thickness) Cornea of normal to moderately increased diameter Cornea thinnest near limbus Present at birth and generally non-progressive Acute hydrops possible Perforation of cornea is frequent and generally occurs < 20 YO High myopia, high astigmatism Associated with Leber's congenital amaurosis, blue sclera May be genetically linked to keratoconus Treatment: difficult due to thinning; RGP's ARE CONTRAINDICATED, EPIKERATOPHAKIA surgery usually best prognosis, BSCL - BAD FITTING |
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Posterior Keratoconus
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Steep concavity of posterior surface with normal anterior curvature
UNILATERAL > bilateral Corneal scarring anterior to "cone" Associated with anterior and posterior synechia, retinal and choroidal sclerosis, lens problems May be congenital or follow trauma No treatment unless corneal scarring severe, then do PKP Still get scissoring |
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Sclerocornea
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RARE
Diffuse marble-like opacification of the entire stromal thickness usually involving peripheral 1-2mm but sometimes involving central cornea as well Involved cornea blends with sclera and obliterates normal limbal architecture Collagen fibrils in this area are larger than normal and are oriented in scleral formation vs. corneal formation Bowman's absent Most have flat corneas - called CORNEA PLANA, and associated with angle closure glaucoma Usually BILATERAL FEMALES = MALES, UNKNOWN HEREDITY |
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Posterior Embryotoxon
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Thickened or hypertrophied Schwalbe's line which is anteriorly displaced
Thin, sharply demarcated peripheral corneal opacity 15% of patients - pretty normal Autosomal dominant |
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Peter's Anomaly
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Leukoma (whitening of the cornea) in the central or paracentral cornea bordered by one or more iris strands that cross the anterior chamber from the collarette
Endothelium and Descemet's are absent in area of opacity May be associated with - anterior pyramidal catarct, microcornea, sclerocornea, infantile glaucoma UNILATERAL > bilateral FEMALES = MALES Unkown heredity Thought that during third month of fetal development anterior hyaloid plexus touches the cornea, damaging the endothelium and Descemet's, leaving adhesions Lens may or may not be attached to the cornea as well |
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Axenfeld-Reiger Syndrome
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Continuum of disorders involving anterior chamber abnormalities
ALWAYS BILATERAL, may be asymmetric Autosomal dominant 1) Axenfeld's anomaly - posterior embryotoxon to which peripheral iris strands adhere 2) Axenfeld's syndrome - axenfeld's anomaly PLUS GLAUCOMA 3) Reiger's anomaly - axenfeld's anomaly PLUS HYPOPLASIA of the iris stroma - other ocular and systemic associations are possible 4) Reiger's syndrome - reiger's anomaly PLUS DEVELOPMENTAL DEFECTS OF TEETH AND BONES |
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Corneal Dystrophies
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BILATERAL
Alterations of cornea that are NOT associated with prior inflammation or systemic disease Most are autosomal dominant in inheritance and are USUALLY present within first few decades of life May be stationary or slowly progressive DON'T CONFUSE WITH DEGENERATIVE (POST-TRAUMATIC, POST-INFLAMMATORY, AGE-RELATED CHANGES THAT ARE OFTEN ACCOMPANIED BY OTHER OCULAR OR SYSTEMIC DISEASE) |
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Meesman's Dystrophy
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Epithelial dystrophy
a.k.a. Juvenile Hereditary Epithelial Dystrophy RARE BILATERALLY SYMMETRIC Autosomal dominant Microscopic epithelial cycts that may first appear in the first year of life Symptoms begin usually in early adult life when these cysts rupture (treat supportively) Uniform size and shape Most numerous in interpalpebral area and may coalesce to form larger cysts NO CORNEAL STAINING WITH NaFl UNLESS CYSTS RUPTURE Unknown cause - "peculiar" substance within epithelial cell Treatment: supportive when rupture, BSCL may help, superficial keratectomy if severe |
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Epithelial Basement Membrane Dystrophy (EBMD)
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Epithelial dystrophy
a.k.a. Cogan's microcystic dystrophy, map-dot-fingerprint dystrophy, anterior basement membrane dystrophy (ABMD) MOST COMMON ANTERIOR CORNEAL DYSTROPY Three forms: 1) "Maplike" or "Geographical" whorl line patterns - maps are circumscribed areas of central ground-glass appearance often punctuated with clear lacunae - NEGATIVE staining over elevated areas 2) "Dots" may occur under or close to the maplike patches, which are pseudocysts and may rupture (WILL STAIN) 3) "Fingerprints" are concentric, often curvilinear parallel lines clustered in central or midperipheral cornea, often surrounding maps Maps and Fingerprints are histologically found to be aberrent multilaminar projections of thickened basement membrane into the overlying epithelium, which interferes with connections of epithelium to basement membrane Could get recurrent epithelial erosion which would be painful in the morning because of ripping off of loose epithelium Treatment: for RCE - anterior stromal puncture, which helps b/c scar tissue draws Bowman's in...SEE NEXT SLIDE |
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Dystrophic Corneal Erosion (RCE)
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Epithelial dystrophy
Spontaneous traumatic erosion of corneal epithelial tissue Associated with trauma (most commonly), or inherited alone or with several corneal dystrophies (EBMD) 50% of patients with RCE have EBMD Microcysts, epithelial edema, and bullae formation from loss of hemidesmosomes may occur in acute phase Patient typically reports waking from sleep with acute pain - due to opening eyes and loose epithelium tearing off - causes extreme pain, photophobia, tearing, lid swelling Also associated with Reis-Buckler's, macular dystrophy, lattice dystrophy Treatment: IF SEVERE - antibiotic ung, cycloplege, PP, oral doxycycline 50mg BID for two weeks and 50mg QD for two weeks combined with topical steroid QID for two weeks and then BID for two weeks if not using PP, IF MODERATE - prophylactic antibiotic drops (azasite offers additional anti-MMP activity to hasten healing), BSCL, possible topical and/or oral NSAIDS, IF MILD - prophylactic antibiotic drops with AT, possible topical NSAIDS and oral NSAIDS FOLLOW OPEN CORNEA EVERY DAY UNTIL HEALED NaCl 5% drops/ung used during the healing phase and in between erosion episodes may decrease epithelial edema and therefore help with adherence, bland ung may be equally helpful as NaCl used prophylactically Debridement of cornea may result in normal epithelial growth Anterior stromal puncture - which helps b/c scar tissue draws Bowman's in PTK or superficial keratectomy are LAST RESORT TREATMENTS |
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Reis-Buckler's Dystrophy
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Bowman's layer dystrophy
BILATERAL AND SYMMETRICAL Central corneal dystrophy - anterior opacification causing irregular astigmatism and reduced VA Presents in childhood with recurrent attacks of photophobia and irritation Early signs: fine reticular opacities at Bowman's membrane - membrane degenerates and is replaced by collagen and microfibrils Late signs: irregular corneal surface with varying thickness of epithelium, usually no edema Highly variable presentation of gray-white opacities in subepithelial area of central and paracentral cornea; periphery usually spared Opacities are from ridges or "spokes" from Bowman's membrane into the epithelium No NaFl stain seen unless RCE occurs Autosomal dominant with strong penetrance Non-inflammatory RCE usually occurs 3-4 times per year Progression/diminution highly variable Usually see Hudson-Stahli lines, distorted keratometry Treatment: RCE treatment when it occurs, may require PTK, superficial keratectomy, lamellar keratoplasty, penetrating keratoplasty if VA severely affected |
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Central Crystalline Dystrophy (of Schnyder)
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One of the rarest but least severe corneal dystrophies
Autosomal Dominant Yellow-white opacity made up of cholesterol crystals; may appear polychromatic BILATERAL AND SYMMETRICAL Associated with ARCUS HIGH PERCENTAGE OF PATIENTS HAVE HYPERLIPIDEMIA |
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Posterior Polymorphous Dystrophy (PPMD)
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Endothelial dystrophy
