Lids Lashes Adnexia Flashcards

1
Q

Function of eyelids

A
  1. Prevent ocular desiccation (Drying of eye)
  2. Protects the globe
  3. Grandular secretion - maintain pre-ocular tear film
  4. Spontaneous blinking (10-15/min at near 5/min)
  5. Reflex blinking - responce to irritants
  6. Closure during sleep
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2
Q

Lid Coloboma (Incomplete closure of tissue)

A
  • Not Hereditary
  • Gaps notches in lids
  • Superior - junction of inner to middle 1/3 of lid
  • Inferior - junction of middle to lateral 1/3 of lid
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3
Q

Lid coloboma

  • Ocular complications
  • Management
A

Complications:

  • Tear film unstable
  • Corneal epithelium disruption
  • Ocular dissication
  • Sec infections

MX and treatment

Gel during the day (increase viscosity) ung PM / Gtt 6/pd

Oculoplastic SX

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4
Q

Epicanthal folds

A

Common - Autosomal dominant - Inherited

Redundant folds of skin from upper lid to inner canthus and covers cruncle

Can self resolve / Px with down syndrome

Pseudo-strab (esotropia)

MX - Optional SX

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5
Q

Epicanthal folds

CT + variation

A

Reversed epicanthal fold - only bottom lid has fold

Cover test: Norm Hirsberg 0.5mm nasal of midline

Every 1/2mm = 11 pd

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6
Q

Distichiasis

A

Hereditary - Autosomal dominant

Meibomian glands replaced by lashes / Hair growing out of meibomian glands

Lashes irritate cornea / cause tracking staining

Px - FB sensation, tearing, prone to corneal infection + scarring

MX - Epilation , Bandage CL, Electrolysis, cryo treatment, Art gel lubricant, Laser treatment

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7
Q

Blepharophimosis

A

Hereditary - Autosomal dominant

Narrowing of lid fissure Horizontally and vertically

Ddx - Epicanthal folds and Ptosis

RISK - Amblyopia

MX - Sx

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8
Q

Alcohol Fetal symdrome

caused 1st + 2nd trimester

A

Blepharophimosis (Epicanthal folds + Ptosis)

Other facial features:

  • Wader Nares (flaring nostrils)

Philtrum - flatter(no ridge) larger in dist betwwen nose and lip

Flat thin upper lip

Micrognatia (Smaller lower mandible)

Rail road ears (sup notch not fully rounded) ears lower down

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9
Q

Ectropion

A

Outward eversion of lower lid, away from globe, Poor lid apposition

Symptoms: Red eye, hypereamia of bulbar conjuctiva

FB sensation

Signs: Increased lacrimation

Hypereamia , Conjuctival drying, Exposure keratitus

MX - Horizontal shorming of lids SX

Artificial tear lubricant. AM gtt 6/pd PM ung

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10
Q

Ectropion

Classifications (causes)

A

Congenital - Rare

Involutional - Horizontal taxity 2nd to Aging

Paralytic - 7N palsy (Temp or perm)

Spastic: dt trauma / Orbicularis muscle contraction everts lid

Cicitricial - Skin contraction due to scarring

Allergic - Thickend skin, pul lid from globe

Mechanical - Growth in lid margin

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11
Q

Bell’s Palsy

A

Unilateral Facial Palsy

Sudden onset, Mild to severe paralysis

Symptoms: Sensitive to sound (Hyperacusis)

Pain in ear and jaw, Facial droop

Inability to raise eyebrow

  • Etiology - Viral (Herpes zoster)
  • Acoustic Adenoma
  • Ideopathic
  • Ischemia
  • Lyme’s disease (tick bite fever)

MX - ave 3wk. - 6 mnth recovery

  • Lubricate - gtt unpreserved 6/pd gel
  • Ung PM
  • Tape lids
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12
Q

Entropion

A

In turning of ids of eithe superior or inferior lid

Symptoms: Tearing - inc corneal sensitivity

  • FB sensation
  • Hypereamia

Ethiology

  • Congenital
  • Involutional - Aging
  • Cicatricial - Chemical injury
  • Trachoma (chronic infection Bacterial)

MX:

  • Epilation
  • Electrolysis
  • Cauterization
  • Bndg CL
  • Art lubricants 6/pd gel better
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13
Q

Trichiasis

A

Random misdirected lashes turn in

Causes: Entropion, Chronic lid/ conjuctival disorders,

Symptoms: Tearing / Irritation / Redness / FB sensation

Signs: Eye lashes abrading conj + cornea (NaFl staining)

MX:

  • Epilation
  • Electrolysis
  • Cauterization
  • Bndg CL
  • Art tears 6/pd Ung pm
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14
Q

Blepharochalasis

A

Repeated Idiopathic episodes of acute eyelids swelling

Rare + idiopathic

Skin stretches large amounts - has a redundent lose skin with premature wrinkling

Mx - Blepharoplasty, Only considered after disease is quit

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15
Q

Dermatochalasis

Common in older px /

A

Loosend or redundent skin on upper eyelid more sup-temp

Middle to older Px’s

Common - cause Aging

Eyelid looses elastisity

Symptoms:

  • Reduced visual acuity + Fields (in front of nodal point) SUP TEMP
  • Brow ache (using frontalis muscle to lift lid)
  • Induced trichiasis - upper lid weight
  • Pseudo Ptosis
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16
Q

Ptosis

Features + Signs

A

Features

  • Damage or developmental failure to the levator muscle
  • dystrophy of superior rectus muscle,
  • damage to CN 3 which can cause the upper eyelid to droop

Signs/Findings

NORM : the upper eyelid usually sits in between the limbus and the top of the pupillary margin (2mm from the limbus and 2mm from the top of the pupillary margin)

→ in ptosis, the upper eyelid droops

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17
Q

Congenital Ptosis

Cause and Signs

A

Secondary to development of or isolated dystrophy of the levator muscle

  • ● Primary gaze ptosis
  • ● Absence of tarsal folds
  • ● Impaired movement of lids in upgaze and downgaze

CAUSES

  • ● Marcus Gunn Jaw Winking Syndrome (5% of cases)
  • ● Blepharophimosis (5% of cases)
  • ● Superior rectus weakness (25% of cases)
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18
Q

Acquired Ptosis

Findings and causes

A

Findings

  • Brow/frontal headaches
  • Presence of tarsal fold
  • Acute seeing double or droopy eyelid

Causes of acquired ptosis

● Trauma → damage to CN 3 and muscle innervation

● Surgical damage

Oculomotor/CN 3 palsy → the pupil undergoes noticeable changes like having a fixed, dilated pupil and the eye would turn downwards and outwards due to the lack of muscle innervation

Horner’s syndrome → would result in a little ptosis

Diabetes → ischemic changes along the CN 3 pathway

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19
Q

Treatment and Grading of PTOSIS

A

Surgery - oculo-plastic surgeon

Lid Crutch - spring on the edge of RX

● Gradient of Ptosis

Mild Ptosis - lid top of pupil - visual axis unobstructed

Moderate Ptosis - lid covers sup pupil - visual axis obstructed or unobstructed

Severe Ptosis - lid mid to inf pupil - visual axis significantly obstructed (could possibly cause amblyopia)

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20
Q

LID EXCURSION TEST (explain)

levator muscle

A

Steps ■ Immobilize the frontalis muscle by placing the thumb firmly against the patient’s brow with the eyes in downgaze

■ The patient then looks down as far as possible and the amount of excursion is measured with a ruler

■ Ask patient to slowly look up

■ Patient then is looking up as far as possible and the amount of excursion is measured with a ruler

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21
Q

Turning in of lashes

A

Trichiasis

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22
Q

small, focalized area of eyelash loss

A

Madarosis (missing)

Can be caused by chronic blepharitis (most common cause) or injury (the lid structure is changed which could leave scar tissue)

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23
Q

complete loss of hair/eyelashes

A

Alopecia (alles uit)

chemotherapy + other causes

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24
Q

whitening of the eyelashes

A

can be 1 or 2 eyelashes or a whole row of eyelashes

○ Can be caused by albinism, chronic lid problems (like blepharitis), some systemic diseases

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25
Q

abnormal rows of lashes coming out of Meibomian orifices

A

Districhiasis

lashes coming out of Meibomian orifices

usually misdirected eyelashes

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26
Q

thickening of lid margins

A

Tylosis thick

○ More common/observable on the lower lids

○ Thicker and darker lid

○ Usually permanent

Apposition can be normal with Tylosis or apposition can be abnormal if an ectropion forms due to the extra weight of the eyelid ○ Can be caused by chronic inflammation to the lid

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27
Q

Lid Nevus / Nevi

A

flat and uniform Benign

  • Slightly darker/more concentrated pigmentation
  • Usually congenital
  • born but noticeable until puberty

~8 to 10 mm in size

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28
Q

Papilloma

space between lesions / Rasberry surface

A

Benign epithelial growth → epithelial cells grow upwards from skin ○ Non-infectious → happens secondary to toxins in the environment or UV light exposure

○ Can be pigmented or non-pigmented

○ Can be singular or multiple

AvascularRaised surface

Well defined/textured lesions

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29
Q

Type of Papiloma ?

A

Sessile

■ Broader base

■ Dome-shaped

■ Slightly bumpy

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30
Q

Type of papiloma?

and Mx

A

Pedunculated

  • ■ Smaller base
  • ■ Very narrow in shape
  • ■ Raspberry-like bumps

MX:

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31
Q

Treatment Papilloma

A

Document the papilloma and monitor its growth + Size

Excision

Laser treatment

Chemical cauterization (uncommon)

Bichloroacetic acid → is an older treatment option that is not really used much anymore as it uses a strong acid to ‘burn off’ the papilloma (con: this procedure is done very close to the eye, and it would be very bad for acid to get into the eye)

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32
Q

Xanthelasma

A

Multiple soft yellow deposits (plaques) under the skin on the inner aspect of the lower and upper lids

deposits are slightly elevated / asymmetric

-Causes/Etiology -

elevated serum cholesterol levels

  • Younger patients (40-50 year old) with Xanthelasma chances of having high cholesterol > older patients
  • Medical evaluation is indicated -
  • Case HX medication is called Lipitor or last check up
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33
Q

Treatment and Management

A
  • Laser treatment

- Excision - stability in their management of cholesterol → 1 year or more

  • Side note: will not go away on their own and can return if cholesterol inc
  • Bichloroacetic acid → is an older treatment option that is not really used much anymore as it uses a strong acid to ‘burn off’ the xanthelasma (con: this procedure is done very close to the eye, and it would be very bad for acid to get into the eye)
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34
Q

Sudoriferous Cyst

A

○ Involves clogged or blocked sweat glands (Glands of Moll)

focalized (Alone) benign lid lesions along the lid margin

○ Surfaces are smooth

fluid-filled

■ This build-up of fluid causes the cyst to have a very taut surface

Clear, oily fluid

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35
Q

Identify

Treatment and Management

A

Sudoriferous Cyst

○ Excision with drainage

■ Should “lance” (cut the cyst) across quite drastically and then allow the contents to drain

■ If popped and not LANCED the skin would regrow and the cyst would form again

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36
Q

Sebaceous Cyst

A

blocked sebaceous glands (Meibomian Glands)

  • focalized benign lid lesions that occur along the lid margin sup + inf
  • The surface smooth
  • filled with oil/sebum
  • This buildup of sebum causes the cyst to have a very taut surface
  • Yellow, opaque and lipid in content
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37
Q

Identify

Treatment and Management

A

Sebaceous Cyst

- Excision with drainage

  • Should “lance”/cut the cyst directly across and allow for drainage
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38
Q

Malignant lid lesions

ABC

A

● “A, B, C” → Asymmetry, Bleeding, Color

Asymmetry → mirror images if line drawn through? asymmetrical in size

Bleeding → bleeds? Tumors typically have really rich blood supply

Color → is the lesion uniform in color? Does it have patches where it is lighter or darker?

History of growth/changes in size

Vascularization or ulcerationSkin surface changes → is the area drier than normal? Is the area peeling more than normal?

Loss of hair growth in the area of the lesion and surrounding the lesion

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39
Q

Basal Cell Carcinoma

A
  • Most common eyelid malignancy 90%
  • Predominantly derived from epithelial tissue
  • Non-metastatic → doesn’t move from one organ to another
  • Extensive local destruction

Slow growing (unusual for tumors)

  • Grows laterally then posteriorly
  • Basal cell carcinomas can recur if not properly removed
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40
Q

Basal Cell Carcinomas

Risk Factors?

A
  • Age (>60 years of age)
  • Vocation (outdoors during sunlight)
  • Exposure to UV radiation
  • Race (Caucasian or more fair-skinned)
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41
Q

Types of Basal Cell Carcinomas

A

Nodular Type - Most common, early stages of Basal Cell Carcinoma - Slightly raised - Dome/rounded shape → in the center, there is a small depression

~5 to 10 mm in size - Pearly and translucent edges → the surface around the eroded/indented center shines a bit

  • Fine telangiectatic blood vessels

2) Ulcerative Form

  • The surface loses its fine skin lines - Umbilication and subsequent erosion (surface becomes more indented)
  • Ulcerative center - Flaky skin around the periphery
  • Increase vascularization of the telangiectatic blood vessels
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42
Q

Identify, Treatment and Management

A

All must be referred for removal!

