Lecture 9 – The Red Eye

1. External Lid Problems

a. Hordeolum
i. Acute infection/inflammation at the eyelid margin
ii. Sebaceous Zeis or Apocrine Moll
iii. Red and painful
iv. Warm compress, lid antibiotics cream – systemic antibiotics for cellulitis, I&D if persistent
b. Chalazion
i. Chronic, painless, granuloma
ii. Warm compress, lid antibiotics cream – systemic antibiotics for cellulitis, I&D if persistent
c. Dacrocystitis
i. Acute onset, maybe some preceding trauma
ii. Epiphoria – tears down the cheek
iii. URGEN TREATMENT – drain and antibiotics
d. Blepharitis
i. Itching, burning, FB sensation, crusting of eyelids in morning
ii. Anterior = Demodix mites, sleeves of protein on the eyelashes (pilocarpine treatment)
e. Masquerade Conditions
i. BCCA/SCCA – ulcer like, lose eyelashes and glands
ii. Sebaceous – cancer of the Meibomian glands, white creamy
iii. Melanoma – black, dark pigment
2. Cellulitis
a. Preseptal
i. Tenderness, swelling, erythema
ii. Sinusitis, skin abrasion, hordeolum, insect bite
iii. NO PROPTOSIS, NO PAIN ON EOM, NO EOM ABNORMALITES
iv. May not be able to open the lid themselves
b. Orbital
i. Fever, chills, toxic appearing, elevated WBC
ii. PROPTOSIS, DIPLOPIA, PAIN ON EOM
iii. Treatment requires IV antibiotics and possible drainage
3. Conjunctiva
a. Subconjunctival Hemorrhage
i. Blood under the conjunctiva, usually in one sector
ii. Valsalva, trauma, HTN, bleeding problem (disease or anticoagulants), bleeding mass
iii. Exam – look for conjunctival lesion, check EOM, resistance to retropulsion of the globe, BP, CT?
iv. Treatment – nothing, maybe lubricants
b. Algorithm
i. Follicles
1. Preauricular Lymphnode
a. Yes
i. Herpetic Signs
1. Yes = HSV
2. No = Chlamydia
b. No
i. Toxic
ii. Molluscum
iii. Peduculosis
ii. Papillae
 1. Severe Purulent = GC
2. Scant Purulent = Bacterial
3. Water = Allergic or Atopic
c. Follicles
i. Lymphocytic aggregates with avascular centers (white in the middle)
ii. Viral – adenoviral, HSV, chlamydia, Molluscum
d. Papillae
i. Response to bacterial or allergic insult
ii. Vascularized red centers to the bumps
e. Acute Viral Conjunctivitis
i. Red eye (conjunctival hyperemia), watery stringy discharge, eyelid crusting in the AM, VA NL
ii. Preauricular lymph node, often asymmetric
iii. May have a membrane/pseudomembrane
iv. Prolonged cases may have the sub epithelial infiltrates
v. DDx – adenoviral, bacterial other than GC, GC, Allergic, Toxic, Atopic
vi. Tx – don’t need to culture, acute lasts 4-7 days, cornea can be 2-3 weeks
vii. Highly contagious for 10-12 days
viii. If membrane or SEI develops refer to ophthalmologist
f. HSK
i. Eye doesn’t improve with conservative treatments
ii. Can affect vision if central lesion
iii. Needs referral to optho
iv. Dendritic lesions with end bulbs on fluor stain
v. Trifluoridine and or Acylcovir/Valtrex
g. Allergic
i. Usually bilateral, itchiness, watery discharge, no crusting
ii. Tx – eliminate agent, cold compress, mild – tears, moderate – allergy drops, severe – steroid IO
h. Vernal
i. Causes – genetics, allergy stuff in the family, asthma, eczema – young males in the spring/sum
ii. Sx – Burning/itching/watery, photophobia, limbus/upper eyelids swollen and rough, white muc.