BILATERAL AND AUTOSOMAL DOMINANT Isolated or coalescent posterior corneal vesicles usually without corneal edema; variable presentation ("polymorphous") THICKENED DESCEMET'S MEMBRANE Bandlike figures on posterior corneal surface Treatment: Usually none, BUT if corneal edema present, treat as Fuch's dystrophy |
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Fuch's Dystrophy
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Endothelial dystrophy
BILATERAL AND ASYMMETRICAL Females > Males Also see stromal clouding and decreased corneal sensation 3 Stages: 1) Guttata (Hassal-Henle bodies) - excrescenses from thickened Descemet's membrane; DIRECT ILLUMINATION shows golden refractile mounds on the posterior corneal surface; SPECULAR REFLECTION shows black holes in the endothelial mosaic; INDIRECT/RETRO shows vacuole-like structures - MOST GUTTATA DO NOT PROGRESS TO FUCH'S 2) Stromal Edema/ Epithelial Edema - if endothelium fails, aqueous penetrates, signs include wrinkles in Descemet's membrane, corneal striae, corneal haze, bullae, and microcysts; tight junctions between epi cells prevent fluid exit with cause cysts/bullae and decreased VA, symptoms usually worse in morning b/c of overnight corneal swelling *Bullous Keratopathy - end stage of ANY endothelial problem, large bullae form in the epithelium and eventually rupture, causing severe pain/photophobia - treat like HYDROPS but probably no corneal transplant (must distinguish from HYDROPS - keratoconus history) 3) Subepithelial scarring - from chronic corneal edema Treatment: 5% NaCl ung/gtt QHS and A.M. - if later in disease may give throughout day, hair dryer at arm's length aimed at eyes (on low or medium heat to dry out corneal surface), topical beta-blockers to reduce IOP (reduces imbibation pressure) |
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Coat's White Ring
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Corneal degeneration
Small oval ring made up of discrete white dots Usually inferior cornea Associated with previous corneal metallic foreign bodies No symptoms - no treatment |
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Iron Deposition
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Corneal degeneration
Hudson-Stahli line May be green, brown, yellow, white Located in deep epithelium at the line of palpebral closure, about .5mm wide Horizontally oriented, variable in size, location etc... Tear film is source of iron Seen in 75% of patients over 50 Causes no symptoms - no treatment |
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White Limbal Girdle of Vogt
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Corneal degeneration
Fine white lines that run radially in the periphery of the cornea, appears similar to corneal arcus on low mag May or may not have clear zone Directly associated with age Subepithelial hyperelastosis and mild hyaline degeneration - similar histologic changes to pingueculae No symptoms - no treatment DISTINGUISH FROM BAND KERATOPATHY (ON HIGH MAG LOOKS LIKE SQUIGGLY LINES) |
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Corneal Arcus
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Corneal degeneration
Grayish white or yellow deposits, made up of fine dots, separated from the limbus by a clear interval .2 to .3mm wide Occurs initially inferiorly, then superiorly, circumferentially in later stages Sharp peripheral (outer) border and diffuse central border Incidence increases with increasing age in otherwise healthy patients; men and blacks develop arcus before women and whites Often associated with hyperlipidemia if seen in patients less than 30 to 40 years old - and remember demographics also Refer at-risk groups for lipid profiles |
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Calcific Band Keratopathy (Band K)
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Corneal degeneration
Result of several inflammatory and degenerative conditions, and is not itself a specific entity in most cases In superficial stroma Most commonly seen after chronic uveitis, chronic glaucoma, corneal edema, elevated serum calcium also Usually begins near limbus at 3/9 as a grayish haze at Bowman's layer with sharp peripheral border - separated from limbus by a clear zone "Swiss Cheese" appearance from gaps in haze, probably where nerves pierce Bowman's As disease progresses, bands progress centrally and become more chalky-white Seen only in interpalpebral zone, presumably from evaporation of tears (if lower, probably arcus) Treatment - none unless VA decreased or mechanical irritation, in which case Chelation with EDTA - remove epithelium, apply EDTA in drop form, let heal - can also try manual scraping of deposits, PTK may be most useful when combined with EDTA and/or lamellar keratoplasty in severe cases |
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Salzmann's Nodular Degeneration
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Corneal degeneration
Elevated blue/gray fibrous lumps in the superficial stroma just beneath epithelium (lumps are made of collagen) Gradually developing process that appears in corneas that have been inflamed many years earlier Most common association is phlyctenular kerato-conjunctivitis (but also associated with trachoma, vernal disease, K sicca, exposure keratopathy, scarlet fever, measles, etc...) Females > Males Iron pigment rings may be seen at the base of the lesions Usually no symptoms unless lumps form in the line of sight or marked elevation causing drying, dellen, RCE Treatment - usually not necessary, lumps can be removed individually if not heavily vascularized, Lamellar KP or PTK also used |
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Lipid Keratopathy
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Corneal degeneration
Similar in appearance to corneal arcus, but seen in one area only Associated with previous blood vessel ingrowth into cornea in response to prior trauma, ulceration, IK, herpetic keratitis Lipid deposition occurs from leakage of blood vessels |
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Terrien's Marginal Degeneration
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Corneal degeneration
BILATERAL BUT ASYMMETRICAL thinning of peripheral cornea Usually begins superiorly as a fine punctuate stromal opacity similar to arcus with a lucid zone Area then becomes vascularized from limbus, followed by indentation of the limbal area Irregular or against the rule astigmatism may form as the area involved is flattened Epithelium remains INTACT but the thinned area may bulge ectatically Perforation may occur spontaneously or after minor trauma Usually non-inflamed and painless, only symptoms occur as a result of any visual disturbance Treatment - no effective treatment, peripheral lamellar keratoplasty is necessary in cases of extreme thinning or perforation MUST DISTINGUISH FROM MOOREN'S ULCER - peripheral corneal thinning disorder but is INFLAMMATORY (lots of injection) in origin and involves epithelial disruption (ulceration) |
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Senile Furrow Degeneration
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Corneal degeneration
Shallow, non-vascularized thinning in peripheral cornea, often just peripheral to arcus Furrow is usually .5mm or less in width More common in elderly patients No symptoms - no treatment |
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Corneal Guttata
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Hassal-Henle bodies
See Fuch's dystrophy card |
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Iridocorneal Endothelial Syndromes (ICE)
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Clinically UNILATERAL
Generally involve corneal edema, progressive iris deformity, glaucoma Fundamental defect is corneal endothelial abnormality, abnormal endo cells migrate over the anterior chamber and contract, causing secondary glaucoma and PAS All patients have "hammered silver" appearance of posterior cornea, and variable corneal edema, iris atrophy, corectopia (displaced pupils), PAS, iris nodules, glaucoma Most frequently patients complain of decreased VA and abnormal-looking irides 3 types |
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Chandler's Syndrome
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Iris is normal or has mild stromal atrophy, blurry vision
Patient usually complains of decreased VA MOST EDEMA OF THE THREE TYPES Decreased VA, normal to high IOP, moderate to severe edema, mild to moderate corectopia, 5% have glaucoma |
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Progressive Iris Atrophy
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Also known as EIA - essential
Iris shows extensive changes with marked atrophy and hole formation Patient usually complains of iris changes High IOP, mild to moderate corneal edema, moderate to severe corectopia, 37% have glaucoma |
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Cogan-Reese
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Iris nodules ("raised nevi" in some sources) with any degree of iris atrophy