  • Excision via Mohs’ technique
  • Frozen section surgery → freezing the area of the basal cell carcinoma to kill the cancer cells and then excising it
  • Radiotherapy → high energy beams of light (photons) to damage the DNA of the cancer cells
  • Cryo-surgery → using liquid nitrogen to cause irreversible tissue damage
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43
Q

Moth’s Technique

A
  • Step 1 → surgically remove the visible part of the tumor
  • Step 2 → biopsy the specimen
  • Step 3 → pathologist prepares frozen sections of the biopsy on glass slides
  • Step 4 → cells are microscopically examined to confirm the presence of basal cell carcinoma cells
  • Step 5 → if residual tumor is found, a further layer of tissue is removed to be analyzed under a microscope by a pathologist
  • Step 6 → once all cells have been microscopically examined and there is no more tumor found (normal cells will be surrounding the cancerous cells), the wound is reconstructed by the surgeon
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44
Q

Acute and Chronic Staphylococcal Blepharitis

Bacteria Involved?

A

Most common lid disorder - Affects the eyelids 75% of the time and the conjunctiva 75% of the time

  • Gram positive
  • 2 types: Staphylococcus Aureus and Staphylococcus Epidermis
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45
Q

Acute Staphylococcal Blepharitis

Hx , signs and Symptoms

A
  • Sudden onset , Acute inflammation → 1 week
  • ○ Can be unilateral or bilateral
  • worsens in the first 24 to 48 hours and then decrease severity

● Symptoms

  • Red eye
  • Lids are sticky with a crusty material on the lids/lashes
  • Difficulty opening eyelids AM
  • Burning/“foreign body sensation”(If cornea involved)

Signs/Objective Findings

  • Lid margin hyperemia
  • Collarettes / crusty/sticky material located at the base of the lashes, close to the lid margin
  • Bulbar and palpebral conjunctiva are redder and the blood vessels are more dilated (hyperemia)
  • Cornea - Exotoxins from bacteria can cause SPK
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46
Q

Identify, Treatment and Management

Px Entance test expected results

A

ACUTE STAPHYLOCOCCUS BLEPH

Management and Treatment

1)Warm compresses - Commercial / Non-comercial. ★ non-commercial warm compress 4x a day (QID) for 10 minutes → in the morning when they wake up, at lunch time, in the early evening and at bedtime

2)Lid Scrubs - Non-commercial lid scrubs , acute/short term use / J&J no-tear Baby Shampoo 9:1 GENTLY rub along the upper and lower lid ★ Official treatment protocol: non-commercial lid scrub should be done 4x a day AFTER the warm compress

■ Topical broad-spectrum antibiotics Polytrim / 1gtt TID 1week after hydiene Polysporin 1 ung qhs / 1 week

■ Artificial Tears : 1 gtt TID or QID / 1 week if SPK

■ Discontinue and discard any eye make-up products

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47
Q

Chronic Staphylococcal Blepharitis

Features

A
  • HX - Chronic disease → weeks to months & recur
    • Typically Bilateral
    • Usually associated with other ocular surface findings
    • The bacteria can be resistant to antibiotics
    • The elderly population- immune systems weaker

Symptoms

    • Red eye
    • Lids are sticky with a crusty material on the lids/lashes
    • Difficulty opening eyelids in the morning - Burning/“foreign body sensation”
    • “Lumps and bumps” → patients will describe the condition like this
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48
Q

Chronic Staphylococcal Blepharitis

SIGNS

A
  • Upper or lower lid hyperemia
  • complications along lid margin - Madarosis / Poliosis / Tylosis
    • Irregular lid margins
    • Collarettes at the base of lashes
    • Rosettes along lid margin
    • Internal and External Hordeolum - Acute infections of glands
    • Chalazion
  • Corneal findings SPK - Exotoxins on the inferior or superior part of the cornea
    • Consequential dry eye issues - The ocular surface of the eye is changing which results in poor tear stability (the lipid → aqueous → mucin layers of the tear film are changing)
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49
Q

Identify and full treatment / Management plan

CHRONIC

A

Chronic Staphylococcal Blepharitis

  • Warm compresses / Commercial 10min QID OU
  • Lid Scrubs Commercial after warm compresses QID, For 2weeks then taper to TID 2weeks - up to 8wks while improvement noted then 1wk / month to prevent return
  • Topical Steroid- antibiotic combination. Pred-G TID / 7-10 days
  • Artificial Tears unpreserved Shorthand: 1 gtt TID or QID / 6 weeks - 6 months
  • Oral Antibiotics Doxycycline 50 mg daily PO for ~3-6 months
  • BlephEx / Mechanical lid scrubber

- Hypochlorous acid BID / 10 days

  • Discontinue and discard any eye make-up products
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50
Q

Seborrheic Blepharitis

Symptoms and Signs

A
  • Common ‘dandruff’ on the lid margin area
  • Can affect the scalp, face and brow area
  • Caused variety of factors including hormones, infection, stress and nutrition
  • Underlying Staphylococcal Blepharitis infection

Symptoms

  • Isolated Seborrheic Blepharitis Asymptomatic but if Seborrheic Blepharitis is in combination with an Staphylococcal Blepharitis infection, the patient will probably have symptoms ○ Burning/“foreign body sensation” in eyes ○ Bilateral involvement of both eyes
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51
Q

Seborrheic Blepharitis

Signs

A

Very mild lid hyperemia if any

Collarettes might be found on the lashes → can either be found at the base of the lashes or suspended on the lashes

○ No lid margin ulcerations

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52
Q

Identify

Treatment and Management

A

Seborrheic Blepharitis

Warm compresses (3-4x a day for 10 minutes for 1 week)

Lid scrubs J&J shampoo 3-4x a day for 1 week

Hair/scalp treatment with selenium sulfide shampoo (Run-off onto lids

○ Discontinue any make-up products

○ Follow up appointment 2 to 4 weeks after first appointment

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53
Q

Angular Blepharitis

Features and Symptoms

A

Frequent in dry/warmer climates

  • Commonly found in the elderly - Staphylococcus aureus

- Alcoholics - Moraxella

Symptoms

Red eye on one part of the eye”

  • Skin changes - Irritation/itchy sensation
  • Could be described as “all of a sudden” onset
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54
Q

Angular Blepharitis

Signs

A
  • In the lateral canthus area, there could be redness/hyperemia
  • Dermatological findings
  • Excoriation → “cracked” skin
  • Maceration → “softened” skin
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55
Q

Identify

Treatment and Management (2 variations)

A

Staphylococcus aureus infection - topical antibiotics for bacteria along lid margin

Gentamicin : 1 gtt TID / 1 week

Moraxella infection, prescribe zinc sulphate solution to reduce the number of bacteria along lid margin

  • 1 gtt QID / 1 week
    • Discontinue any make-up products
    • Could also recommend patient to follow lid hygiene protocol (warm compresses + lid scrubs) for 1 week
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56
Q

Meibomian Gland Dysfunction (Meibomianitis)

Features

A
  • Characterized as a hypersecretion of lipid production
  • Inflammation along the lid margins and ocular irritation
  • Excessive secretion of lipids
  • Affecting tear production/tear film in eye
  • Meibomian orifices are blocked

Lipids from the Meibomian glands in the eyelids

Lipids allow for a smooth surface in the eye and consistent refraction of light

Lipids prevent evaporation of the underlying aqueous layer

Lipids provide the forces for redistributing the tears evenly across the tear film after blinking

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57
Q

Meibomian Gland Dysfunction (Meibomianitis)

Symptoms and Diagnosis

A

Symptoms Variable if their tear film is unstable complain

DrynessBlurrinessBlinking irritationTired eyesBurning sensation

● Diagnosis - look at lid margins

○ Examine the Meibomian gland orifices blocked or clogged

○ Press gently on the lid margin - clear/oily fluid comes out → if not, more yellow and sebum-like?

○ If blocked/clogged and yellow/sebum is coming out → indicates the Meibomian glands are not functioning at an optimal level

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58
Q

Identity

Treatment and Management

A

Meibomian Gland Dysfunction (Meibomianitis)

○ Lid hygiene/warm compresses

○ Expression of oil glands ■ Allow patient to sit with a warm compress in the office for 10 to 15 minutes ■ “Express” their Meibomian glands

● 1 drop of proparacaine 20/20 ● Place one wetted Q-tip patient’s inner lid margin and also outside role and express to top

○ Oral antibiotics - Doxycycline calm down inflammation and control the secretions of the Meibomian glands

■ Not a common method to manage this gland dysfunction, but can prescribe a low dosage over several months ● Doxycycline 50 mg daily PO for ~3-6 months

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59
Q

Meibomian gland dysfunction classification

2 types

A

Classifications

Meibomian gland hypersecretion

■ The Meibomian gland isproducing lipids but the ducts/orifices are blocked

■ The lipids are not getting on to the tear film

○ Meibomian gland anatomy is changing

■ This can happen with age

■ The Meibomian glands can shrink and become stunted (atrophy) ■ Can check for this using infrared imaging to anatomically see the extension of the Meibomian glands

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60
Q

External Hordeolum

Features and Symptoms

A
  • Acute Staphylococcal infection of the Gland of Zeiss - - Characterized by a focal swelling on the lid margin
    • Tends to worsen on the 2nd or 3rd day
    • Bump pointing outwards - Red - Tender to the touch (pain) - Warm in temperature to the touch
    • May develop a “pus point”

Symptoms

  • Sudden and recent onset
    • Progressively getting worse
    • Reg bump along the upper or lower lid margin
    • Bump enlarging over a couple of days
    • Tender to the touch (“pain”)
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61
Q

External Hordeolum

Signs

A

Signs/Objective Findings

    • Focal area along lid margin elevated
    • Red
    • Dome-shaped
    • Tender to the touch
    • Warm to the touch
    • Pus point pointing outwards towards the observer
    • Swelling/edema
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62
Q

Identify

Treatment and Management

A

May resolve on its own (usually within a week)

  • Warm compresses - QID for 10 mins for 1 week - If improve, can lessen warm compresses to BID for 10 mins until week is finished - Warm compresses can accelerate the process of healing
  • Lid Scrubs - underlying Blepharitis - initiate the lid hygiene protocol (warm compresses + lid scrubs 4x a day for 10 mins for 1 week) - Broad spectrum topical antibiotics
  • Debatable treatment method - Can prescribe: Polytrim 1 drop TID (3x/day) for 1 week
  • Discontinue and discard any makeup products
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63
Q

Internal Hordeolum

Features and Symptoms

A

Acute onset and infection

Staphylococcal infection to Meibomian glands

○ Infection will involve **more surface area of the tarsal area **

○ Infection leads to acute inflammationRednessTenderness/pain in the area ■ Swelling/edemaWarmth

● Symptoms

○ came on very suddenly (recent onset)

○ The bump is progressively getting worse

Focal area of elevation along the upper or lower lid margin

○ The bump has been enlarging over a couple of days

○ Very tender to the touch (pain)

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64
Q

Internal Hordeolum

Signs and considerations

A

Focal area along lid margin that is elevated

Redness in the area

peak of elevation does not point outwards / no pus point

○ Tender to the touch ○ Warm to the touch

An internal Hordeolum can lead to Preseptal cellulitis

■ The internal hordeolum usually stays in one spot, but it can spread on to the lid adnexa area → will not be a focalized region anymore → this can lead to the preseptal cellulitis → if this occurs, we should act more aggressively in treatment

Orbital cellulitis ■ Rarer condition than preseptal cellulitis ■ This condition is considered an ocular emergency → an Ophthalmologist or ER doctor should be contacted ■ Orbital cellulitis usually occurs due to ocular injury/trauma

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65
Q

Identify

Treatment and Management

A

INTERNAL HORDEOLUM

Warm compresses ● 10 minutes QID 1 week

● The heat from the warm compresses will “get the infection going” as the heat will increase the infection so it will heal faster

Lid hygiene ● If underlying blepharitis is suspected, suggest the lid hygiene regimen

● Remember lid hygiene = warm compresses + lid scrubs

■ Discontinue and discard any eye makeup products

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66
Q

Identify

Treatment and Management

A

Preseptal cellulitis

● Broad spectrum topical antibiotics ● Polytrim 1 gtt TID / 1 week

● Polysporin: 1 ung qhs / 1 week

Combine the Polytrim and Polysporin antibiotics for one week!