iii. Often requires steroids or cyclosporine
iv. HORNER TRANTAS DOTS – perilimbal bumps filled with eosinophils, refer to optho
i. Bacterial (Non-GC)
i. Purulent discharge
ii. Staph aureus (blepharitis), Staph epidermidis, H. influ (children), Strep pneumonia
iii. GS and culture ONLY if severe, recurrent, or recalcitrant
iv. Trimeth/polymixin or Cipro QID, if H. influ add systemic amox/clavulanate
j. Gonococcal
i. Severe, purulent discharge, marked chemosis, preauricular nodes
ii. Begins over 12-24 hours
iii. May progress to corneal perforations (examine for ulcers)
iv. Can be seen in neonates
v. GS and Culture – blood and chocolate
vi. Tx – PO/IV antibiotics, consult I&D, topical antibiotics, eye lavages
k. Chronic Chlamydial
i. Symptoms greater than a month, sexually active may have cervicitis or urethritis
ii. Inferior follicles, Giemsa staining for cytoplasmic basophilic inclusion bodies
iii. Azithro or Doxy, topical erythromycin for 2-3 weeks
l. Trachoma
 i. Arlt line or scarring of the superior tarsal conjunctiva
ii. Azithro or Doxy, topical erythromycin for 2-3 weeks
m. Molluscum Contagiosum
i. Dome shaped, umbilicated shinny nodules on lid or margin
ii. Chronic follicular conjunctivitis from viral particles
iii. Simple excision or curettage or cryosurgery
4. Sclera
a. Scleritis
i. Serious inflammation of the sclera
ii. Redness/purple of sclera and conjunctiva, severe eye and templ/jaw pain, photophobia,
tearing, decreased VA, maybe blindness
iii. Associated with SLE, RA, Ank spond, arthritises, polyarteritis nodosa, MCTD, wegners, Sjogren,
GCA, IBS, allergic angitis
iv. Differentiate from Episcleritis with pheylephirne or neosynephrine drops (blanches in epi)
v. Diffuse, Nodular, Necrotizing, Posterior
vi. Mild cases = NSAIDs
vii. Oral corticosteroids
viii. Severe = long term immunosuppression
b. Episcleritis
i. Mild eye pain, redness, watery eyes
ii. Benign, self limiting, WORSE IN TOBACCO SMOKERS
iii. Artificial tears if needed
iv. Severe cases oral NSAIDs or topical corticosteroids
c. Pingulecula
i. Yellow/white adjacent to limbus, sup epithelial collagen degrades to elastic like, no excision
d. Pterygium
i. Wedge shaped fibrosis into the cornea, extends onto the cornea, may distort vision, removed
5. Cornea
a. Contact Overwear Syndrome
i. Corneal Inflammation without Ulcer but is an ulcer until proven otherwise
ii. Can be devastating
iii. Acanthomeba – ring
iv. Pseudomonas – central and entire
b. Corneal Ulcer
i. Result of inflammation or infection
ii. Extremely painful due to exposed nerve endings
iii. May also have anterior uveitis symptoms of miosis, aqueous flare, redness

Lecture 10 – Adult Vision Abnormalities

1. Cataracts
a. Opacification of the lens, blurring of vision
b. Normal lens – ectoderm epithelial cells, lens capsule that a=surrounds and is zonular fiber attachement
c. Morgagnian – hypermature liquefied
d. ANteiror polar – pin hole
e. Fetal nuclear – red reflex disturbed, prevent amblyopia, operate at two weeks
f. Nuclear – yellow brownish
g. Cortical – spokes
h. Posterior Sub-Capsular – steroids used, posterior subcapsule is hazy
i. Metabolic – galactosemia
 j. Ectopia Lentis – Marfans = up Homocystinuria = down
k. Phaco Emulsification = most common technique
2. Age Related Macular Degeneration
a. ARMD – most common irreversible vision loss over age of 60
b. MOST COMMON IN WHITES, then black/Hispanic/other
c. Risk Factors
i. Aging, smoking, family history, HF1/CFH gene, HTN, UV exposure, female
d. Retinal Pigment Epithelium