Patient usually complains of iris changes High IOP, mild to moderate edema, moderate to severe corectopia, 50% have glaucoma |
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Metabolic Diseases of Cornea
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Cause clouding
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Adult Inclusion Conjunctivitis
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Caused by Chlamydia Trachomatis (TRIC)
STD - usually new sex partner within 1-2 months Incubation is 5-12 days Acute follicular (large - usually on bulbar conjunctiva and in caruncle - and also more inferior) AND papillary conjunctivitis with scant mucopurulent discharge, often described as "STICKY," mild PAN possible, may have SEI's and mimic EKC, monocyts and neutrophils, chronic red eyes non-responsive to traditional therapy should prompt investigation, females usually unaffected genitally, or couuld have UTI-like symptoms (could eventually cause pelvic inflammatory disease) NEONATE HAS NO FOLLICLES, HAVE RED, SWOLLEN LID Treatment: azithromycin 1g QD x 1 dose, or doxycycline (has anti-inflammatory properties too) 100mg BID 1st day then 100mg QD x 21 days (alternate is tetracycline 250mg QID x 21 days - DO NOT GIVE THE CYCLINES TO KIDS UNDER 8 OR IN PREGNANT/LACTATING MOMS), or erythromycin 500 QID x 21 days CO-MANAGE WITH GYNECOLOGIST/UROLOGIST & TEST SEX PARTNERS |
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Trachoma
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Caused by Chlamydia Trachomatis (TRIC)
Underdeveloped countries, rarely in US, MOST COMMON CAUSE OF PREVENTABLE BLINDNESS OR DECREASED VISION IN THE WORLD, transmitted eye to eye via flies Follicular hypertrophy occurs first (upper/lower palpebral conjunctiva, limbus), papillary response associated with obliteration of follicles, photophobia, tearing, mild mucopurulent discharge, ARLT'S LINE - represents superior tarsal horizontal conjunctival scarring and leads to entropion, trichiasis and mucin-deficient dry eye from goblet cell destruction; punctal stenosis possible secondary to scarring but isn't enough to combat dry-eye symptoms, superior SPK, pannus, edema, HERBERT'S PITS - scarred limbal follicles, small depressions around limbus - DIAGNOSTIC Stages: 1) Incipient: immature follicles on superior tarsus with minimal papillary hypertrophy, may see early SPK or pannus 2) Florid/Established: 2a=Follicular hypertrophy - superior tarsus has predominance of mature follicles, large, soft, liable to rupture under pressure, limbal follicles, pannus, corneal SEI's; 2b=Papillary hypertrophy - intensification of the inflammatory response with obliteration of follicles by papillae, necrosis of follicles 3) Cicatrizing Trachoma: beginning of scar formation, Herbert's pits, Arlt's line begins to form, entropion/trichiasis may form 4) Healed: inflammation resolved, replaced by scar tissue, no follicles/papillae, no SEIs, could have corneal involvement from secondary bacterial keratitis which may lead to blindness and results from corneal insult via trichiasis/scarring Treatment: same as adult inclusion conjunctivitis |
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Neonatal Inclusion Conjunctivitis
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Chlamydia is leading cause of neonatal infectious conjunctivitis in the US
Incubation of 5-14 days Papillary response only, mild/moderate mucopurulent exudate, lid edema, chemosis, pseudomembranes, can cause pneumonitis Treatment: erythromycin 50mg/kg/day divided into 4 doses x 10-14 days, NO CYCLINES!!, can add erythromycin ung also adjunctively, a second course of treatment is often required b/c e-mycin is not 100% effective Prophylaxis is standard now with erythromycin |
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Toxic and Irritative Follicular Conjunctivitis
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Caused by long-term use of certain ocular medications, particularly strong miotics, also seen as a toxic response to heavy makeup use, environmental irritants, radiation, soaps, hypersensitivity reaction...CHECK HISTORY
May be minimal mixed papillae and follicles Usually UNILATERAL Treatment: switch ocular medications, remove antigen, AT for supportive therapy |
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Superior Limbic Keratoconjunctivitis
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Chronic/recurrent inflammation of the superior palpebral and bulbar conjunctiva and cornea (10-2)
Disease course may last several months to years Etiology unknown (associated with dry-eye, thyroid disease) but is thought to result from repeated microtrauma of the superior bulbar conjunctiva which is abnormally lax, tight upper lids, SCL wear (remove), prominent globes (like in thyroid disease) Marked hyperemia, thickening, general irritation of superior conjunctiva and cornea, abnormal densities of goblet cells and abnormal limbal epithelial cells, MAJOR DIAGNOSTIC SIGN IS RB STAINING OF ENTIRE ARE INVOLVED - also LG, usually BILATERAL and ASYMMETRICAL, symptoms usually more severe than would be predicted by clinical picture - FBS, photophobia, pain, filaments Treatment: in order of mild to severe - AT, punctal occlusion, steroid pulse - acetylcysteine drops (mucolytic - not commonly used) - cromolyn sodium drops - mast cell stabilizers - .5% silver nitrate causes sloughing of conjunctiva which may grow back normally - BSCL - thermal cautery of conjunctiva (sloughing) - surgical conjunctival resection with or w/o amniotic membrane graft/transer DON'T USE ANTIBIOTIC - CORNEA USUALLY NOT SIGNIFICANTLY STAINED |
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Phylctenulosis
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Two forms: conjunctival/corneal
Conjunctival: focal nodule(s) of limbal tissue usually in response to staph exotoxins, less commonly from TB, staph bleph usually present so will go away with bleph treatment Corneal: appears as a whitish plaque on the cornea itself, same associations as conjunctival variety, but may be protracted in its course (could be TB or sarcoid) USUALLY ANYTHING ON LIMBUS IS INFLAMMATORY, NOT INFECTIOUS Treatment: for staph bleph - lid hygiene, combo QID, mild vasoconstrictors, IF TB SUSPECTED - REFER TO HEALTH DEPT FOR CXR/PPD, could also use topical cyclosporine-A (restasis) |
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Ophthalmia Neonatorium
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Conjunctivitis in a neonate 1 month post-partum
3 routes: 1) Ascending infection from cervix to vagina secondary to premature membrane rupture 2) Mom has an infection in birth canal, baby infected during passage 3) Postpartum contact 5 Classes: 1) Chemical - related to former use of silver nitrate solution as prophylaxis 2) Chlamydial 3) Gonococcal - usually 24-48 hours after birth, hyperacute purulent discharge, lid edema, chemosis; Treatment: ceftriaxone IV or IM, 30mg/kg/day divided, e-mycin ung, frequent lavage 4) Non-gonococcal, non-chlamydial, bacterial - similar picture to adult acute bacterial conjunctivitis, Treatment: e-mycin/bacitracin ung for Gram+, tobramycin/gentamicin gtt for Gram-, MUST DISTINGUISH FROM GONOCOCCAL 5) Herpetic/Viral - usually appears within 2 weeks of birth, may be preceded by lid vesicles if herpetic, Treatment: similar to adult herpetic infection, viroptic 1% q2h and taper according to response and treat for 3 weeks for HERPES SIMPLEX ONLY Prophylaxis is mandatory in all states now - use e-mycin ung, used to use Crede's prophylaxis: silver nitrate which is effective against gonococcus but causes chemical conjunctivitis itself |
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Neurotrophic Keratopathy
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Loss of corneal innervation causing epithelial defect
Caused by s/p infection by varicella-zoster, HSV, stroke, complication of CN V surgery, irradiation to eye, tumor (acoustic neuroma) Signs - loss or reduction of corneal sensation, epithelial defects with NaFl stain, perilimbal injection, possible corneal ulcer with associated iritis - ulcer has gray heaped up border, oval in shape, and is usually located in lower half of cornea Symptoms - red eye, FBS, swollen eyelid - protective ptosis Workup - history, test corneal sensation, signs of corneal exposure, CT/MRI if tumor suspected Treatment - AT if mild, antibiotic ung, cyclo, PP or BSCl if corneal defect, if infected treat as corneal ulcer, tarsorrhaphy, BSCL, pain management, if from HSV/HZV use oral prophylaxis |
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Thermal/UV Keratopathy
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Damage to cornea from thermal burn or UV exposure, symptoms usually appear 8-12 hours following exposure