● Make sure the patient is informed on their responsibility to complete their prescribed antibiotic → if the patient stops mid-week, they could be causing bacterial resistance ● Polytrim is implemented AFTER lid hygiene

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67
Q

Identify

Treatment and Management

A

Orbital cellulitis

■ If a patient presents to your office with orbital cellulitis, write a prescription for a strong topical antibiotic (ex: Vigamox drops) that they can pick up from a pharmacy on their way to the hospital

See attached table

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68
Q

Chalazion

Features and Symptoms

A

Chronic lipo-granulomatosis inflammation of Meibomian glands → caused by retention of granular and granulomatous tissue

NO ACUTE SIGNS OF INFLAMMATION

result from non-resolved internal hordeolums

  • Waste product secretions Meibomian glands don’t dissipate

Symptoms

    • Raised, red bump
    • Focal area of elevation along the upper or lower lid adnexa - Bump enlarges over a long period of time (gradual!)
    • Hard round nodule
    • Not tender to the touch! No pain!
    • Slow onset, sterile swelling
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69
Q

Chalazion

Signs

A

Signs/Objective Findings

  • Elevated focal lesion
  • Dome-shaped
  • Not tender/painful to touch!
  • Not warm to touch!
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70
Q

Identify

Treatment and Management

A

Chalazion

  • Warm compresses AGGRESSIVELY! - The chalazion might resolve Only if small
  • Commercial warm compress and urge the patient to do the warm compresses 6 times a day for 10-15 minutes for 2 to 3 weeks
  • Excision and Biopsy - aggressive warm compress treatment and the chalazion is still unresolved or large to start with recommend excision
  • excision should biopsy the specimen afterwards to confirm or reject the presence of sebaceous cell carcinoma

Steroid Injections

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71
Q

Demodex

Features and Symptoms

A

Very common type of mite (8-legged)

○ Human manifestation is called demodicosis

bilateral

○ Risk factors ■ Elderly population ■ Warmer climates

Symptoms

Sore lids/redness in the morning

○ Itching AM (Defining symptom)

Burning sensationCrusting on lid margins and lashesBilateral ○ Chronic

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72
Q

Demodex

Signs

A

○ Bilateral lid involvement

○ Inflamed lid margin

○ Collarettes are “wrapped like a sleeve” on cilia → start from the base and move up cylindrically along the cilia

Remember, the collarettes in Acute and Chronic Staphylococcal Blepharitis are mainly found on the base of the lashes and the collarettes in Seborrheic Blepharitis are usually suspended on the lashes

Microscope in Lab

Pull 4 lashes from each lid using a tweezer ■ If there is >6 demodex, considered excessive

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73
Q

Identify

Treatment and Managment

A

DEMODEX

○ Topical Steroids - the itching and inflammation

○ Lid Hygiene ■ Warm compress 4x a day (QID) for 10 minutes followed by lid scrubs

Newer Treatment = Tea Tree Oil 50% consentration

■ Should recommend the commercial brands of Tea Tree Oil (Oust Demodex Cleanser, Cliradex wipes, etc.)

■ Official treatment protocol: Cliradex BID / 10 daysAfter 10 days, use 1x a day for another 10 days

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74
Q

Phthiriasis Palpebrarum

Features and Symptoms

A

Pediculosis: a parasitic infection - Lice (plural); louse (singular)

  • 2 types: Phthiris pubis: crab louse on lids due to spacing and density
  • Transmitted sexually/promiscuity

Symptoms

    • Sore lids/redness
    • Itching (all day long/constant!)
    • Burning sensation (tear film is affected)
    • Crusting on lid margin/lashes - Bilateral lid involvement
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75
Q

Identify

Treatment and

A

Phthiriasis Palpebrarum

  • Ointment - Antibiotic + steroid ointment : Pred-G TID ung / 1 week
  • Antibiotic to fight the blepharitis infection and steroids to control itching/soreness
  • Remove nits manually - sterilized forceps and pull off every nit from the lashes and destroy
  • return to clinic in 2-3 days
  • Patient might have lice still alive that could still be reproducing - Continue having the patient come in every 2-3 days until the lashes look completely clean - Lid Hygiene - Can also recommend warm compresses + lid scrubs
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76
Q

Phthiriasis Palpebrarum

Signs

A
  • Bilateral lid involvement
    • Inflamed lid margin (hyperemia)
    • Secondary signs of blepharitis (collarettes at the base of lashes)
    • Red/black deposits on the eyelashes - Fecal material of the louse → usually causing the itching/allergic reaction - Nits (eggs) wrapped around the cilia
    • Eggs are laid by the female louse on the lashes - The female lays 2-3 eggs in 24 hours - Adult louse is mature for 15-25 days - The eggs look like translucent balloons on the cilia
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77
Q

Phthiriasis Palpebrarum involves other necessary steps

A
  • Hygiene - Wash affected clothes and sheets on high heat for 20-30 minutes or place in a sealed bag to suffocate/kill lice

Family Considerations - Partner: need to let significant others know they might have same condition - Family: other family members might have same condition especially if due to cramped living quarters

  • General Physician - Need to involve general physician as there may be lice on other parts of the body
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78
Q

Molluscum Contagiosum

Features and symptoms

A

○ Often seen in children

○ Found in the HIV/AIDS population Used to be larger (due to immuno-compromised systems)

DNA pox virus: epidermal (skin) infection

○ Insidious onset (the disease “creeps up” and forms)

○ Characterized by painless wart-like lesions

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79
Q

Molluscum Contagiosum

Signs

A

Multiple lesions transmitted by contact → auto-inoculation

→ found on the lid adnexa area

○ Usually 2-10 mm round, central depression

■ If HIV is involved, the lesions are a lot larger (>1 cm)

Center of the lesion has cheesy-colored contents

Hair follicles and skin surrounding the lesion look normal!

○ May cause secondary follicular conjunctivitis

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80
Q

Identify

treatment and Management

A

MOLLUSCUM CONTAGIOSUM

○ Sometimes the lesions go away on their own

■ Tell the patient not to touch their face/orbital area

○ Excision wait ~1 year to make sure the virus isn’t active anymore (no new lesions appearing)

○ Cauterization

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81
Q

Verruca

Signs and Symptoms

A

Viral involvement (Human Papilloma Virus - HPV)

  • Can affect the lower or upper lid adnexa
  • Signs - Characterized by “frondular” growth
  • Little lesions together (look like cauliflower or broccoli florets) - Branched together, no space between them and pointing outwards
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82
Q

Identify

Treatment and Management

A

VERUCCA

May regress with time

  • Cauterization when no longer active
  • After many months, if no growth is occurring, can cauterize or laser
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83
Q

Contact Dermatitis

Features and symptoms

A

○ Allergic reactions

○ Exogenous source (plant or cosmetic product)

○ Can affect other parts of the face

○ Unilateral or bilateral ocular presentation

Symptoms

Itching ○ Redness to lid adnexaIncreased lacrimation (if close to lid margin) ○ Adnexa swelling

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84
Q

Contact dermatitis

Signs

A

○ Redness to skin surface

Edema (swelling of lid adnexa)

○ Maybe bilateral or unilateral

○ Excessive tearing

○ Flaking of the skin surface

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85
Q

Identify

Treatment and Management

A

Contact Dermatitis

○ Cold compresses 4 to 6 times a day for 1 week

○ Antihistamine

○ Topical steroids ■ Cream or ointment applied to area for 1-2 weeks

■ Steroids not used langer than 2 wks ● If steroids get in the eye, IOP can increase If steroids are used for a long time, the skin in that area can thin out

○ Remove exogenous agents ■ If a specific cream or beauty product was the culprit, get rid of it!

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86
Q

Conjunctival Follicles

A

Focal hyperplasia (enlargement of an organ or tissue due to increased reproduction of cells)

Little pockets of lymphocytes found in the conjunctival stroma (newly formed lymphoid tissue)

● Size 0.5mm to 2mm

● Location - palpebral conjunctiva (can check lower palpebral and evert the lid to check upper palpebral)

Pathophysiology - Localized cell-mediated immune response (could happen when you have a toxic reaction to an eye drop)

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87
Q

Follicular conjuctivitis

Signs + Causes

A

Appearance

ElevatedClear/milky/translucent centersBlood vessels located at the BASE of the follicle

○ If the eye is red and the patient is presenting with follicles, the problem is the follicles and need to determine the cause!

CausesToxins: irritants to patient’s eye cause patient to develop hypersensitivities ○ Examples: Molluscum contagiosum, chemicals, viruses

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88
Q

Folliculosis

A

○ A condition that children and young adolescents might have (NOT a disease and NOT caused by a virus or toxin)

○ Eye is very “quiet” → not red or hyperemic

○ Due to hyperactive lymphatic system

Disappears with age

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89
Q

Papillae

General

A

Histopathology - Non-specific response to irritants (allergy or bacteria related) to conjunctiva

Fibrovascular in origin

  • Small to very large
  • Location - Elevations usually found on the upper and lower palpebral conjunctiva (upper more common)
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90
Q

Papilae

Signs and Causes

A

Appearance

    • Elevated
    • Deeper red (very vascular looking) → “meaty red”
    • Blood vessels at the core of the papilla
    • Increased neutrophils to area to fight bacterial infection or increased eosinophils to fight allergic reaction

Causes - Bacterial infections - Contact lens overwearing - Allergies

  • Other Facts - Giant papillae occur in vernal conjunctivitis (seasonal allergies) - Giant papillae also occur due to contact lens wear
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91
Q

Retention Cysts

A

● Appearance Elevated, smooth/taut surface

Clear-like fluid (vacuoles) → blister appearance

● Location - found in the interpalpebral zone / Found on the bulbar and palpebral conjunctiva

● Causes

  • Cellular degeneration (epithelial cells not sloughing off correctly)

● Treatment - Removal by lancing (lance → drain → flatten) if of cosmetic concern

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92
Q

Gross Anatomy of the lacrimal system

Drainage pathway

A

Drainage Pathway: puncta (small opening) → lacrimal canaliculi → lacrimal sac (tears drain into here) → nasolacrimal duct → finally drains into the inferior meatus

  • Puncta - upper and lower

Canaliculus - upper and lower canaliculus → join form the common canaliculus

  • Lacrimal pump - _Valve at the entry point of the common canaliculus /_prevents backflow
  • Lacrimal sac - Attached to the periosteum - Fibers from the orbicularis oculi muscle help with blinking and spread the tears along the eye - The negative pressure in the lacrimal sac helps to push tears along passageway
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93
Q

Jones Test 1 + 2

Explain

A

Test patency or blockage between the puncta and the inferior meatus

● Jones Test 1 Procedure

○ Place NAFl in the eye ○ several minutes, blow their nose into tissue paper OR use a Q-tip and swab nose

○ Examine the tissue paper or Q-tip for fluorescein residue → if the yellow stain is present, then there is good drainage/patency ●

Jones Test 2 - force NaFl solution into caniculus

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94
Q

Regugitation test

Explain

A

Regurgitation Test Procedure

  • Put NAFl in eye
  • slit lamp /cobalt blue filter
  • Pull the lower lid slightly away and locate the lower puncta
  • Press on the nasolacrimal sac - Tears should go back out the way they came from (emerge from the puncta) - If the yellowish tears reemerge, the system is patent
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95
Q

Common Disorders of the lacrimal system

list

S / ECT / EN

A

Stenosis/blocked puncta / AGE / Inflamation of the area

MX & TX - Probing or Sx if not sucessful

Entropion of the lid → inversion of the puncta

Ectropion of the lideversion of the puncta

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96
Q

Nasolacrimal Duct Obstruction

Features / MX & TX

A

Infants

Stenosis of puncta and canaliculi opening in the nasolacrimal d

● 1 month old, nasolacrimal duct should open NORM

● Uni / Bilateral ● asymmetric

MX & TX ○ Reassure lacrimal system should open up in time by their own (canalize)

○ Accelerate ■ Gently massage nasolacrimal sac ■ Use warm compresses (4-5x a day for a few minutes)

○ Surgery ■ If not open ~1 year after birth, might refer for surgery ■ Dacryocystorhinostomy (DCR) ■ Infection because of stenosis

■ In this case, the lacrimal sac area would be red, tender/painful to the touch, elevated and warm ■ refer pediatrician oral antibiotics

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97
Q

Dacryocystitis

Features / Symptoms

A

Acute infection and inflammation of the lacrimal sac due to closing of the puncta

  • 50-60 yrs old - women dt anatomical difference Smaller opening

Symptoms

    • Sudden and recent onset
    • Progressively getting worse
  • - Red
    • Tender/painful
    • Elevated
    • Excessive tearing
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98
Q

Dacryocystitis

Signs

A

Signs

    • Red focal elevated lesion
    • Tearing
    • Inner canthal area to lacrimal sac involved
    • Firm nodule
    • If infection spreads further, complications like preseptal cellulitis
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99
Q

Identify

Treatment and Management

A

Dacryocystitis

  • Warm compresses
  • Topical antibiotics - Broad spec. Polytrim / Gentamycin

Tobramycin QID 1 week

  • Oral antibiotics 1 week
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100
Q

DRY EYE

Definition

A

Dry eye is a multifactorial disease of the ocular surface

Loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles

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101
Q

DRY EYE

Approach

A

Dry Eye in clinic

  • ○ Determine the risk factors for the patient AGE / SEX
  • ○ Determine the symptoms the patient is experiencing
  • ○ Determine the ocular surface damage - Na Fl Staining / Inflamation all lacrimal structures
  • ○ Determine tear film stability Tear Qaulity
  • ○ Determine tear production TBUT
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102
Q

Overview of Lacrimal system

A
  • Lacrimal gland → type of exocrine gland; consists of lobular ducts and acini aqueous layer / innervated by the ophthalmic branch of the trigeminal nerve (CN 5) and has some sympathetic innervation
  • Accessory glands of Krautz and Wolfring → contribute to aqueous secretions; found in the subconjunctival tissue
  • Meibomian glands → found in the tarsal plate; produce lipid/oil