i. Maintains photoreceptors, absortion of stray light, outer blood retinal barrier, phag/regen cells
ii. Bruch’s Membrane seperates RPE from choroid
iii. Choroid capillaries prevent overheating and provide O2 and nourishment to RPE
e. Dry ARMD
i. Early stage, less severe, 90% of cases
ii. Blurry or faded vision
iii. Drusen, incipient atrophy, then geographic atrophy
iv. Insufficent nutrition damages photreceptors, with age RPE cant digest photreceptors,
accumulation of metabolic debris (druesen), RPE membrane and cells degenerate and atrophy
v. Lose central vision
vi. Drusen appear as focal areas of eosinophilic material between BM or RPE and Bruch’s
vii. Mild drusen = normal VA, more light
viii. Larger drusen = risk of late form, progression to wet
ix. Geographic atrophy = severest form of Dry without Wet – RPE atrophy and choroid exposed
f. Wet ARMD
i. More severe, 10%
ii. Early symptom is wavy lines
iii. Develop central vision blind spots
iv. Age related Bruch’s changes (thickening, drusen, metabolic deposits) and lose connection RPE
v. Pigment epithelial detachment may occur
vi. Photreceptors and pigment epithelium send distress signal to choriocapillaries to make new
vessels
vii. New vessels grow underneath macula, breakdown Bruch’s, new vessels are fragile
viii. Leak blood, fibrovascular scarring of macula
ix. Potential for rapid and severe vision damage
x. SRNVM or CNVM (NVM = neovascular membrane)
xi. Leakage of blood or serum in CNV develop sudden loss of central vision, often other eye too
g. Diagnostic Tools
i. Visual acuity
ii. Amsler grid test – distorted vision or central irregularities
iii. Ophthalmoscope – direct visualization
iv. Fluroescein and ICG – NVM and location
h. Management
i. Ocuvite – Vitamins C/E, Zinc, Cu, DHA, EPA, Lutein, Zeaxanthin
ii. Wet AMD – VEGF inhibitors, PDT – cold laser, surgery, other laser photocoagulation
i. Rehabilitation
i. Low vision aids – reading lamps, magnifiers, CCTV, Alexa
ii. Don’t smoke, exercise, good diet, sunglasses, take meds, see eye doctor
iii. Q1-2 years for 65+ healthy patients to see eye doctor
3. Viral Keratitis
a. HSV 1&2, VZV 3, EBV 4, CMV – 5, Roseola 6, Pityriasis Rosa 7, Kaposi’s -8
 b. HSV, VZV, EBV, and CMV
c. Leading cuse of corneal blindness
d. Atopy = increased risk for bilateral disease
e. Primary infection of epithelial cells, retrograde transport to CN V ganglion, latent, reactivation = eye sxs
f. Primary HSV1
i. Rarely seen, vesicular belpharoconjunctivitis, corneal infolvement, children
ii. Hutchisons Sign – vesicles on the nose before eye problems
g. Recurrent HSK
i. Triggered by – fever, UV, trauma, mensturation, immunosuppression
ii. Cornela ulceration, branching with end bulbs
4. Retinal Detachment
a. General
i. Always occur at the periphery, floaters and flashers first then black curtain
b. Degenerative
i. ARMD
ii. Epiretinal Membrane and Macular Hole
1. Vitreous jelly contracts and activates fibroblasts cracking the central macula
c. Metabolic
i. Diabetic Macular Edema
ii. Proliferative Diabetic Retinopathy and Vitreous Hemorrhage
d. Vascular Occlusive
i. CRVO
1. HTN or DM, can cause the black curtain vision loss but on exam no retinal detachment
ii. CRAO
e. Vitreoretinal Traction
i. Retinal Detachment
f. Trauma
i. Injury, Eye Wall Rupture, IO FB
1. Contraction of the vitreous
2. Flashers and floaters
3. Peripheral retinal tears
4. Scotoma initially in periphery – never isolated central scotoma
ii. Post-surgical
5. Common Retinal Surgeries