Symptoms - moderate to severe ocular pain, FBS, red eye, tearing, photophobia, blurred vision Signs - confluent SPK in interpalpebral area, conjunctival injection, eyelid edema, absent or minimal corneal edema, typically miotic pupils, may present as droplet keratopathy - yellowish oily deposit in subepithelial cornea and conjunctiva Treatment - treat as corneal abrasion; antibiotic ung, cylco, BSCL for mild, BILATERAL PATCHING is ideal if feasible for patient |
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Thygeson's SPK
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Coarse punctate epithelial keratitis of unknown etiology, thought to be related to subclinical viral infection and/or immune-based disease
S/S - photophobia, FBS, tearing, faint gray coarse PEK defects usually round to oval or stellate and made up of miniscule opacities - these stain with RB and are slightly elevated, if microerosions occur with opacities then NaFl staining occurs (stippling), usually BILATERAL and can be ASYMMETRICAL, QUIET, WHITE EYE, strictly epithelial, no stromal involvement, usually chronic with recurrences up to 30 years, only corneal involvement, TRUE SPK, may look like large infiltrates but are actually many small ones grouped together Treatment - weak topical steroids, alrex, pred mild QID for 3-4 days then quickly tapered, BSCL and PP has been advocated by some, however most wear CL already so removing them is essential, NO ANTIBIOTIC |
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Non-Herpetic Interstitial Keratitis
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Look at previous cards
Vascularization and infiltration affecting all or part of the corneal stroma Usually associated with systemic disease Ghost vessels from previous processes of active inflammatory vascularization are common (look like gray lines or small tubes) IF RED EYE WITH ACTIVE IK - USUALLY HERPETIC IF WHITE EYE WITH GHOST VESSELS, STROMAL OPACIFICATION - NON-HERPETIC/SYPHILITIC 90% of non-herpetic IK are secondary to syphilis - immunologic reaction to spirochete organism For congenital syphilitic cases, 80% are bilateral and 2/3 of these are ages 5 and late teens In aquired syphilis, 60% are UNILATERAL and usually condition is more mild and easier to treat IF NON-SYPHILITIC AND NON-HERPETIC - TB Acute phase shows infiltration, edema of endothelium, KP's, miosis, small stromal opacities Most cases encountered will be residual effects - diffuse stromal scarring, opacification, ghost vessels In TB cases, cornea is typically involved in peripheral inferior sector only and is RING shaped Treatment - keratoplasty if vision impaired, in active IK, steroids may be necessary for 1-2 years, cyclo, IDENTIFY AND TREAT SYSTEMIC CONDITION |
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Juvenile Syphilis
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Caused by spirochete, treponema pallidum
Congenital or acquired, acquired is chronic, systemic STD Males>Females, nonwhites>whites, higher in low socioeconomic patients, HIV patients, homeless, etc... "The great imitator, the great mimic, the great masquerader" because it looks like many other ocular diseases Associated with IK, epscleritis, scleritis, uveitis, chorioretinitis, papillitis, retinal vasculitis, exudative RD Three forms: 1) Primary - genital chancre (papules that become painless ulcers), these appear about a month after infection and heal in another 1-2 months, organism enters blood and lymphatics and disseminates, secondary will almost always progress if not treated 2) Secondary - generalized rash and lymphadenopathy 4-10 weeks after infection, especially prominent on palms of hands and soles of feet, these areas heal with scarring, patients feel unwell during this phase, only 10% in this stage have ocular involvement, usually go into a latent phase next (without treatment) 3) Tertiary - can have cardiac and systemic-dermatologic involvement but for our purposes the NEUROSYPHILIS findings are most important - light-near dissociated pupil (Argyl-Robertson pupil), optic neuropathy, uveitis, other ocular and intraocular inflammatory findings Ocular involvement at any stage - conjunctival chancre/injection, uveitis, iris nodules, scleritis, epsicleritis, IK, cataract, uveitic glaucoma, retinal periplebitis, optic neuropathy Congenital Syphilis - can present with many of the same ocular findings PLUS "Hutchinson's triad" = peg-shaped notched teeth, deafness, IK - if mother passes to unborn child, developmental problems will occur if mother isn't treated with penicillin, treating the child after birth but developmental problems will be permanent DEFINITIVE DIAGNOSIS OF SYPHILIS - FTA-ABS = flurosceing treponemal antibody absorption (will pe positive for patient's entire life if ever infected with syphilis), VDRL = veneral disease research lab, RPR = rapid plasma reagin Treatment - IV or IM penicillin with probenecid |
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Ocular Cicatricial Pemphigoid
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A type of systemic-associated conjunctivitis
Chronic autoimmune disease characterized by scarring of the mucous membranes (conjunctiva, soft palate, nasal mucosa, genito-urinary system, esophagus, skin) Average age of onset is 65 years, females>males, 70-75% have ocular involvement, first sign is usually chronic, recurrent unilateral conjunctivitis, scarring, perivasculitis, squamous metaplasia, loss of goblet cells, waxes and wanes Stage 1: subepithelial fibrosis Stage 2: fornix foreshortening Stage 3: symblepharon - eyelids adhere to eyeball Stage 4: ankyloblepharon (eyelids adhere to each other) and surface keratinization - eye becomes immobile Dry eye present in late disease Vision is lost from keratopathy, corneal neovascularization, corneal ulceration and scarring FIRM DIAGNOSIS REQUIRES IMMUNOHISTOCHEMICAL CONFIRMATION PRIOR TO INITIATING TREATMENT Treatment - Non-preserved AT aggressively, topical retinoid ung (vitamin A) - helps goblet cells, treat chronic bleph aggressively with lid hygiene, oral doxycycline, topical antibiotics, chemotherapy for active and rapidly progressive cases - prednisone (always start with steroids) 1mg/kg/day, eventually tapered over 8-16 weeks, cyclophosphamide, for cases that are less active and not rapidly progressive - prednisone, dapsond REFER TO RHEUMATOLOGIST FOR IMMUNOSUPPRESSANTS/CO-MANAGE, REFER TO OPHTHALMOLOGIST FOR SYMBLEPHARON REMOVAL |
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Stevens-Johnson Syndrome
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a.k.a Erythema Multiforme
Can appear clinically similar to OCP, but is not relentless and progressive, occurs idiosyncratically in some patients, and is seen as mucosal inflammation in response to the administration of various drugs or following systemic infectious disease During acute phase, patient may appear to have a severe pseudomembranous conjunctivitis, following resolution, fibrosis of the conjunctiva with associated entropion and trichiasis may be present, may have predisposition to autoimmune disease Can remove antigen and will resolve Treatment - aggressive topical steroids - pred forte q1h, and refer to ophthalmologist from scar tissue removal |
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Ocular Rosacea
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Seen in patients with acne rosacea
General increase in lipid secretion See hyperemia of lid margins, FBS, BURNING, recurrent chalazia Treatment - doxycycline 100mg BID first day, 50-100mg QD for 21 days, or tetracycline 250mg QID, or retinoic acid |
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Psoriasis
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Affects 1-2% of population, average age of 28
Hyperproliferation of keratinocytes in epidermis Conjunctiva usually shows non-specific inflammation, chronic in nature, and is almost always associated with eyelid margin involvement Plaques seen in this disorder can extend onto the conjunctiva and cause scarring, which can be confused with phlyctenulosis Bleph can take the form of redness, edema, and skin plaques Treatment - supportive, also systemic treatement |
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Connective Tissue Disease
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Thought to have autoimmune etiology
1) SLE - 3rd-4th decade, females>males, butterfly rash on face, nonspecific conjunctival findings (hyperemia, fine papillae) Treatment - conjunctiva supportively, systemic treatment with aspirin, chlorquine, steroids 2) Polyarteritis nodosa - arteritis of small and medium vessels, from severe hypersensitivity, many systemic findings with non-specific conjunctivitis (may see subconj hemorrhage), males>females Treatment - supportive, systemic conditions with steroids 3) Relapsing polychondritis - recurrent inflammation of cartilage, seen in 3rd-6th decades, females=males, mild conjunctivitis, more often episcleritis Treatment - supportive, system with steroids 4) Reiter's syndrome - triad of nongonococcal conjunctivitis, urethritis, arthritis, may be associated with chlamydial infection, males>>females, mild, nonspecific conjunctival findings Treatment - some success with oral tetracycline, steroids for systemic Others: rheumatoid arthritis, scleroderma, dermatomyositis, RF....supportive |