Conjunctival Goblet cells → found in epithelium of conjunctiva; aqueous/mucin production

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103
Q

Tear Film Lipid Layer

Defects of lipid Layer

A
  • Meibomian Glands and the Glands of Zeiss
  • Stabilizes the tear film
  • Reduces evaporation of aqueous content
  • ○ Composed of cholesterol, fatty acids and phospholipids
  • Lowers surface tension
  • ○ Allows for smooth refraction of light
  • ○ Provides forces for redistribution of tear film after the blink

● Deficiencies Causes

  • ○ Lid problems (entropion, ectropion, blepharitis)
  • ○ Contact lenses
  • Meibomian Gland dysfunctions
  • ○ Bell’s Palsy Lag opthalmos
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104
Q

Aqueous Layer tears

Defects of Aqeous layer

A

Lacrimal Gland and Accessory Glands of Krause & Wolfring

○ Basic aqueous tear secretions

○ Composed of salts, proteins, glucose, lactate, water soluble molecules, lactoferrin and lysozymes

● Deficiencies due to…

  • Decrease in lacrimal gland tear production
  • Atrophy AGE
  • Decreased sympathetic innervation or problem with CN 3
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105
Q

Mucin layer of tears

Defects of Mucin Layer

A
  • Mainly by Goblet cells in the conjunctiva + crypts of Henle and glands of Manz
  • On corneal epithelium microvilli → converts corneal epithelium from hydrophobic to a hydrophilic

● Deficiencies dt

  • Lack of Vitamin A
  • ○ Trachoma → thicker upper lid surface and disrupts Goblet cell mucin production
  • Lasik surgery → during surgery, a suction ring is placed around the cornea and can disrupt Goblet cell mucin production
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106
Q

Mucin layer Glycocalyx

A

Mucin Layer and Glycocalyx

○ Mucins 1, 4 and 16 (MUC) are associated with corneal and conjunctival epithelial layers and helps to develop the glycocalyx

○ The glycocalyx is produced by the corneal epithelium, which attracts mucin and allows for good adherence between mucin layer and corneal epithelial microvilli

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107
Q

Tear film Structure

Traditional & Contemporary

A

Traditional**

■ 3 distinct layers (lipid → aqueous → mucin)

Contemporary

■ Still 3 layers but instead of all the layers being separate from each other, there is different concentrations of mucin spread out through the aqueous layer

Higher concentrated towards the corneal epithelium and less mucin concentrated towards the top of the aqueous layer

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108
Q

What is tear Osmolarity, how does it affect dry. eye

A

Elevated tear osmolarity is characteristic of dry eye

  • A decrease in goblet cell density would have a decrease in mucin
  • Lactoferrin and Lysozymes in the aqueous layer - immunological components
  • If aqueous production decreases, the concentration of lactoferrin and lysozymes would also decrease which would affect tear osmolarity
  • Surface changes to the epitheliums in the eye (cornea, lens, conjunctiva) can cause inflammatory mediators to be released in too high of concentrations in the tear film which will also increase tear osmolarity
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109
Q

DRY EYE

GENDER / AGE

A

Patient History & Risk Factors for Dry Eye

Age / Meibomian glands atrophy - decrease in oil production and decrease in androgen hormone production → regulate leads to a decrease in tear production ○ Androgen hormones regulate Meibomian and Lacrimal gland production

● Gender

Androgens immuno-suppressive (inflamation mediators)

○ Females levels change menopause, pregnancy, breast feeding, and oral contraceptives

○ Less ANDROGEN than ESTROGEN

instead of inflammatory mediators being kept at a lower level on the ocular surface, there will actually be more inflammatory mediators on the ocular surface

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110
Q

DRY EYE

Environmental & Lifestyle

A

● Environmental factors

Air quality ○ Pollution ○ Smoking ○ Air dryness ○ Altitude ○ Lack of humidity

● Vocation/Lifestyle

Prolonged computer usage ○ Frequent air travel ○ Working in arid conditions ○ Prolonged reading

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111
Q

DRY EYE

Systemic Med HX and Systemic Drugs

A

Systemic Medical History

Rheumatoid Arthritis ■ An increase in inflammatory mediators ○ Sjörgen’s Syndrome ■ Autoimmune disease that is one of the main causes of dry eye

■ The autoimmune disease disrupts lacrimal glands

■ 9:1 ratio females to males ■ Sjörgen’s Syndrome Triad: dry eye + dry mouth + arthritis

Grave’s Disease ○ Acne Rosacea ○ Diabetic patients

● Systemic Medications

○ Antihistamines/decongestants (Benadryl) ○ Hypertension medications (diuretics, beta blockers) ○ Antidepressants (Prozac, phenothiazines) ○ Oral contraceptives (birth control pills) ○ Alcohol derived medications (NyQuil) ○ Parkinson Disease medications

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112
Q

Risk factor for dry eye specific to the ocular HX , MX used and Ocular Sx

A

Ocular Medications

  • Preservatives cytotoxic (Benzylcodium Chloride BAK)
  • BAK only short term - cytotoxic (increase inflammatory mediators, decrease Goblet cell mucin production) and can change tear osmolarity

● Contact Lens Wearer

Pre-lens tear film is thinner / DECr tear exchange and INCr evaporation

● Refractive Surgery (Lasik)

  • 3 to 6 months post-op
  • Damaged Goblet cells Dt ring suction around the limbus
  • Goblet cell mucin production DECr
  • Px uses Gtt and the goblet cell regenerate
  • Lasik surgery neurotrophic theory → nerve endings damaged and no sensory information to lacrimal gland DECr production Aqueos
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113
Q

Underlaying CAUSES of dry eye - 2 Primary causes

Broad 1st tier devision

A

1) Aqueous Deficiency

  • not producing enough tears
  • T cell mediated inflammatory reaction to the lacrimal gland causes a decrease in tear production
  • ocular surface irritated and inflammation is increased
  • Constant cycle of low-grade inflammatory states

2) Evaporation

  • Due to Meibomian gland dysfunction altered lipid metabolism OR age/atrophy of the Meibomian glands
  • Meibomian gland oil changes from trans unsaturated fats to saturated fats causing OBSTRUCTION
  • Obstruction leads to hyperosmolarity and INCr evaporation → inflammation will occur
  • Age/atrophy of the Meibomian glands /
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114
Q

2n tier of dry eye Causes following the Primary AQUEOUS DIFFICIENT and EVAPORATIVE DRY EYE

A

A) Sjörgen Syndrome

Autoimmune disease associated with Triad of dry eye + dry mouth + arthritis

B) Non-Sjörgen Syndrome

lacrimal gland blocked or lacrimal gland atrophy

C) Intrinsic

    • Meibomian glands not producing enough oil
    • Lid structure has been altered
    • Not blinking enough
    • Drug induced

D). Extrinsic

    • Contact lens wearer
    • Preservatives like BAK
    • Vitamin A deficiency
    • Ocular surface diseases
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115
Q

DRY EYE

Symptoms

A

Burning/stinging sensation dt tear film changing

FB sensation dt corneal epithelium damage to the

epithelium → a feeling of scratchiness/grit/irritation

Tearing/increase in reflex tearing → compensation leads for dry eye leads to the brain realizes the eye is dry and thus sends a signal to counter / excessive tearing

Dryness

Fluctuating Blurry vision during 7A Tear film not evenly distributed

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116
Q

Anterior segment diseases Causing

DRY EYE

A

PX: ALLERGIES , BLEPHARITIS and MEIBOMIANITIS >> Risk Dt lipid layer being disrupted

LID appositional disorders

(ECTROPION, CHRONIC LID INFLAM, LID CLOSURE , BLINK PATERNS)

  • Anterior lid problems - Staphylococcus blepharitis

- Seborrheic blepharitis

  • Posterior lid problems. - Meibomian dysfunction
  • Eye drops - Preservatives are cytotoxic BAK / Thimerisol
  • Viral conjunctivitis - loss of Goblet cells = release of cytokines and leukotrins

which are inflammatory mediator

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117
Q

SIGNS to look for in DRY EYE

A

★ Lid Evaluation

  • Lagophthalmos
  • lid apposition abnormalities - ectropion cause punctal eversion
  • lid margin - Chronic Blepharitis / / Meibomeinitis Decreased lipids

★ Evaluate blink rate and tear flow

  • ● Flow lacrimal gland medially + down to drainage /medial canthus
  • ● Tear flow facilitated by the blinking action of the eye
  • DECr Blink rate. tear flow might be compromised
  • Blink rates NORM 15/MIN. NEAR work 5/MIN
  • ○ Incomplete blinking / DECr quality of the blink
  • ○ Can advise patients on the correct way of blinking

■ Side note, “20-20-20” rule and advise on correct blinking

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118
Q

Evaluate Blinking Paterns and Drainage system

A

Look for lid blinking patterns

  • Inferior corneal staining pattern NaFL / SPK on lower cornea dt a lack of Lubrication
  • Blink evaluation (LipiView II Ocular Surface) How well lipids distribute
  • Uses infra Red to examine structure of meibomian glands for Atrophy

● Look at the Lacrimal Drainage pathway

stenosis/blockage of puncta OR blockage of the nasolacrimal duct might

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119
Q

How to measure TEAR VOLUME

5 Options

A
  1. Tear MENUSCUS Height
  2. Schirmers 1 and 2
  3. Strip Meniscometry
  4. Phenol Red Thread
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120
Q

Tear Meniscus HGT

Schirmirs 1 + 2

explain + Norms

A

Tear Meniscus / Prism - Add NaFl and measure tesr lake with Cobalt blue filter

  • The normal amount of meniscus height is 0.2 to 0.5 mm

● Schirmers I Testing (Reflex and Normal)

  • Norms
  • ■ >15 mm in 5 minutes = normal
  • ■ 5 mm to 10 mm in 5 minutes = significant dry eye
  • ■ <5 mm in 5 minutes = severe dry eye

● Schirmers II Testing (Basic tear only)

■ proparacaine anesthetic NB Dry eye

  • Norms
  • ■ <5 mm in the eye in 5 minutes = dry eye
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121
Q

Phenol Red Thread

Strip Meniscometry

Norms and explanation

A

Phenol Red Thread Test

15 seconds ○ Norms

■ >20 mm in 15 seconds = normal

■ 10 mm to 19 mm in 15 seconds = borderline dry eye

■ <10 mm in 15 seconds = severe dry eye

Strip Meniscometry Tube (SM Tube)

○ Norms

■ >5 mm in 5 seconds = normal

■ <5 mm in 5 seconds = abnormal (dry eye)

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122
Q

Variations of tear film Stability

TBUT & New TBUT

A

Invasive Tear Film Break Up Time (TFBUT) (As I DID)

  • ■ Repeat this procedure 3 times and then average the results
  • ○ Norms
  • ■ 20 to 30 seconds = average
  • ■ >10 seconds = normal
  • ■ <10 seconds = abnormal (dry eye)

● New Tear Film Break Up Time (TFBUT)

  • microquantities of fluorescein dye (5 μl)
  • ○ Newer Reference Values
  • ■ >5 seconds = normal
  • ■ <5 seconds = dry eye

● Non-Invasive Tear Film Break Up Time

  • ■ Machine concentric rings how long it takes in seconds for
  • the concentric rings to lose their structure
  • ○ Norms
  • ■ >10-18 seconds = normal
  • ■ <10 seconds = abnormal, dry eye
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123
Q

Corneal Staining

Different Agents Used

What stain which defect better

A
  • NaFl● Using a slit lamp + cobalt blue filter + fluorescein dye examine the corneal staining and loss of epithelial cells
  • ● Isolated loss = superficial punctate keratitis (SPK)
  • ● Coalesced areas = punctate erosions

Lissamine Green

  • ○ devitalized (dead) cells
  • ○ cyan/blue-green color on conjunctival surface /WHITE light
  • ○ Dye washes out of the eye very quickly

Rose Bengal Pink

○ evaluate devitalized (dead) cells

○ Looks like a pink/red color on the conjunctival surface / White

○ Dye lingers for longer (10 to 15 minutes) and is also slightly cytotoxic

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124
Q

Identify Condition and what to use to diagnose

A

● Filamentary Keratitis and Rose Bengal Staining

  • Filamentary Keratitis dead epithelial cells become Mucin coated and form filaments.
  • These filaments drag up and down with lid movements and scrape against the cornea causing a FB sensation and burning pain

severe dry eye

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125
Q

★ Mucocutaneous Junction

Line of Marx (LOM)

A

○ The Line of Marx delineates the wet and dry parts of the epithelium Sup and Inf

Posterior to the Meibomian gland openings

Stained with Lissamine Green to see any ocular surface changes

NORM very thin / Become thicker and move anteriorly in certain diseases

CLEAN KERITANISATION with SPUD

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126
Q

Lid Wiper Epitheliopathy (LWE)

A

Lid Wiper Epitheliopathy (acquired condition)

■ Dt abrasions of the lid and cornea due to a small tear film on the eye → if there is a small tear film, there is potential lid and cornea interaction and this can cause friction and alter the lid margin area

○ Stains Lissamine Green and extends more posteriorly down the palpebral conjunctiva from the Line of Marx

○ The thickness, width, convexity and surface area of the staining how much irritation is occurring

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127
Q

Bio Marker analysis, Norms

Meibomien Gland Evaluator ?