a. Macular hole repair, detachment repair, diabetic hemorrhage removal, IO FB, droppec cataract
b. Pars Plana – fixes IO abnormalities and retinal detachment
c. Scleral Buckling for Retinal Detachment – thin silicon band swe in around the eye to give a surface to
reattach retina
d. Retinal Eye Laser
i. Ablation of ischemic tissue – burn away the poorly perfused tissue, thicken leaky vessels
ii. Form adhesions to seal retinal tears
6. Vitreous Substitutes/Eye Gases
a. Temporary, removed at end of operation
i. Perfluron used to flatten tissues
b. Slow absorbing, may be left in
i. Sulfar hexaflorane SF6
ii. Propane octaflurane C3F8
c. Non-absorbing, premant
i. Silicon oil
Lecture 11 – Ocular Manifestations of Systemic Diseases
1. Diabetes
a. Blacks and Mexcans, older than 40s, men>women
b. Age, duration of DM, pregnancy, insulin dependency, diastolic pressure, smoking Type1>2
c. Pathogenesis
i. Endothelial cell damage/prolif + capillary BM thickening, increased plasma viscosity leads to…
ii. Decreased capillary blood flow and perfusion leading to retinal hypoxia
iii. AV shunt IRMA
iv. VEGF leads to neovascularization and fibrovascular proliferation
d. NPDR (Background Retinopathy)
i. Cotton wool spots
ii. Venous beading
iii. Intra-retinal microvascular abnormalities
iv. Intra-retinal hemorrhages
e. PDR
i. Temporarily benefits from anti-VEGF, eventually requires Pan Retinal Photocoagulation laser
ii. Complications – poor perfusion leads to vitreous hemorrhage and fractional membranes to RD
f. Recommended Screen Schedule
i. Type 1 – 3-5 years after diagnosis then yearly
ii. Type 2 – at time of diagnosis, then yearly
iii. Pregnancy – before conception, early in first trimester, then 3-12 months mild/mod or 1-3 sev.
g. Follow Up
i. Normal, mild, mod, severe NPDR, CSME, PDR
ii. 1 year, 9, 6, 4, 2-4, 2-3 months
h. Treatment of DR
i. Laser photocoagulation, anti-VEGF/steroids injections, surgery
ii. Panretinal Photocoagulation
2. Hypertensive Retinopathy
a. Most are asymptomatic, some have HA or blurred vision
b. Exam
i. Arteriolar narrowing, changes in AV crossings, flame hemorrahges, microaneursym, exudates
ii. Cotton wool spots, optic disc swelling
c. Grading
i. 0 = No changes
ii. 1 = Barely detectable arterial narrowing
iii. 2 = Obvious arterial narrowing with focal irregularities
iv. 3 = Retinal hemorrhages = grade 2
v. 4 = Optic disc swelling + grade 3
d. Complications
i. CRVO (complete or hemi)
ii. Blown Capillaries
iii. Ischemia, neovascularization – proliferative retinopathy – will need PRP
3. Increased ICP
a. Normal is 7-15 mmHg, if increased, CPP=MAP-ICP, so CPP decreases
b. ICP of 25-40 has normal alertness, 40-50 LOC, then brain death further
c. Causes – mass effect, brain swelling from liver, HTN, increased venous pressure, CSF production
d. Signs
i. Papilledema or optic disc swelling, usually vision is unaffected
ii. BILATERAL AND SPARES VISION – maybe enlarged blind spot
 iii. Neuroretinitis – inflammation of retina and optic nerve – firework appearance
4. Blood Dyscrasias and Embolic Disease
a. Anemia
i. Retinal hemorrhage, CWS, vitreous hemorrhage, CRVO like picture, papilledema
b. Polycythemia
i. Retinal venous dilation and tortuoisity, intraretinal hemorrhages
c. Leukemia
i. Hemorrhages (flame, dot-blot, white Roth spots, boat shaped), microaneurysm, hard exudate
d. Coagulopathies
i. Serous detatchment of retina, retina and choroidal hemorrhage, vitreous hemorrhage
e. Plasma Dyscrasias
i. Retinal venous dialation and trotrousity, sausage like, microanerysus, CRVO, intraretinal hem.