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Subconjunctival Hemorrhage
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Red/pink lesion
Subconjunctival blood from breaking of small capillaries Caused by hypertension, bleeding disorders, valsalva maneuvers, trauma, aspirin overuse, some forms of conjunctivitis, idiopathic (MOST COMMON) - CHECK HISTORY Similar to bruise under skin, may involve entire globe Treatment - none, can use alternating hot and cold packs as frequently as possible but not more than 10 minutes - cold for first 24 hours then hot after - still alternate, if you have to choose one do cold, usually resolves within 2 weeks, changing colors rather dramatically during resolution, consider full medical evaluation if recurrent |
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Capillary Hemangioma
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Red/pink lesion
Raised broad-based conjunctival vascular mass - benign More commonly seen in inner canthus or in fornix Usually congenital, or first appear in young years, may enlarge with age, and are worse if child is crying The only concern is cosmesis, may be excised or cauterized if treatment is desired - refer MAY NEED TO DISTINGUISH FROM KAPOSI'S IN ELDERLY |
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Kaposi's Sarcoma
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Bright red/purple masses and hemorrhages
Tumor of endothelial origin, associated with AIDS, probable herpes virus association, if mucous membranes are involved (conjunctiva) usually means a later manifestation of AIDS 18% of KS patients have conjunctival tumors Treatment - radiation, or topical IFN a2b with or without IFN injections, refer for biopsy |
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Lymphoid Tumors
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Light pink/salmon-colored
May be benign ("benign reactive lympoid hyperplasia") or malignant ("lymphoma") May appear in bulbar conjunctiva, FLESHY MUST EXCISE ALL SUSPECTED LYMPHOID TUMORS AND BIOPSY TO DETERMINE IF BENIGN OR MALIGNANT (CLINICALLY INDISTINGUISHABLE) Refer to ocular oncologist |
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Concretions (Lithiasis)
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Small white/yellow calcium deposits usually 1-3mm in size
May be in upper or lower palpebral conjunctiva, patient usually asymptomatic, but if causes irritation (FBS) can cut and remove, single or multiple, common Only refer if serious problem for patient |
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Retention Cysts
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Fluid-filled cysts, usually clear, seen anywhere in conjunctiva, vessels under look magnified
May be lymphatic fluid or with secretions from glands of Krause and Wolfring Usually asymptomatic, if they are treated by draining, they usually refill with several days If recurrent and symptomatic, refer or surgical excision of entire gland involved |
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Pinguecula
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Hyperplasia of conjunctival tissue, probably in response to some environmental irritation, usually seen on sun-exposed areas of bulbar conjunctiva
Usually asymptomatic, may become inflamed, may be a cosmetic concern, may cause corneal dellen (area of non-wetting) Treatment - lubricants/decongestants (to help shrink vessels on pinguecula), use protective wear, rarely may surgically excise (if dellen, excise) |
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Pterygium
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Basophilic degeneration of bulbar conjunctival stroma which invades the cornea, most nasal
Triangular or wedge-shaped fleshy mass with the apex pointing towards center of cornea Usually see an iron line preceding growth pattern (Stocker's line - only associated with Pterygium) Often become inflamed/irritated, if this occurs, treatment is the same as for pinguecula Ultimately will require surgical excision when expands to 2mm before pupil border, if surgery alone up to 67% will recur - conjunctival sliding flap procedure is best option |
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Dermoid Cyst
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Congenital tumors from mesoderm and ectoderm (dual origin), not malignant, primarily composed of collagen
Raised circumscribed white to pale yellow lesion, usually located in inferior temporal limbal area May have hair associated with lesion, may involve cornea, conjunctiva, sclera Usually don't enlarge, but excise if cosmesis a problem |
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Axenfeld's Loops
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Blue/Black ciliary nerve loops on scleral surface, usually seen near limbus - pigment due to blood vessels/nerves going through wrong layers (bring pigment with them)
Generally no symptoms involved, no treatment necessary, anatomical variation only |
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Nevus of Ota
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Congenital subepithelial melanosis, appears blueish in color because the pigmentation is in the dermis rather than the epidermis
Appear along first and second division of cranial nerve V Overall rare, but relatively more common in Japanese patients than other races Approximately 4% of these patients will develop melanoma, so patients should be followed (photodocument) annually for changes |
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Conjunctival Nevus
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Usually congenital, or develops in early years
Smooth, flat surface lesions with well-circumscribed edges, may see clear (most likely benign) cysts within lesion, more common nasally Treatment - photodocument, refer for biopsy if lesion enlarges or shows threatening changes (ulceration, hemorrhage, change in pigmentation, feeder vessels), may grow more during puberty but still follow |
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Adenochrome Deposits
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Black, well-circumscribed pigment lesions as a result of epinephrine or Propine therapy
No treatment |
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Melanosis
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1) Primary Acquired Melanosis (PAM) - spontaneous development of irregular diffuse flat patches of conjunctival pigmentation
Usually appears between ages of 30 and 40, asymptomatic except for cosmesis, up to 15% may develop malignant melanoma with highest percentage of conversion in choroidal melanoma May disappear over 1-3 years Treatment - photodocument, refer for biopsy if suspicious, follow closely at first diagnosis (q 3-6 months) 2) Racial Melanosis - dark skinned patients often have bilateral patches of pigment clustered in the interpalpebral and peri-limbal areas, these are stable throughout life and no reason for concern Lighter skinned more likely to be cancerous |
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Conjunctival Malignant Melanoma
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Pigmented lesions which may resemble benign melanosis or nevus, may be de novo or in areas of previous benign pigmentation
Males=females May be multiple lesions (more suspicious) Treatment - photodocument any patient with acquired pigmented lesions (or at first diagnosis if onset unknown) and follow q3-6 months, refer for biopsy/excision at first signs of threat, can spread to adjacen tissues Note: primary ocular melanoma is rare - almost always associated with Dysplastic Nevus Syndrome (DNS), which is a disease in which MANY nevi form on both covered and non-covered (sun-exposed) areas during the life span of patient, DNS has autosomal dominant inheritance pattern, the lifetime risk in a patient with DNS of developing cutaneous melano is nearly 100% COULD ALSO BE METASTISIS FROM OTHER MELANOMA |
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Papilloma
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Sessile (flat) or pedunculated (on a stalk) lesions with irregular surface
More common in patients over 40 years old, usually seen in fornix or caruncle Two forms: viral (recurrences common, more likely to be multiple) and non-viral (single lesions more common, may be pigmented, more likely to be pre-cancerous) MUST REFER BECAUSE CAN'T DISTINGUISH FROM OSSN Note - Basal cell carcinomas of the conjunctiva are extremely rare, but can appear similar to a papilloma |
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Sebaceous Cell Carcinoma
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Not a typical "tumor" because it's not in the form of a lump or bump, may mimic blepharitis