A
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128
Q

Inflamatory Marker MMP

important for which patients?

A

Use for Sjorgens Syndrome Px

Rapid Pathogen Screening

Elevated protein in tears, Only tests for Matrix Metalloproteinse

MMP-9

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129
Q

What 2 test can be done with a trans illuminator

related to Dry eye

A

Meibography

To view the anatomy of the meibomian glands / Usually done with Infra Red

KORB-Blackie method to check for lid seal

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130
Q

Posterior Embryotoxon

A

Autosomal Dominant

DEF: exaggerated Schwalbe’s line (Termination of Descemet’s membrane)
posterior cornea at 3 & 9 o’clock , also be a ring.

  • Schwalbe’s line is visible only with gonio, but in 15% normals it is displaced anteriorly.
  • It is seen as an irregular line or ridge up to 2 mm central to limbus and posteriorly.
  • The corneal surface between the line and the limbus is usually clear.
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131
Q

PANNUS

2 types

Normally superficial limbal vessels do not extend onto the cornea for more than 1mm

A

Any growth beyond the normal arcade

  • New vessels deep or superficial can be accompanied by sub-epithelial fibrous tissue or stromal scarring.
  • Scarring/fibrous tissue - clarity of the stroma is reduced
  • *Micropannus** - 1 to 2 mm beyond the normal arcade
  • *Causes**: inclusion conjunctivitis, staphylococcal blepharitis, contact lens wear, vernal conjunctivitis

Gross pannus - Extension greater than 2 mm

Causes: trachoma, phlyctenulosis, acne rosacea, atopic keratoconjunctivitis, contact lens wear, staphylococcal blepharitis

Conclusion: - if it is new or large, try to find etiology

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132
Q

Dellen

A

Localized thinning of stroma next to raised area, secondary to poor wetting and resultant stromal dehydration.

  • -Adjacent to raised mass : pinguecula or thick contact lens edge.
    • Stroma not hydrated - scarring and vascularization.
  • -Dellen have intact epithelium
  • -pinguecula and pterygiums don’t cause Dellen. So, a specific human antigen factor involved.
  • -Llittle or no risk of perforation.

Conclusion: treated to prevent scarring and vascularization. Remove cause / treat with lubricants, bandage CL etc.

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133
Q

Identify and also stain used

A

Herpes Simplex

Rose Bengal stains dead devitalized cells very well

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134
Q

Identify and what should be considered

A

NEGATIVE staining

Consider: Possible recurrent corneal abrasion / Erosions

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135
Q

Identify

A

SPK

Superficial punctate Keratistis (DRY EYE)

FB scar, 2nd NaFl diffused into epithelium at site of injury after some time

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136
Q

Cornea

Functions

Parameters

Layers

A
  1. Stay Transparent
  2. Refractive – 75% of refractive power
  3. Protective – protects internal eye from the outside environt

NORMS:
• Dimensions – 11.6 mm horizontally and 10.6 mm vertically

cornea at birth – +- 10mm H x10 mm V
• Central thickness is 0.53 mm and 0.70 peripherally.

Corneal Layers:

  • Epithelium
  • Basement Membrane
  • Bowman’s Membrane
  • Stroma
  • Dua’s Layer
  • Descemet’s Membrane
  • Endothelium
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137
Q

Corneal Epithelium

A

5-7 Layers 50 microns in depth

Basal columnar cells, which are attached by hemidesmosomes to basement membrane

Wing cells are in two or three rows

Surface cells are long and thin with flat nuclei arranged in 2 layers and joined by bridges.

The surface area of the outermost cells is increased by micro-plicae and microvilli to facilitate the absorption of mucin. This is important in corneal wetting.

7-14 days from division to desquamation

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138
Q

Basement Membrane

Bowmans Membrane

A

Basement Membrane

  • • Secreted by basal cells
  • • 6-8 weeks to regenerate
  • • Anchors to Bowman’s/stroma
  • Disruption may lead to recurrent corneal erosions

Bowman’s
Strong barrier to injury, pressure, and infection 11-17 micron in depth
Homogeneous condensation of the anterior stroma lamellae - continuous with the corneal stroma
• It is an acellular structure and does not regenerate when damaged
it stops approximately 1 mm short of the corneoscleral junction
• It scars when it is disturbed

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139
Q

Stroma

+ dua

A

90% of the thickness of the cornea

  • • ]Collagen producing fibroblasts (keratocytes), collagen fibrils, and ground substance.
  • • The fibrils are of uniform size and extend across the entire length of the cornea as bundles (lamellae). his regular lattice structure is why we have the extreme transparency of the cornea.
  • • The ground substance,- composed of proteoglycans. The proteoglycans help keep the fibrils in shape.

DUA

well-defined, acellular, strong layer in the pre-Descemet’s cornea.
may have impact on posterior corneal surgery and the understanding of corneal biomechanics and posterior corneal pathology such as: acute hydrops, pre-
Descemet’s dystrophies.

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140
Q

Decements Membrane

Endothelium

A

Descemet’s Membrane
Basement membrane of endothelium - Terminates in Schwalbe’s line, anterior limit of angle
• Elastic but can easily be broken away from stroma
• Composed of a fine lattice work of collagen fibrils consisting of an anterior banded zone,
• Normal thickness of Descemet’s is 3-4 microns at birth but increases to 10-12 microns
Endothelium

  • Single layer of flat, amiototic cells arranged in a hexagonal
  • Barrier function
  • Pump function key in maintaining corneal transparency
  • • Babies range from 3,500 to 4,000 cells per mm2.
  • In normal adult corneas, cell density is approximately 3,000 to 3,500 cells per mm2.
  • If cell density falls below 500 to 700 cells per mm2, it is increasingly difficult to maintain optical
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141
Q

Cornea Innervation

&

Blood Supply

A

Innervation
Sensory innervation - ophthalmic division of the trigeminal nerve(V) via the long ciliary nerves that branch in the outer choroid, near the ora serrata
middle third of the cornea / lose their myelin sheath after traversing 0.5-2.0 mm into the cornea

Bowman’s take an approximate 90 degree turn and terminate in the epithelium.

  • *nine months** for regeneration of damaged nerves
  • *Cornea Blood Supply**
  • conjunctival episcleral and scleral vessels that are around the corneo-scleral limbus
  • • The oxygen and nutritional requirements - atmosphere/ tear film anteriorly and the aqueous posteriorly.
  • Eyes are shut, oxygen is derived from conjunctival capillaries.
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142
Q

Palisades if Vogt

A
  • Contain blood vessels and lymphatics
  • Source of neovascularization
  • Dentate conjunctival projection into cornea
  • Important in epithelial regeneration

• The palisades & corneal stem cell population same area.

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143
Q

Loss of Corneal Clarity

A

It is not a disease
• The normal cornea is 78% water.
• 5% above the normal level, begins to scatter light
• response to/clinical sign of insult
• Clarity - pump function of the corneal endothelium
balances the fluid accumulating effect of intraocular hydrostatic pressure and corneal swelling pressure.
• Disturbances of the balance occur with problems in the epithelium and endothelium.
• When corneas imbibe water and swell, the distance between the fibrils increases but the fibril radii are not changed
Normal epithelium and endothelium have tight junctions that restrict the flow of electrolytes and fluid through.

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144
Q

Epithelial Edema

A

Epithelial edema - hydropic basal epithelial cell degenerativechanges and the development of extra-epithelial cellular fluid-filled spaces cysts/bullae.

Epithelium edema, the surface turns gray and loses its luster. The patient will suffer from decrease vision and glare.

Epithelial edema can present as epithelial microcysts, microcystic edema or epithelial bullae.

Epithelial microcysts are small, round, refractile lesions that originate in the basal layers migrate toward the surface, and stain.

Bullae - excess fluid accumulates / epithelial layers to separate from the basement membrane. They appear as flat, pebble- like lesions

Bullae break it exposes the nerve endings and your patient can be in significant pain.

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145
Q

Important factors to consider when taking the HX of CORNEAL Edema

A
  • Age of onset
  • Duration of symptoms
  • Unilateral or bilateral
  • Family Hx of corneal disease
  • Ocular medications
  • Previous ocular disease or surgery
  • Diurnal variation
  • Environmental effects on symptoms
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146
Q

Possible CAUSES of

Corneal Edema

A
  • Contact lenses
  • Epithelial defects (i.e. abrasion, ulcer)
  • Swimming
  • Medicamentosa (Inflamation of nasal mucosa / nasal spry overuse)
  • Angle closure glaucoma or high pressure open angle glaucoma
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147
Q

Signs and Symptoms of

Corneal Edema

A

SIGNS

  • An irregular, distorted corneal reflex
  • central circular clouding CCC (sclerotic scatter)
  • Epithelial Defect - halo of edema
  • Swimming and Medicines - roughened epithelium and loss of transparency

• Clinical Symptoms

  • Usually significant, Discomfort / FB sensation
  • Decreased visual acuity
  • Halos around lights, foggy vision
  • Spectacle blur after wearing RGP
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148
Q

Treatment for

Corneal Edema (Epithelial)

A

o Removing the cause (i.e. refit contacts)
o Non-preserved carboxymethylcellulose
o Hypertonic NaCl Muro 5 & 2 %
o Increase evaporation (fan, hair dryer)
o If secondary to stromal edema, remove the cause of the stromal edema
o Lower IOP
o Topical glycerin is used in acute angle glaucoma to clear the cornea so you can look at the angle
o Bandage Contact Lens therapeutic for bullous changes

For treating recurrent corneal erosions:

o Eyes with poor vision – you can use anterior stromal cautery scars to form firm adhesions between epithelium and underlying stroma

o Amniotic membrane
o Anterior Stromal Puncture
o Excimer laser
o Collagen Cross linking – riboflavin and UVA

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149
Q

Stromal Edema

A
  • Endothelium pump or barrier function decreased
  • Advanced stromal edema leads to epithelial edema (Buckling of Epithelium
  • mildly disordered fibrillar distributions and regions called “lakes”
  • Lakes - fluctuations in the refractive index, which increase light scattering
  • Corneal hypoxia leads INCr of lactate in the stroma. This increases the osmotic pressure Causes edema ensues. Acidosis impairs endothelial cell function, exacerbates stromal edema.
  • clinically appears as a painless, cloudy, thickening of the corneal stroma.
  • There is usually only mild reduction is va and mild glare
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150
Q

Causes of

STROMAL EDEMA

A
  • Hypoxia - Soft contact lenses
  • Fuch’s endothelial dystrophy
  • Focal keratitis
  • Surgical trauma or trauma
  • Endothelial dysfunction
  • Infections (corneal ulcers or endophthalmitis)
  • Uveitis , with keratic precipitates
  • Rupture of Descemet’s membrane (birth trauma or keratoconus)
  • Acute angle closure glaucoma
  • Long-standing increased IOP from open angle glaucoma
  • Toxic substances in the anterior chamber
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151
Q

Signs and Symptoms

Stromal Edema

A

Signs

  • Increase in width of the slit beam, folds in the Descemet’s
  • Pachymetry increases as edema does
  • >5% you begin to see vertical striae in posterior stroma
  • 10-12% of cases, folds in Descemet’s membrane
  • The stroma can be clear and still be edematous.

• Clinical Symptoms
o Minimal, until very advanced

o May complain of glare

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152
Q

Treatment of

Stromal Edema

A

If possible, treat underlying causes (CL, treat iritis)
Lower IOP (above 21mmHg)
Steroids if edema caused from inflammation (temporarily increase
endothelial cell tight junctions)
Topical glycerin in acute angle glaucoma to clear the cornea
IOP exceeds stromal swelling pressure epithelium edema occurs
o However if endothelium function is compromised epithelium edema can happen with

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153
Q

Surgical interventions at Endothelial layer

Prevent Corneal Edema

A

DSAEK
Descemet and endothelial layers and a very small amount of stroma are stripped

from the donor and placed on the inner surface of the cornea of the recipient o Adheres to new cornea / air bubbles
o Patient lies on his back for 24 hours to allow the air bubbles to tamponade the graft to the posterior stroma

DMEK

Descemet and endothelial layer are stripped same a DSAEK only tissue is thinner, better results but more difficult to do.

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154
Q

How IOP influences which part of the Cornea swells

A

IOP

In normal eyes, IOP has little effect on stromal thickness

However, when IOP exceeds stromal swelling pressure epithelium edema occurs

However, if endothelium function is compromised epithelium edema can happen with

pressures as low at 30

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155
Q

Corneal Scarring

A

Decreased vision and glare if on the visual axis
Bowman’s layer and the stroma scar

Grading Scars
o Nebular - faint
o Macular - translucent
o Leukoma - opaque
Scars are the result of an insult to the stromal matrix, activating keratocytes cells to gather at the site of insult and synthesize new collagen.
o This new collagen is a different type from the old collagen and is not as transparent.

