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105 Cards in this Set
- Front
- Back
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Coloboma |
Absence of portion of eyelid |
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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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) |
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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 |