f. Histopathology
i. Flame shaped are in the nerve fiber layer
ii. Dot-blot are in the inner and outer plexiform and inner nuclear layers
g. Hollenhorst Plaque
i. Cholesterol plaque from the carotid breaks off, occasionally after CEA or heart surgery
ii. Vision loss suddenly in the corresponding field to the emboli location
iii. Painless, sudden loss of vision that is not permanent
iv. If no HH plaque seen, then vasculitis is considered
v. Temporal arteritis may cause sudden vision loss
h. Amaurosis Fugax
i. Embolic – carotid or cardiac with afib or valve disease
ii. Hemodynamic – giant cell arteritis, vasospasm, hypercoagulable states
iii. Ocular – angle closure, iritis, severe dry eye
iv. Neurologic – optic neurits, MS, migraine, ICP, psychogenic
v. Idiopathic
i. Sickle Cell
i. Due to sluggish blood flow and occlusion of vessels, most often in the SC disease form
ii. Swelling of the hands and feet is often the first symptom, eye findings are late
iii. Sickle Cell Non-Proliferative Retinopathy
1. Venous tortuosity
2. Salmon patch hemorrhage
3. Schesis cavity
4. Black sunburst
iv. Sickle Cell Proliferative Retinopathy
1. Peripheral arteriolar occlusions
2. AV anastomosis
3. Neovascular proliferation
4. Vitreous Hemorrhage
5. Retinal Detachment
6. Most severe form, progressive, need to treat neovascular tissue with PRP
5. Thyroid Eye Disease
a. 30-50, females
b. TSH receptor antigen in the orbital fat and connective tissue, autoimmune assault
c. Findings
i. Eyelid retraction, lid lag on infraduction (Von Graefe), eye globe lag on supraduction (Kocher’s)
ii. Inability to completely close lids
iii. Chemosis, punctate epithelial erosions, superior limbic keratoconjunctivitis, lacrimal problems
 iv. Inferior rectus muscle most commonly affected – diplopia on upgaze and limited elevation
v. Lymphs, plasma, mastocytes on histiology
vi. Deposition of collagen and GAGs causes fibrosis
vii. Lipogenesis by fibroblasts and preadipocytes increase orbital volume
6. Metastatic Carcinoma
a. Breast most frequently, can be bilateral in 20% or so
7. AIDS
a. Early Stage – Kaposis, Zoster, Candida, Lymphoma
i. Kaposi’s HHV 8 - VEGF
b. Middle Stages – Toxoplasma, TB, PCP
c. Late Stage – CMV, MAC
i. CMV retinitis (HHV-5) – intravitreal flame hemorrhages – pizza box, Gancyclovir
8. Occular Inflamations
a. Young people, primary without systemic assocaitong
b. RA, lupus, Sarcoidosis, Wegner, Infections
9. Uveitis
a. Anterior
i. Iris, anterior chamber – 90% of all uveitis
ii. Unilateral/bilateral, pain, photophobia, blurred vision, redness, miosis
iii. Single episode, treated with drops
b. Intermediate
i. Pars plantitis, vitiritis
ii. Macular, less pain or photophobia, floaters, blurred vision
iii. Snowbanking
c. Posterior
i. Chorioretinits
ii. Photopsia
d. Diagnosis
i. Complete visual exam, skin test for TB, toxo, histo – full blood testing CBC, ESR etc
e. Treatment
i. Underlying disease – cycloplegics and steroids to the eye