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156
Q

Stages of Wound healing

CORNEA

A

o After wounding, transparent keratocytes differentiate into migratory fibroblasts
o Fibroblasts migrate into the wound margin
o At the wound margin, fibroblasts differentiate into non-motile, contractile myofibroblasts

o After wound closure, myofibroblasts disappear
o The persistence of myofibroblasts in a wound correlates with fibrotic healing
o There is also disorganized fibrillar and lamellar structures; vacuoles within and around keratocytes; convolutions and discontinuities in the basement membrane

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157
Q

Corneal Neovascularization

A

Corneal Neovascularization

Beyond 1-2 mm of limbus is neovascularization.
• Neovascularization Causes

  • tight soft contact lenses
  • trachoma
  • superior limbal keratitis
  • Anoxia appears to trigger some neovascularization.

• Neovascularization- decreased VA if cross visual axis.
Neovascularization in the stroma is more characteristic of interstitial keratitis, 90% secondary
to congenital syphilis but can be secondary to other systemic diseases (i.e. TB, mumps)
• Vessels not perfused with blood are called ghost vessels
• Infectious neo is usually deep in the stroma

158
Q

CORNEAL INJURY

Sources

A

• Infections
Bacterial / Viral. / Fungal
• Foreign bodies
• Contact lens wear and over wear
• Burns
o Heat o Radiation o Chemical

Majority involve epithelium. Bowman’s layer is very tough. Epithelial injury to the eye is very painful.
• An abrasion of the cornea involves removing corneal epithelial cells. Certainly, deeper abrasions will also involve deeper corneal structures.

159
Q

5 Main Symptoms

to evaluate with Corneal Injury

A

• Pain or Discomfort
first division of the trigeminal nerve, it has a subepithelial plexus and a stromal plexus. In eyes with corneal abrasion or bullous keratopathy, the direct stimulation of bare nerve endings causes severe pain. Patients with only mild punctate erosions may complain only of slight irritation which is made worse by blinking. Pain from inflammation or spasm of the ciliary body

• Halos
• Impairment of Visual Acuity
May be secondary to the loss of transparency from the wound itself or from the tears leaking into the wound

• Photophobia
Caused by abnormal, strong light induced miosis to an inflamed iris and ciliary spasm

• Lacrimation (excessive tearing)
Secondary to reflex stimulation of corneal nerves. Its degree frequently parallels the severity of the photophobia.

160
Q

How does Epithelium HEAL

A

Sliding of adjacent epithelial cells to cover denuded area starts within an hour

An enzyme is released from the damaged cells to loosen the tight attachments so they can slide

Fibronectin is also secreted by the cells and this acts like glue to hold cells together.

Mitosis begins within 24 hours from the distant cells. Within 3 days from the damaged area

The healing goes quicker if the temperature is increased

Only the basal cells, amplifying cells, and stem cell undergo mitosis

Corneal transient amplifying cells (TACs) are migratory cells which move from the limbus towards the cuboidal basal layer of the central cornea and become corneal basal

Jagged shaped edges are harder to heal.

If the basement membrane is involved, the process is markedly slowed

The basement membrane takes between 6-8 weeks to regenerate.

The epithelium cannot adhere to Bowman’s without the basement membrane

When the whole cornea is denuded, such as in a chemical burn, re-epithelialization occurs

from migration of conjunctival cells from the Palisades of Vogt’s

161
Q

Treating Corneal ABRASION

A

First make sure no foreign body still in eye / Evert sup lid
Before dye check for cells in the anterior chamber
QID / q4h
• gtts: Polytrim (polymyxin B and sulfate trimethoprim), Vigamox (moxifloxacin), Tobrex (tobramycin), or Ciloxan (ciprofloxacin).
OR
• ung: Polysporin(polymyxin B and Bacitracin) or tobramycin BID or QID
• If abrasion is from a finger nail or piece of paper these abrasions are more prone to recurrent corneal erosions and you should use an ung at night for at least a month
Cycloplegia prevent a reflexive iritis
• Depending on the size and location, monitor daily or within 24 hours and then every other day until it is healed
Pressure patch if area is greater than 10 mm2

(do not patch an abrasion soft contact lenses or
material is organic matter) DO NOT leave on for longer than 24hrs

• T patching / treatment with bandage contact lens / collagen shield. / amniotic membranes

162
Q

Corneal Abrasion treatment

SUPLEMENT MX

A

Prevent a traumatic iritis Topical cycloplegic agent

cyclopentalate 1% bid (cyclogel), Homatropine 2% or 5% bid to tid ALT Acular / Levro nepafac TID

Mild pain: Acetaminophen 500 mg every 4 to 6 hours,

ibuprofen 400 to 600 mg every 4 to 6 hours, naproxen 250 to 500 mg twice a day
Moderate pain: Acetaminophen with codeine (30 mg codeine) every 6 hours

163
Q

How would you treat PX that presents at 24hr post injury

A

NEGATIVE STAINING

Antibiotic if positive staining still present

UNG for as long as negative staing persists
Systane Nighttime Lubricant Eye Ointment (3.5 g )
Refresh PM, Refresh Lacrilube
Ocusoft Retain PM Ointment
Genteal Ointment

cyclo when to d/c- if no iritis and not a red angry eye and epithelium is all healed

164
Q

Penetration VS Perforation

Corneal injuries

A
  • A penetrating wound passes into the structure
  • A perforating wound passing through a structure

You can diagnose if something has Perforated the cornea by using the Seidel sign test to see if any aqueous fluid is leaking out.

You perform this by wiping a wet strip of fluorescein over the wound and viewing how the dye appears. With a positive Seidel, you can see the clear aqueous running through the yellow stain

165
Q

Recurrent corneal Erosions

TREATMENT

A
  • UNG - PM Preventative
  • Pressure patch, then UNG Pm and Gtt AM
  • Punctal Plugs
  • Debridement of Epithelium
  • Bandage contact lenses (Prolonged)

Newer therapies:

  • blood-derived eye drops
  • amniotic membrane graft application
  • judicious application of topical corticosteroids.

Surgical procedures

  • Epithelial debridement with diamond burr polishing (DBP),
  • Anterior stromal puncture (ASP)
  • Excimer laser phototherapeutic keratectomy
166
Q

Treatment example:

Recurrent Corneal errosions

A

Muro 128 ointment 5.0%, h.s.

FreshKote t.i.d.

Loteprednol 0.5% q.i.d. for two weeks, then b.i.d. for six weeks. (Check the patient’s IOP around week three or four.)

Doxycycline 20mg b.i.d.

Why Doxycycline?

Patients with recalcitrant recurrent corneal erosions often show increased levels of matrix metalloproteinase (MMP) enzymes. These enzymes dissolve the basement membrane and fibrils of the hemidesmosomes, which can lead to the separation of the epithelial layer. ) together with a topical corticosteroid (such as prednisolone)
Some doctors give 50 mg of Doxy bid

167
Q

Definition of Corneal Ulcer

A

Ulcer - Definition according to Dictionary of Ophthalmology
• Corneal Ulcer is a superficial loss of corneal tissue as a result of infection andinflammation which had led to necrosis.
It involves disruption of the epithelial layer with involvement of the corneal stroma T

• A necrotizing lesion with or without an abscess; inflammation-mediated breakdown affects the epithelium and stroma

168
Q

Differentiate between ULCER and ABRASION

A
169
Q

Foreign Body Removal

A

Treatment

  1. o Irrigate
  2. o Cotton swab
  3. o Spud or Magnetic Spud or 25-gauge needle
  4. o Alger brush
  5. o Remember to always flip lids to ensure a foreign body is not embedded under the upper lid.
  6. o After foreign body is removed, treat the corneal abrasion
170
Q

Identify and Discuss

A

Arcus

white or yellowish ring with a clear zone at the limbus
Composed of cholesterol esters, cholesterol, and low-density lipoproteins in stroma
-first in the inferior cornea in the stroma near Descemet’s membrane,
Men >. Women

PX <50 A serum lipid profile should be obtained.
-The presence of unilateral arcus may suggest vascular occlusion on the side without arcus.

Ask for Meds Lipitor

171
Q

Identify and Describe

A

Limbal Girdle of Vogt

Degeneration of sub epithelial collagen - cause may or may not be related to UV exposure

-White crystal-like appearance with or without a clear zone, almost always at 3 and 9 o’clock.

2 types:

Type 1 is separated from the limbus by a clear translucid zone. The reason for the clear zone can be explained by the fact that calcium deposition ends at the termination of Bowman’s, which is not at the same location as the sclero-limbal junction.

Vogt’s limbal girdle is a normal finding in any age:
• 55% of eyes 40 -60
• 93 % of eyes 70 -90
Conclusion: normal finding, no management needed

172
Q

Identify and Describe

A

Hudson-Stahli line

  • Iron deposition at level of Bowman’s
  • Yellowish, brown irregular line just inferior to mid-pupil, near where the margins meet -It may be more common in dry eye patients or patients with tear flow problems.

-Frequency parallels age: 20 = 20%, 60 = 60%

Conclusion: very common, usually a normal finding. When you are first learning to use a slit lamp, this is difficult to see.

173
Q

Identify and Describe

A

Descemet’s Striae

  • Small, linear striation in Descemet’s membrane, often are seen in otherwise normal corneas
  • They are usually vertically oriented but can be tilted slightly

Conclusion: no clinical significance; however, if large, may be associated with stromal/corneal edema

174
Q

Identify and Explain

A

Mosaic Shagreen also called Crocodile Shagreen

  • Grayish white, polygonal opacities separated by clear spaces.
  • They look like crocodile leather.
  • Can be seen either anteriorly or posteriorly; probably results from relaxation of the normal tension on Bowman’s layer.
  • They are most commonly seen centrally.

Conclusion: Normal, no clinical significance except in some rare cases, anterior shagreen can be associated with trauma.

175
Q

Identify and describe

A

Hassal-Henle Bodies/Guttata

-If peripheral, they are called Hassal-Henle Bodies. If central, they are called Guttata.

  • Guttata are nodular thickening of Descemet’s membrane.
  • Composed of collagen - byproducts of the endothelial cells.
  • In specular reflection, they have an orange peel appearance.
  • With direct illumination, they appear as refractile circular excavation in the endothelium.
  • They can also be associated with corneal trauma and inflammation

Conclusions:
First sign of Fuch’s Endothelial Dystrophy.
Consider doing pachymetry.

176
Q

Identify and describe

A

Corneal Farinata

  • Is an age-related corneal change comprising of many tiny, dust-like gray dots and flecks in the deep stroma.
  • The term is derived from farinaceous or flour-like.
  • The deposits are more prominent centrally and best seen with retro-illumination.
  • The condition is usually bilateral and does not interfere with vision.
  • The exact cause is unknown but they are probably lipofuscin, which is a degenerative pigment found in aged cells.

Conclusion: normal finding, no management needed

177
Q

Identify and Describe

A
  • *Corneal Farinata (bilateral)**
  • age-related many tiny, dust-like gray dots and flecks in the deep stroma.
  • *farinaceous or flour-like.**
  • The deposits are more prominent centrally and best seen with retro-illumination.

Conclusion: normal finding, no management needed

178
Q

Identify and Describe

A
  • *Band Keratopathy**
  • Calcium salts deposit in the interpalpebral zone in basement membrane
  • Deposits start as gray and flat, but as they progress, they become white and elevate the overlying epithelium, later they can spread to Bowman’s layer and anterior stroma
  • calcium and phosphate in concentrations that approach their solubility product
  • Evaporation of tears tends to concentrate solutes and to increase the tonicity of tears; this is especially true in the intrapalpebral area, where the greatest exposure of the corneal surface to ambient air occurs.
  • Elevated serum calcium or serum phosphate can tip the balance in favor of precipitation
  • It begins in periphery and extends to visual axis

Band keratopathy is associated with long standing inflammation of the eye, prolonged uveitis, prolonged glaucoma, systemic hypercalcemia (hyper-parathyroid disease), juvenile rheumatoid arthritis, chronic exposure of the cornea to mercury, taking thiazides, Vitamin D toxicity, silicon oil in the eye, and in rare cases it can be inherited.

179
Q

Considerations for Band Keratopathy

HYPERPARATHYROIDISM

JUVENILE RHEUMATHOID ARTHRITIS

SARCOIDOSIS

A
  • *labs:** serum calcium. / albumin. / magnesium. / and phosphate levels; blood urea nitrogen, and creatinine.
  • *ACE (Angiotensin-converting enzyme) levels** if you suspect SARCOIDOSIS
  • *uric acid** levels if gout is suspected.