Consider a tissue biopsy if the patient has a highly recalcitrant case of blepharitis, usually takes the form of intraepithelial dysplasia (abnormal cell changes), so it is extremely difficult to detect clinically May arise de novo, but is usually related to an underlying invasive tumor of Meibomian or Zeis gland or both |
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Ocular Surface Squamous Neoplasia (OSSN)/ Conjunctival Intraepithelial Neoplasia (CIN)/ Squamous Cell Carcinoma
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Third most common ocular tumor in older population (after melanoma and lymphoma)
Higher risk characteristics = pale skin/iris, residing less than 30 degrees latitude from equator, male gender Average age of patient = mid 50s, related to UV-B exposure, perhaps from abnormal stem cell development at limbus, lesions have many different presentations, but generally are slightly elevated, sharply demarcated, with feeder vessels, and may range in color from gray to reddish gray, generally seen at the limbus within palpebral fissure opening Very difficult to diagnose properly without cellular analysis Treatment - topical IGN a2b drops with or without injections also, if surgery done - either Moh's microscopic technique or a wide excision with 2-3mm clear margins Usually see firework like pattern (but could be papilloma) Average recurrence is 30% overall but the recurrence rate seems to be lower with IFN treatment CIN - when tumor completely confined to the epithelium (subtype of OSSN) |
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Anterior Uveitis Intro
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Uveal tract is the densely pigmented, vascular tunic of the eye between the sclera and retina, made up of IRIS, CILIARY BODY, CHOROID
Primary function of the uveal tract is to supply nutrition to the eye, secondary functions are to assist in refraction through accommodation and pupillary constriction Uveal tract mirrors all systemic vascular diseases due to its dense vascular makeup IRIS - most anterior of uveal structures, provides nutrition of anterior segment by diffusion through the aqueous humor, also has sphincter and dilator muscle to control amount of light entering eye CILIARY BODY - the inner layer of the uveal tract which secretes aqueous, also contracts producing variable tensions on the lens zonules, thereby changing refraction CHOROID - expandable vascular plexus supplying nutrition to the rods and cones (outer retina) Anterior uveitis is inflammation of anterior uvea - COMPRISED OF IRIS AND CILIARY BODY, IRIS ONLY = IRITIS, CB ALSO = IRIDOCYCLITIS Many causes possible, usually co-managed with rheumatologist, internist, infectious disease specialist, immunologist etc... CRITICAL SIGNS = cells/flare in anterior chamber Not a static condition, could present differently every time, most widely accepted scheme is based on the appearance of KPs NONGRANULOMATOUS - KPs are small, dry, discrete white cells on the corneal endothelium, more separated from each other GRANULOMATOUS - KPs are wet, "mutton-fat" clusters of white blood cells on the endothelium, see Koeppe's nodules (clusters of cells on the pupillary border of the iris), Busacca's nodules (clusters of cells on the anterior iris surface) Better way to classify is based on pathophysiologic mechanisms Trauma, Infection, Immunologic, Masquerade (vascular, infectious, congenital, metabolic/degenerative, neoplastic) Anterior usually inflammatory, posterior usually infectious Leading cause is IDIOPATHIC - second biggest group of anterior uveitis is caused by HLA-B27 associated conditions HLA-B27 is a genotype located on the short arm of chromosome 6, sometimes associated with specific rheumatologic disease, present in 1-8% of general population but in 50-60% of patients with anterior uveitis Examples are ankylosing spondylitis, Reiter syndrome, IBD, psoriatic arthritis - these patients do not have a +Rh factor but do have a positive HLA-B27 (check for symptoms), typically present with acute, nongranulomatous anterior uveitis |
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Anterior Uveitis Active Signs/Symptoms
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CELLS AND/OR FLARE REQUIRED FOR DIAGNOSIS OF ANTERIOR UVEITIS
Cells = WBCs and pigmented cells in AC - WBCs released from uveal vessels Flare = milkiness of aqueous, visible as the conical beam of light passes through it - protein is transudate from uveal vessels Photophobia = mild light sensitivity to severe pain and blepharospasm (b/c iris inflamed) - trigeminal stimulation from ciliary spasm Pain = mild to severe, may be referred to periorbital region, aggravated by light - irritation of ciliary nerves, ciliary muscular spasm SOME SERIOUS LOOKING CASES MAY NOT BE THAT PAINFUL - LOOK FOR SYSTEMIC CAUSE B/C PATIENT MAY BE USED TO LOW-LEVEL PAIN Lacrimation = trigeminal irritation of lacrimal gland Small pupils = not always present, usually relative to other eye - vasodilation of iris vessels, prostaglandin release IOP Variation = usually indicates CB involvement, most cases of acute uveitis have lower IOP, HZV USUALLY HIGHER - low from decreased aqueous production, high from trabeculitis Blurred vision = mild to moderate, related to severity of inflammation - clouding of media, poor tear film, macular edema, or other posterior uveitis KPs = deposits of inflammatory cells on endothelium, usually inferior - WBCs from iris and uveal vessels Fibrin (cyclytic membrane) = coagulation of exudates in AC (severe cases) - extreme inflammation with accumulation of fibrin (be careful of sticking on pupil - b/c causes high pressure within minutes) Iris Nodules = Koeppe/Busacca - inflammatory cellular infiltration into iris stroma Hemorrhage = blood in AC (hyphema - rare) - uveal vessel hemorrhage Hypopyon = purulent exudate in lower AC (severe cases) - purulent exudation from inflamed uveal vessels NOTE: if not from trauma, hypopyon is highly suggestive of HLA-B27 disease, Behcet disease, or endophthalmitis Ankylosing Spondylitis = always think of this when shown an X-ray of sacro-iliac joint (lower back pain) When seeing a CXR, think of TB or Sarcoidosis (could be Horner's) |
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Anterior Uveitis Chronic Signs
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IOP Variation = low IOP is characteristic, however glaucoma may develop as complication during acute or chronic stages - decreased aqueous production, high IOP if TM becomes clogged or inflamed (HZV)
Iris atrophy = SUGGESTIVE OF HZV, diffuse, patchy, or focal atrophy of iris pigment epithelium - prolonged inflammation of iris stroma and epithelium Synechiae = POSTERIOR: posterior surface of iris adheres to lens in pupillary zone, PERIPHERAL ANTERIOR SYNECHIAE: adhesion of anterior surface of iris to angle structures (PAS) - heavy exudation of protein (posterior), shallowing of AC from pupillary block, organization of exudates in the angle or from swelling of iris root (PAS) Band Keratopathy of cornea = deposition of calcium in Bowman's memrane - can be seen in any chronic inflammation Lens Precipitates (LPs) = cells on anterior lens capsule - from exudation of uveal vessels, same as KPs except located on lens vs. cornea Cataract = opacification of lens - from nutritional deprivation of lens fibers, or as a toxic response to inflammatory cell breakdown, or from topical or systemic steroid use Retinal Complications = CME, neovascularization, epiretinal membrane formation etc... |
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Anterior Uveitis Evaluation
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Complete history with systemic health history and ROS, complete ocular examination with TONO and DFE (even if patient is walk-in or emergency patient)
If a UNILATERAL NONGRANULOMATOUS uveitis develops for the first time and the history/examination are unremarkable, then usually no further workup is required If uveitis is BILATERAL, GRANULOMATOUS, OR RECURRENT (mandatory after third recurrence), many of the tests listed can and should be ordered, based upon the patient history and examination findings Consultation with a GI specialist, rheumatologist, neurologist, or other appropriate subspecialists is warranted CBC with differential, ESR, HLA-B27 and/or HLA B-5, ANA, RPR or VDRL (tests for active case of syphilis), FTA-ABS or MHA-TP (tests for syphilis during patients lifetime), PPD, CXR, Lyme titer, ACE, Toxoplasmosis titer when posterior findings present (HIV patients especially), HIV testing These are also tested for in scleritis/epscleritis |
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Anterior Uveitis Treatment
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Mandatory:
1) Address any accompanying infections, or other conditions when present - refer, co-manage 2) Cyclo - Atropine QD (preferred), Scopolamine BID, Homatropine TID, Cyclopentolate QID - contraindications include narrow angles, iris-fixed IOLs, hypersensitivity 3) Steroid - prednisolone acetate remains the most effective intraocular anti-inflammatory, dose depending on severity, for moderate start with 1 gt q 1-2 hours then taper, in severe/early cases could be up to q 15 minutes - still need topical even if on orals If a patient is only on steroid for a few doses (less than 10) no taper is generally needed For taper, usually start with last dose reduced by one drop per day for that same amount of days, keep doing this until patient takes one drop for one day If there is a risk for ocular infection, use cyclo first, then add steroid after epithelium fully heals, or in conjunction with an antibiotic as prophylaxis against infection, remember absolute contraindications!! - bacterial ulcer suspected, fungal infection which still has disrupted epithelium, acanthamoeba infection with epithelial disruptment, herpes simplex 4) Periocular/Systemic steroids - if the uveitis is severe and not responding to topical steroids 5) Treat elevated IOP if present - on test just say IOP agent 6) Immunomodulatory and/or cytotoxic agents - only used as a last resort for severe, sight-threatening inflammation which has been unresponsive to steroids 7) Surgery - for complications of uveitis (cataract, corneal edema etc...) |
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Acute/Non-granulomatous Anterior Uveitis
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Trauma (surgical/nonsurgical)
Ankylosing spondylitis - seen in young adult men, lower back pain, abnormal sacroiliac joint area by x-ray, elevated ESR, positive HLA-B27 IBD Reiter syndrome (can't see, can't pee, can't bend knee) - young adult men, conjunctivitis, urethritis, polyarthritis, occasionally keratitis (usually not enough to contraindicate steroids - if you need to prophylax, combo is too weak), elevated ESR, positive HLA-B27, may have recurrent episodes Psoriatic arthritis Glaucomatocyclitic crisis - acute IOP elevation with OPEN angles, corneal edema, fine KP, mid-dilated and fixed pupil, mild iritis, tends to be recurrent Lens-induced (Phacolytic) - lens proteins cause inflammation by leaking out (hypermature cataract, trauma etc...) Herpes simplex/zoster/varicella Postoperative iritis UGH syndrome (uveitis, glaucoma, hyphema) Behcet's disease - young adults, acute hypopyon (BIG), iritis, mouth and genital ulcers, erythema nodosum, often retinal vasculitis and hemorrhages, tends to be recurrent Lyme disease Mumps, influenza, adenovirus, measles, chlamydia Toxoplasmosis - obligate intracellular parasitic protozoan, usually causes a necrotizing retinochoroiditis with accompanying vitritis and anterior uveitis - congenital or acquired Others - tight CL, leptospirosis, Kawasaki's disease etc... |
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Chronic/Non-granulomatous
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Juvenile rheumatoid arthritis (JRA) - usually young girls, eye may be white and quiet, often BILATERAL, positiva ANA, negative RF, elevated ESR, occasional fever and lymphadenopathy, lots of cells/flare - usually already diagnosed
Chronic Iridocyclitis of children - same as JRA but no arthritis Fuch's heterochronic iridocyclitis - usually unilateral, few symptoms, diffuse iris stromal atrophy and loss of pigmentation causing a lighter colored iris, iris transillumination defects, blunting of iris architecture, fine KP over entire endothelium, vitreous opacities, glaucoma, cataracts common |
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Chronic/Granulomatous
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Sarcoidosis - blacks most often (African not Caribbean), usually BILATERAL, may have dense posterior synechiae, conjunctival nodules, posterior uveitis, mild to moderate anergy, abnormal CXR, elevated ACE
Syphilis - "great masquerader" - do FTA-Abs with VDRL (review syphilis) Tuberculosis - positive PPD, typical CXR, occasionally phlyctenular keratitis, posterior uveitis SLE - more common in females, may have associated retinal signs |
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Also cause AC reaction...
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Rhegmatogenous retinal detachment
Posterior segment tumor Juvenile xanthogranuloma Intraocular foreign body Sclerouveitis (uveitis secondary to scleritis) HIV |
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Congenital/Developmental Anomalies of the Iris
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Aniridia - autosomal dominant condition in which there is an absence of the iris, usually a small shelf of iris is visible gonioscopically, frequently associated with glaucoma, if spontaneous associated with Wilm's tumor (renal) - much more subject to lenticular/macular changes
Polycoria - AD, multiple pupils Ectopic pupils - AD, decentered pupil, a.k.a. corectopia Congenital pupillary mydriasis or miosis - most common form of anisocoria seen in infants, children, adults Persistent Pupillary Membrane - PPM - see lens cards Iris coloboma - inherited as irregular AD, missing wedge of iris tissue, usually situated inferior-nasally, results from non-closure of the fetal fissure at 7-8 weeks of gestation, often accompanied by coloboma of the lens, choroid, optic nerve Oculocutaneous Albinism - inherited as autosomal or x-linked recessive, deficiency of pigment of skin, hair, eyes, iris hypopigmentation ranging from light blue with pink reflex to light hazel, lack of pigmentation causes transillumination defects of the iris on retroillumination, associated with nystagmus, reduced VA, strabismus, macular hypoplasia - purely cutaneous albinos have no ocular complications Heterochromia - irregular AD, see difference in iris color between the two eyes or in different parts of the same eye in a patient |
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Cysts/Tumors of the Anterior Uveal Tract
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IF CLEAR ON B-SCAN, THEN PROBABLY A CYST
Epithelial cysts - ectodermal origin, seen in iris and CB, usually result from separation of pigmented and non-pigmented layers of iris or CB, can be congenital, post-inflammatory, post-traumatic and secondary to medicomentosa, BENIGN, fairly common, enlargement may lead to secondary glaucoma Benign Iris Nevus - "freckle" on the iris, neuroectodermal origin, proliferation of normal uveal melanocytes, very common occurence, appear as discrete or clustered pigment spots on the iris surface, more visible in light irides, may be slightly raised but usually flat Malignant Melanoma - neuroectodermal origin, seen in iris and CB, melanocyte is the cell of origin, most common primary intraocular tumor, more common after age 50, may be amelanotic or heavily pigmented tumor may necrose causing secondary inflammation Secondary Malignant tumors - may arise from intraocular structures via local invasion or metastasis from any organ in the body, most common site for "mets to the eye" is from the breast in women, from the lung in men, appearance varies |
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Degenerative and Atrophic changes of the Anterior Uveal Tract
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Iris stromal atrophy - overall thinning, especially in pupilary zone from sclerosis of stromal vessels
Pupillary miosis with slower pupillary response - from sclerosis and hyalinization of stromal vessels and muscles Iris depigmentation - pupillary frill is replaced with grayish border, translucent stroma with retroillumination, from sclerosis of stromal vessels |
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Effects of Trauma on Iris
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Iritis
Pigmentary dispersion - pigment deposition on iris, corneal endothelium, TM, and lens (Vossius ring), pigmentary glaucoma may subsequently develop, Kruckenberg spindle - seen in pigmentary glaucoma, vertical, not KPs Hemorrhage of Iris stromal vessels - infrequently seen, will cause hyphema Pupillary Miosis - from sphincter irritation and release of prostaglandins which in themselves cause miosis, may be accompanied by accommodative spasm Pupillary Mydriasis - transient sphincter paralysis Sphincter ruptures - may be partial or full thickness tear Iridoschisis - splitting of anterior leaf layer of iris from iris stroma Iridodialysis - separation of the iris root from the ciliary body and scleral spur |
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Effects of Trauma on the Ciliary Body
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Angle Recession - cleft in the ciliary body between muscular fibers, clinical appearance varies from subtle separation of the trabecular strands (iris processes) to "blown" angle with complete visibility of ciliary body, must compare angle in every quadrant in the affected eye to the non-affected eye, looking for deepening of the angle in any quadrant, frequent cause of glaucoma which can occur anytime between 2 months to 15 years post-trauma - bad b/c CB isn''''t pulling open TM - ALWAYS DO GONIO OF HISTORY OF TRAUMA