Conclusion: Treat by removing the epithelium and scraping with a knife and applying a chelating agent. Repeated application of calcium binding agent, EDTA (ethylenediaminetetraacetic acid) and scraping of the corneal surface after removing the epithelium is usually effective to treat relatively mild cases. Excimer laser keratectomy may be used for cases with deep involvement

180
Q

Epithelial Basement Membrane Dystrophies

Def:

Hereditary, symmetric, bilateral disease that usually affects the central cornea

  • Avascular
  • Begins early in life
  • Unrelated to other systemic or local diseases
A

Most common corneal dystrophy
They are interchangeably called Cogan’s, Fingerprint, and Map-Dot
women > men. 40-70
autosomal dominance but then presents as Early onset 4-8 yrs
Identified mutations: TGFB1/BIGH3 gene

181
Q

Medication Deposits in Cornea

Chlorpromazine (thorazine)

A

Phenothiazine (antipsychotics) – mechanism of action is related to blockage of dopamine receptors in the central nervous system.
o Most common drug is Chlorpromazine (thorazine)
o Fine yellow-brown white deposits in deep corneal stroma in the intrapalpebral region

􏰀 Deposits are first seen on anterior crystalline lens

o Dose-dependent

o UV triggers

Drug Deposition in/on the Cornea

o Corneal changes reversible and nothing to worry about

o However, retinopathy can be a major problem

182
Q

Identify and describe

A

Epithelial Basement Membrane (BM) Dystrophy

  • *Dots**
  • Gray-white intra-epithelial opacities that very in size and shape
  • The intra-epithelial microcysts (pseudocysts) contain nuclear debris, cytoplasmic debris, and lipids.

They are probably inverted basal cells which continue to
proliferate
- Cysts may discharge spontaneously onto the corneal surface and disappear, producing an erosion in the process

183
Q

Identify and Describe

A

Epithelial Basement Membrane dystrophy

  • *Fingerprints**
  • Clusters of concentric, contoured lines that occur in any area of the cornea
  • Fingers are actually basement membrane projecting up and trapping the anteriorly migrating cells
  • They are best seen by retro-illumination, in which they appear refractile
  • Some lines branch out and other terminate with clubs
184
Q

Identify and Describe

A

Epithelial Basement Membrane Dystrophy

Maps

  • Irregular, geographic-shaped, circumscribed areas that are commonly seen, usually alone or combined with dots
  • Maps can be surrounded by gray-white borders or may blend gradually into the normal cornea
  • Map-like changes are related to multilaminar thickening of basement membrane with extension of the aberrant membrane into overlying epithelium
  • Extensions contain fine fibrillar granular material and are 2 to 6 mm in thickness
185
Q

Epithelial BM Dystrophy Symptoms

All caused by:

All of these patterns are due to problems with the epithelium anchoring to the basement membrane → the epithelial cells anterior to the abnormal basement membrane (BM) do not form hemidesmosomal connections to the membrane

A
  • *Epithelial BM Dystrophy Symptoms**
  • Most ASYMPTOMATIC (Observed)
  • Major complaint → dry eye
  • Tear film is disturbed epithelium UNeven
  • Other complaints → recurrent erosions Usually on Awakening
  • Patients experience a foreign body sensation, pain, photophobia, or tearing
  • Usually happens in the morning, upon awakening.
186
Q

Epithelial BM Dystrophy

SIGNS (Staining)

A

Epithelial BM Dystrophy Findings
● Slit Lamp
○ All of the defects may appear under negative NaFl staining
■ Disruptions in the tear film secondary to the uneven epithelium; appears as a black spot in a normally smooth, green appearance of the tear film stained with NaFl

Maps and microcysts are seen as positive staining when they break through
○ Fingerprints can be seen as a combination of negative and positive staining

187
Q

Treatment of Epithelial dystrophies

A

dry eye - Mention
- Lubricating drops Unpreserved
-

  • *Recurrent erosions**
  • Ointment at night or hyperosmotic agents
  • Drops and ointment may be necessary
  • Follow abrasion protocol for acute erosions
  • Discontinue CL wear
  • Other options: bandage contact lens, collagen shields, amniotic membranes
  • Phototherapeutic keratectomy with excimer laser to anterior 2-4 μm of Bowman’s
188
Q

FUCHS Endothelial Dystrophy

Features

A

● Slowly progressive / Bilateral disease
→ results in decreased vision and pain in some cases
● Fuchs’ develops dt Guttata. nodular thickening of Descemet’s membrane abnormal byproducts of the endothelial cells
Stromal and epithelial edema can result
● Female > Males 50/60
● Inherited as an autosomal dominant trait and known Genetic link

189
Q

ENDOTHELIAL COUNT in Fuch’s Dystrophy

A

Endothelial Cell Count
- Normal Pattern:
present at birth, usually about 5,000 cells/mm2
- There is a normal, progressive and slow loss aging
- By the 40’s - 3,000 cells/mm2
- By the 70’s or 80’s - 2,500-2,000 cells/mm2
- With Fuchs’ Corneal Dystrophy, the rate of cell loss is accelerated!!!

  • Fuchs’ Dystrophy Pattern:
  • By the 50’s or 60’s, too many cells may have deteriorated
  • Below 500 cells/mm2 → cornea begins to swell, and the vision becomes blurred

- Tools to measure endothelial cell count
- Specular microscopy counts below 1,000 mm2 indicate
problems with cataract surgery

190
Q

Underlying Defect in Fuchs’

● A gradual decline in the number of functioning endothelium cells
○ The endothelium cells are noted to be more varied in size (polymegathism) and more irregular in shape (pleomorphism)

A

● Pathway (simplified):
○ Significant Guttata → endothelial cell function (pumps) compromised → stromal edema occurs (separates lamellae and causes lakes to form) → edema alters the epithelial integrity (can be mild or cause major bullae to form) → bullous keratopathy if bullae become large enough → corneal scarring

191
Q

SIGNS of Fuchs endothelial Dystrophy

A
  • Epithelial edema / clear cysts that are causing nodular elevation of the surface (bedewing)Sclerotic scatter
  • Fine, clear cysts will cause negative staining (using NaFl)
  • Fingerprint patterns
  • Subepithelial pockets of fluid can be seen with slit lamp →
    begins in the basal cell layer and later spreads
  • Epithelial bullae develop → due to the coalescence of microcysts
  • Can decrease Visual Acuity
  • Very painful if bullae burst
  • Vascularization and scarring can occur in advanced cases
192
Q

Added findings

Fuch’s endothelial Dystrophy

A

● In the beginning, epithelial edema worse AM - partial Hypoxia and DECr evaporation

● Fuchs’ patients have a higher incidence of glaucoma because problem with the endothelium, also tends to cause same problem with the trabecular meshwork

193
Q

TX and MX Fuchs endothelial dystrophy

Contra-indicated

DIAMOX / TRUSOPT /AZOPTIC

A

● higher incidence of glaucoma Link between endo problem and TM trabecular meshwork
● Patient Edu
● Prescribe topical sodium chloride 5% drops 4 times a day, ointment every night at bedtime.
Apply warm air morning to dehydrate the cornea.
Reduce intraocular pressure with topical medications if pressure >20–22 mmHg. /Done to reduce corneal edema
○ DO NOT use Carbonic Anhydrase

DIAMOX / TRUSOPT /AZOPTIC
Treat ruptured corneal bullae as recurrent corneal erosion
○ Consider cycloplegic, antibiotic ointment, and patching
○ If persistent or large epithelial defect, consider bandage contact lens

194
Q

KERATOCONUS

features

A

- Conical ectasia (bulging) of the central cornea

  • Central or paracentral stromal thinning
  • Apical protrusion (Munson sign)
  • Irregular astigmatism
  • Non-inflammatory
  • 80% of the cases are bilateral
  • No ethnic or gender bias
  • *- An unexpected increase in astigmatism (case history is important!)**
195
Q

CAUSES of Keratoconus

A

● Sporadic and dependent on external factors and stimuli that lead to inception and progression of keratoconus
Eye rubbing dt Allergies
● Familial occurrence
○ Autosomal dominant with incomplete penetrance
○ Familial keratoconus → many of affected members have other connective tissue disorders such as syndactyly, Raynaud’s or brachydactyly
● Slightly higher incidence in South Asia and Middle East
● Also associated with Down’s, Marfan’s, RP, Neurofibromatosis, Ehlers Danlos Syndrome
● Associated with vernal keratoconjunctivitis, atopic dermatitis, and other atopic diseases

○ About 50% of patients reported significant eye rubbing

196
Q

Progression of Keratoconus

Early to Late Stages

337.5 / Diopters

A

Early Stages
scissor type reflex
● Distorted K-reading → central mires are oval
● Usually steeper than 48D
● Photokeratoscopy shows irregular reflected rings
● Topography → cone is usually central and slightly inferior, and asymetry

  • *Later Stages of Keratoconus**
  • Munson’s sign (visible lid protruding outwards)
  • Apex thins then you see stria in the posterior stroma (Vogt’s striae) which disappear with gentle pressure on the cornea
  • Unable to refract to 20/20 with glasses because

irregular astigmatism develops
- Reticular scarring of Bowman’s membrane
- Fleischer ring appears
- Iron deposition in the epithelium around a portion of or the entire base of the cone
- Best seen with slit lamp + cobalt blue filter + fluorescein dye
- Stromal nerves become more visible
- Fine anterior stromal scars seen near cone apex, caused by ruptures of Bowman’s layer
- As stroma thins the number of corneal lamellae decrease
- Diameter of collagen fibrils increases as does the inter-fibrillary distance
- However, hexagonal arrangement of fibrils does not change and distance does not
increase to the point that clarity is lost

197
Q

Classification of different cones in Keratoconus

A

1.) Nipple

  • ● Small (<5 mm)
  • ● Steep curvature
  • ● The apex is often central or paracentral and is slightly displaced inferiorly

2.) Oval

  • ● Medium (5-6 mm)
  • ● Ellipsoid and usually inferotemporal

3.) Globus

  • ● Largest (>6 mm)
  • ● May involve over 70% of the cornea
198
Q

Corneal HYDROPS

(Keratoconus)

A

● Hydrops is a break in Descemet’s membrane and underlying endothelium. This allows aqueous humor to leak into the stroma and cause stromal edema
● Occasional Break in Descemet’s Membrane
increased stromal edema (corneal hydrops)
○ Reduced VA and Pain
○ Edema increase the size of the cornea by 2-3 times
Aqueous leaking into cornea
○ Usually resolves in a couple of months (2-4 months)

● Treatment of Corneal Hydrops
○ Topical antibiotic (ciprofloxacin) QID
○ Hypertonic saline ointment (Muro 128) QID
Ocular antihypertensive (DIAMOX) lower IOP and decrease the posterior forces on the cornea
○ Occasionally, steroid gtts QID (to reduce risk of neovascularization)

199
Q

Treatment of Keratoconus

A
  • Glasses
  • Rigid contact lenses
  • *- Piggyback lenses**
  • Intacs (surgery)
  • Scleral lenses
  • Corneal cross linking
  • Keratoplasty (about 10-20% of patients will need a corneal transplant)
200
Q

CROSS-LINKING

A

Removing the corneal epithelium
and applying riboflavin drops to the eye
● After the cornea is saturated with the riboflavin (Vitamin B2) the eye is exposed to the ultraviolet (UVA) light. The UVA light interacts with the riboflavin stiffer bonds between collagen
● Minimal corneal thickness of 400 μm to avoid problems with endothelium
● increases corneal rigidity by inducing additional cross-links
within or between collagen fibers
● Corneal Collagen Cross-Linking appears to stop the progression of Keratoconus in rapidly
progressing patients! Importantly, it is NOT a cure!
● Corneal Collagen Cross-Linking Complications

  • ○ Pain
  • ○ Epithelium infections
  • ○ Anterior stromal haze
  • ○ Corneal melt
201
Q

Identify and discuss

A
  • *Kayser-Fleischer Ring** - Very rare!
  • Yellowish brown but may appear gold, red, blue, green or any other mixture of these colors
  • 1-3 mm wide circumlimbal ring at level of Descemet’s membrane
  • Caused byWilson ’s disease (abnormal copper deposition)

- Wilson’s Disease:
- A genetic disorder in which excess copper builds up in the body
- Copper deposited in the liver, then the kidney, and eventually the brain and cornea!
- Inherited as an autosomal recessive metabolic defect linked to chromosome 13
common presentation is progressive neurologic diseaseand ataxia from copper deposited in the CNS
- Treatment → low copper diet and chelating

  • CONCLUSION: if you see this very rare condition, refer the patient to internist. Pshychiatric Hospital if in Brain
202
Q

Identify and Discuss

In all Px’s that take

Plaquenil

Amiodarone

Some Rhopressa

A

Krukenberg Spindle
● Vertical, spindle-shaped pigment deposition on endothelium (usually lower half of cornea)
● Associated with pigment dispersion syndrome, pigmentary glaucoma and pseudo
exfoliation syndrome glaucoma

● Iris moves backwards and it hits the zonules → over time zonule pigment ‘rubs off’ and moves into aqueous humor and deposits in the endothelium but also deposits in the trabecular meshwork which causes a problem
● Iris transillumination → the released pigment can cause the Krukenberg Spindle

203
Q

What rare disease is Vortex Keratopathy also a sign of if none of the med causes present?

A

FABRY

204
Q

IRON deposits not associated as Normal Findings

A

Stokers line - At head of pterygium

Fleischers Ring - Base of cone Keratoconus

Coat’s - FB removal site

Ferry line - around filtering Bleb glaucoma

205
Q

Medication Caused

A

Type: Phenothiazine

CHLORPRAMAZINE

Causes fine yellow / brown / white deposits on ant christaline lens

Dose dependent

Triggered by UV / reversable but check for retinopathy

206
Q

CHEMICAL Burns

No staining?