Cyclodialysis - full thickness detachment of CB from sclera, produces a cleft visible on gonio, rare, associated with hypotony (decreased IOP because ciliary processes are damaged) Hyphema - accumulation of free blood in the anterior chamber, increased IOP in 1/3 of cases, microhyphema refers to presence of RBCs only in the AC (not free blood pooling), "eight-ball" is an AC completely filled, older hyphemas look black |
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Uvea Vocabulary
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Iridectomy - cutting out portion of iris tissue
Iridotomy - hole in the iris without any removal of tissue, done with laser or surgically Iridodonesis - iris trembles or flops loosely secondary to a lack of the normal, anatomical support by the lens, seen after lens dislocation or removal Iridoplegia - iris sphincter paralysis Iris prolapse - protrusion of iris tissue into a corneal or conjunctival wound Rubeosis - neovascularization of iris - PROBABLY SOMETHING BAD GOING ON IN BACK OF EYE |
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Thyroid Eye Disease
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Grave's Ophthalmopathy/Grave's Disease
Hyperactivity of thyroid gland, 75% have ocular signs - 15% will develop serious functional impairment - basic problem with ocular involvement is change in orbital tissues: EOMs may be enlarged to 2-5 x nomral, orbital contents under increased pressure "NO SPECS" Classes Class 0: no physical signs or symptoms Class 1 (only signs, no symptoms): upper lid retraction (stare sign), occurs in 90% w/hyperthyroidism, unilater/bilateral, often asymmetric, MOST COMMON CAUSE OF UPPER LID RETRACTION, may be from overaction of Mueller's, overaction of levator from SR excessive stimulation trying to overcome infiltrated IR, or from infiltration of levator muscle, disappears after 15 years in most Class 2 (soft tissue involvement): swelling of lids, prolapse of orbital fat, palpebral lacrimal gland, injection of conjunctival/episcleral vessels especially at insertions of recti muscles, chemosis, may complain of tearing, photophobia, FBS, usually worse in morning Class 3 (Proptosis): not the same as exopthalmos but in used as such in this case, most pts develop 21mm or more, normal: Asian - 18-20mm, White - 20-22mm, Blacks - 22-24mm, should be within 2mm of each other, may cause secondary lagophthalmos Class 4 (EOM Involvement): 33% of pts with TED, become infiltrated and fibrotic, IR MOST COMMONLY INVOLVED, can cause increased IOP and/or diplopia in upgaze b/c more fibrous and can't extend, SR LEAST COMMON, caused by muscle paresis or from mechanical obstruction - do forced duction test Class 5 (Corneal Involvement): significant threat to vision b/c of exposure keratopathy, contributing are exophthalmos, lid retraction, abolished Bell's phenomenon due to IR infiltration, must manage aggressively to avoid secondary corneal ulceration and loss of eye Class 6 (Sight Loss): massive engorgement of EOMs which compress optic nerve, rare - only 2-5%, usually have painless, gradual loss of visual acuity with central or paracentral scotomas, papilledema, papilitis, retrobulbar neuritis possible, color vision disturbances common, APD may be present in asymmetric disease Class 1 disease is the most frequent ocular manifestation of hyperthyroidism Progression from Class 1 to 6 is not necessarily chronological and MAY OCCUR IN THE ABSENCE OF ELEVATED THYROID HORMONE LEVELS Progression to Class 6 disease occurs in up to 5% of patients even after subtotal resection of thyroid gland or treatment with radioactive iodine |
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TED Examination
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History - weight loss, body temperature elevation, rapid pulse, muscle wasting, hand tremor
Ocular - pupillary, color vision (always for anything neuro related), EOM testing, slit lamp with NaFl stain and RB stain, exophthalmometry, forced duction as necessary, automated visual field, orbital imaging PRN, MRI better than CT in detecting infiltration of EOMs and lacrimal gland |
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TED Treatment
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Refer for systemic evaluation with bloodwork with an endocrinologist, internist may prescribe antithyroid medications or RAI (radioactive iodine)
Lubricants to protect cornea - bland ung at night is standard, antibiotic ung if cornea compromised Elevate the head at night if eyelid edema present Local injection of steroids to involved muscle - must specify Botox to involved muscle EOM surgery or plastic surgery to improve cosmesis Diuretic for lid edema - make sure not contraindicated Treat IOP if elevated - oral acetazolamide has added benefit of being a diuretic, beta blockers Tinted spectacles to reduce visibility of cosmetic appearance and shield from wind, dust etc... Prisms or eye patch to relieve diplopia Oral steroids to reduce EOM infilration and optic nerve compression Optic nerve decompression surgery - break ethmoidal bones and make room for orbit (last resort) |
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Orbital Inflammatory Pseudotumor
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Idiopathic inflammation of orbit - MUST RULE OUT EVERYTHING ELSE FIRST
Differential diagnosis - TED, orbital cellulitis, orbital tumors, trauma, orbital vasculitis, infections, varix (like aneurysm but on a vein - doesn't usually blow) Syptoms - red, eyes, pain, blurred vision, double vision, similar to TED but can occur with fever, especially in children, have no history of thyroid function Signs - proptosis, exophthalmos, restriction of ocular motility - USUALLY UNILATERAL ESPECIALLY IN ADULTS, orbital CT scan shows a thickened posterior sclera, orbital fat or lacrimal gland involvement, or thickening of EOMs including tendons - only muscles in TED, eyelid erythema and edema, chemosis, decreased vision, uveitis, increased IOP, hyperopic shift, optic nerve edema Workup - history/symptoms of hyperthyroidism or meds, ocular exam same as TED, vital signs especially body temp, orbital CT/MRI, blood tests Treatment - oral steroids, orbital irradiation when non-responsive to steroids |
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Orbital Cellulitis
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Can occur from direct extension of sinus infection (especially ethmoid - called ethmoiditis, from a focal orbital infection, orbital fracture, or dental infection, vascular extension (bacteremia), follow orbital trauma or eye surgery, most common organisms are staph, strep, h.flu
Symptoms - red eye, pain, blurred vision, fever, headache, double vision Signs - eyelid erythema, edema, warmth, chemosis, proptosis, restriction of EOMs with pain on attempted eye movement, decreased vision, retinal venous congestion, optic disc edema, purulent discharge, fever, APD Examination - history, trauma, infection of ear, nose, throat, sinus, systemic, stiff neck (could be meningitis), mental changes (also could be meningitis - ER), diabetes or immunocompromised illness, check vital signs, CT of orbits/sinuses, blood tests/cultures, gram stain of any infected material, lumbar puncture for suspected meningitis, ocular examination - pupils, EOMs, exophthalmometry, color vision Treatment - IMMEDIATE HOSPITALIZATION with broad spectrum antibiotic IV, follow daily |
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Orbital Tumors in Children
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Dermoid and epidermoid cysts - excise, benign, may rupture and cause an inflammatory response
Capillary Hemangioma - usually exacerbated symptoms when child cries, no treatment unless amblyopia is imminent - then may inject with steroids Rhabdomyosarcoma - malignant tumor with rapid onset and progression, bone destruction is common, treat with local irradiation and systemic chemo Lymphangioma - excise if cosmetic problem, may recur Optic Nerve Glioma - decreased VA and APD, tx controversial Leukemia - systemic chemo Metastatic Neuroblastoma - child is usually ill, local radiation and chemo Plexiform Neurofibroma - associated with neurofibromatosis, surgery if cosmetic problem Teratoma - surgical excision Metastatic - primary sources include breast, lung, GU, GI, treat primary malignancy, ocular treatment varies Cavernous Hemangioma - follow if asymptomatic, excise if compromised visual function or poor cosmesis Mucocele - seen in patients with chronic sinusitis, do surgical drainage, systemic antibiotics Lymphoid tumors - radiation Optic nerve sheath meningioma - middle aged women, APD, vision loss, may see chunt vessels on ONH, surgical excision Localized neurofibroma - surgical excision Neurilemoma - benign, follor or excise depending on symptoms Fibrous Histiocytoma - surgical excision, recurrences are more aggressive and more malignant Hemangiopericytoma - excise because of potential for malignant transformation |