A
207
Q

General Anatomy of lens

“A cataract-free lens is one in which the nucleus, cortex, and subcapsular areas are free of opacities; the subcapsular and cortical zones are free of dots, flecks, vacuoles, and water clefts; and the nucleus is transparent, although the embryonal nucleus may be visible.

A
  • oblate spheroid that is avascular and lacks both nerves and connective tissue
  • Suspended by zonular fibers (made by ciliary epithelium) and insert 1-2um into outer capsule
  • Lens grows only anterior, posterior surface no epithelium.
  • Metabolic needs - aqueous and the vitreous
  • Capsule permeable to water, ions and small molecules
208
Q

Lens Features

A
  1. Transparent
  2. Avascular
  3. Thus the aqueous meets its metabolic requirements
  4. Biconvex structure
  5. Refracts light
  6. Provides accommodation
  7. Lens grows continually - new fibers are laid down continually
  8. ls a wonderful UV-filter to protect the retina
209
Q

Changes of the lens with age

A

o The lens yellows / Brunessence
o Light transmission is decreased
o It becomes harder
o Loss of accommodative ability
o Protein aggregation
o Problems with reactive oxygen species

210
Q

CATARACTS def

A

Definition: An opacity of the lens

May be a small, local opacity or a diffuse, general loss of transparency

Clinically Significant Cataract: causes a significant reduction in visual acuity or a functional impairment

Lens clouding

Lens mostly water (2/3) and protein (1/3)
The protein has a christaline structure / maintains clarity /
highest protein content in the body.
Protein clumping results in opacification of lens

211
Q

Cataract Causes

A

Cataracts can occur secondary to

  1. Aging
  2. Hereditary factors
  3. Trauma
  4. Inflammation
  5. Nutritional disorders
  6. Radiation
  7. Meds
  8. Idiopathic
212
Q

Risk factors for Cataracts

A

Diabetes

Drugs
o Corticosteroids - posterior subcapsular cataracts
o Phenothiazines: stellate cataracts
o Psoralens, a class of drugs used along with light therapy to treat skin disorders, such as psoriasis, can cause central cortical changes
o exogenous estrogen use
Smoking: increased nuclear sclerotic
Increase vitreous syneresis nuclear sclerotic
Alcohol (high consumption)
Myopés
Uveitis, acute angle closure glaucoma
Vitrectomy
Vitreal injection

Obesety Increased body mass index

213
Q

3 Most common found Cartaracts

A
  • Nuclear sclerotic (NS)
  • most common / CaucasiansCortical 27.7%

Slightly more common as first cataract in Asian

  • Posterior Sub-Capsular (PSC) 19.7%

Commonly associated with systemic diseases and medicat

214
Q

CORTICAL Cataracts

A

Clinical Findings

Spoke-like projections in the periphery towards the center

AKA spoke or cuneiform

Pathophysiology
o The cortex is less compact than the nucleus and is therefore more prone to becoming over hydrated as a result of electrolyte imbalance
o intumescence (swelling) / lamellar clefts / opacities
Early changes may include vacuoles, water clefts, and lamellar
separation

o Water clefts

215
Q

Identify

A

Cortical Cataract

216
Q

Nuclear Sclerotic Cataract

A

Diffuse yellow/brown color changes in lens nucleus

Pathophysiology
o Sclerosis: age-related changes in density (index of refraction)
o physiochemical changes in the alpha, beta and
gamma crystallins
• These proteins undergo oxidation, non-enzymatic glycosylation,
proteolysis, phosphorylation, and other processes which lead to
aggregation of high molecular weight proteins

o Reduced amount of glutathione
o Chemical modification of lens proteins leads to yellowing, then
browning

217
Q

Nuclear Sclerosis and CAT sx

A

After a vitrectomy 60-98% get a nuclear cataract within 2 years

Secondary to increased oxygen near the lens after the
vitrectomy

Hyperbaric chambers – increased oxygen exposure can
cause the patient to have huge increases in myopia and a
progression to nuclear cataracts

CARBON MONOXIDE POISENING / SCUBA

218
Q

(PSC) POSTERIOR SUB-CAPSULAR Cataract

A

Dense, granular appearance of the posterior layers of lens cortex

Early iridescent sheen, to more granular and plaque-like

Central opacities and vacuoles

Often located along visual axis

Pathophysiology
o Epithelial cell proliferation at pole with fluid filled areas within
o Associated with UV exposure and steroids
o Younger age than NS or cortical

Most visually distressing type / Pupil Decr in size when you age or read

219
Q

Identify

A

PSC Cataract

220
Q

PSC Medicamentosa

A

STEROIDS

> 15mg/day of prednisone for more than one year have PSC.

Anti-VEGF

  • *intravitreal injection of 4 mg
    (0. 1 ml) of triamcinolone acetonide**

cataract and intraocular pressure
(IOP) rise of at least 5 mmHg (IOP responder).
40
Kena log

221
Q

PSC and STEROIDS

A

Lens epithelial cell seem to express a steroid binding
protein
, altering gene expression which appears to lead to:
o Cell proliferation / Cell differentiation / Cell apoptosis / Modulation of glucose metabolism / Modulation of membrane channels

etiology

transactivation and transrepression of
genes
as well as modulation of the activity of proteins

222
Q

Identify:

A

POSTERIOR SUB-CAPSULAR

CATARACT

223
Q

Cataract GRADING

(Dilated Pupil 1 / 2+ / 3-)

A

Nuclear sclerosis
o Graded by evaluating the average color or opalescence

Cortical cataract
o Grading should be visualized as a total amount of spoking present
o If one of the spokes goes
through the visual axis, Decr in VA

Posterior Sub-Capsular
o Graded on the basis of the percentage of the area of the posterior
capsule obscured

224
Q

GRADING EX

A
225
Q

CATARACT Grading

A
226
Q

Combination CATARACT GRADING

A
227
Q

Cataract Grading

A
228
Q

Symptoms CATARACTS

A

Cloudy or blurry vision
Colors seem faded
Glare around headlights
Reduced contrast sensitivity
A halo may appear around lights
Poor night vision
Double vision or multiple images in one eye
Frequent prescription changes in RX
Decrease in blue perception

229
Q

Evaluation of a Cataract resultant VA

A

O’Scope - Matches what You can see. 20/20 PX should be clos to the same Acuity

Potential Acuity Meter (PAM)

Better to assess NS, Connected to Slitlamp

Laser Inferometry

Best results In mild to Moderate

BAT Brightness Acuity Tester

For Px with Good VA but glare is a problem.

Potential acuity Pinhole technique

230
Q

Cataract Progression

A

Posterior subcapsular
o Usually progresses the fastest
o Usually near vision is more affected than distance
o Not unusual to go from minimal to needing surgery in 6-12 months
o Explain things to the patient

Nuclear sclerotic
o Change in index of refraction results in an increase in minus,

Always consider Add - Keep the amount of Add constant or higher

Cortical
o Progresses the slowest
o In some cases patient becomes more hyperopic

231
Q

CONDITIONS Asociated with CATARACTS

A

Atopic dermatitis – PSC and Anterior SC

A positive correlation was found between atopic cataract development and a decreased inducibility of superoxide dismutase. This suggests that atopic cataract development is correlated with oxidative damage of the lens and related to chronic inflammation.

o Arch Dermatol.

Diabetic: 5-fold increase in the prevalence of
cataracts
o Hyperglycemia is the primary cause
Y Children can demonstrate snowflake, which are reversible
o Snowflake cataracts are white, sub-capsular opacities related to
high blood sugar in children andin patients with type1 diabetes
o Adults demonstrate the usual age-related cataracts, but at an
earlier age
Diabetic patients
may also demonstrateChristmas Tree
cataracts

232
Q

Chrismas Tree Cataract

A

Glittering, multicolored, needle-like opacities

Pathophysiology

o Associated with metabolic dysfunction (i.e. diabetes) o Consists of cholesterol crystals

o “It is concluded that cystine is the most likely candidate for the Christmas tree needles and that the needles probably are formed as the result of an age-related aberrant breakdown of crystallins induced by elevated Ca2+ levels.”

o Associated with Myotonic Dystrophy Y This type of Cataract can be: o Unilateral or bilateral

o Usually does not affect vision Cataracts: cataract _

233
Q

Cataracts Oil Droplet

Metabolic cataract

A

Round, translucent irregularity

Pathophysiology
o Associated with galactosemia (inability to metabolize galactose)
o Cataracts usually form within a few weeks of birth
o Cataract formation due to a high concentration of dulcitol/galactitol
(a product of galactose reduction) within the lens
o Dulcitol causes water to be drawn into the lens fibers (similar to the
sorbitol cataract in DM patients)
o With the Oil Droplet, early modification of diet can cause resolution

234
Q

Traumatic Cataract

( Rosette)

A

Star- or rosette-shaped

Pathophysiology
o Secondary to blunt trauma
o Usually found at interface of anterior cortex and anterior nucleus
o May also occur under anterior or posterior capsule, or both
o Rupture of superficial cortex at the suture lines may account for
rosette appearance
o May be a delayed appearance as initial swelling

Trauma may also lead to findings such as Vossius’ Ring or Focal Cortical Cataract

235
Q

Identify

A

Traumatic Cataract

236
Q

Vossius’ Ring

A

Vossius’ Ring

Deposit of melanocytes from pupillary border of the iris due to blunt trauma

237
Q

Congenital Caratact

TORCH Infectious diseases

Toxoplasmosis, Rubella, Cytomegalovirus, Herpes simplex

A

Opacity present at birth

  • Infantile opacities / occur after birth
  • Unilateral cataracts are usually isolated sporadic incidents.

o Can be associated with:
• Ocular abnormalities (eg, posterior lenticonus, persistent hyperplastic primary vitreous, anterior, segment dysgenesis, posterior pole tumors)
Trauma
• Intrauterine infection (rubella)

Bilateral cataracts are often inherited and associated with other diseases.

o Common causes are:
Hypoglycemia
Trisomy (eg, Down, Edward, and Patau syndromes)
Myotonic dystrophy
• Prematurity

238
Q

Cataracts: Epicapsular Stars
Congenital cataract

A

Epicapsular Stars
Congenital cataract

239
Q

Mittendorf’s Dot

A

Small, round or oval, dense dot approximately 125-350 mm in
diameter white in color black in retro

o Surface of the posterior lens capsule
o Slightly nasal to the center of the lens

o Remnant of the fetal hyaloid vascular system

240
Q

Lamellar Cataracts

A

Affecting ONLY one layer of the crystal lens, which is
surrounded by clear areas

Involves a particular lamella of the lens, both anteriorly and
posteriorly

Most common type of congenital cataract
Usually bilateral and symmetric
VA Good

241
Q
A

Congenital Nuclear Cataract

242
Q

Identify

A

Sutural Cataract

Does not progress / Forms at Y suture

243
Q

Cataracts

A

Round, discoid, opaque mass
Central- posterior part of the lens, involving the subcapsular cortex and capsule
o VA reduced

Pathophysiology
o Autosomal dominant inheritance pattern

244
Q

Cataracts

A

Opacity of the anterior subcapsular cortex and capsule
o Usually bilateral
o Frequently autosomal dominant

o Central opacity involving the anterior capsular

o Associated with: microphthalmos, persistent pupillary membrane,
and anterior lenticonus

245
Q

Congenital Cataracts

A

Small, bluish punctate opacities of
the peripheral cortex

246
Q

Congenital Cataract

Corronary

A

Club-like opacities that lie in deep cortex and surround the lens
nucleus like a crown

autosomal dominant
o Can be associated with Down’s Syndrome

247
Q

Posterior Lenticonus

A

Developmental anomaly of the lens in which the posterior portion
of the lens bulges outward in a cone-shape.

Associations include microcornea, anterior lentiplanus, glycinuria, and Duane’s syndrome.

248
Q

Persistent Hyperplasia of Primary Vitreous (PHPV)

A

Can be associated with retinal detachments and hypoplastic
optic nerves

CAT sx risk of retinal detachment

249
Q

Drug Induced Cataracts

A

Phenothiazine
Steroid

Amiodarone –anterior subcapsular Stellate
Tetracylines
Sulfa drugs

250
Q

Type Of Cataract

A

Mature Complete Cataract

251
Q

Morganian

Cataract

A

Hyper-mature Cataract

Nucleus sinks in lens

252
Q

Entopic Lentis

A

Marfan’s syndrome autosomal dominant genetic disease in which a
fibrillin gene mutation causes weak zonules

o Displacement is usually superior temporal
Homocystinuria autosomal recessive – rare methionine and homocysteine
levels are elevated
o Lens is displaced down and in
Ehlers Danlos Syndrome
Osteogenesis Imperfecta
Contusion injury
Pseudoexfoliation
Syphilis

253
Q

Radial Keratotomy

Not done any more

A

Radial incisions using diamond blade Insisions 90% of corneal thickness deep
ƒ

Refractive effect controlled by

  1. number of incisions,
  2. depth of incisions
  3. size of the central clear zone
254
Q

RK

Complications

A
  • Long-term fluctuation of vision
  • ƒ Halos and glare (When insisions are in the line of sight)

ƒ Progression to farsightedness (hyperopia)

  • ƒ Kerato-ectasia (Corneal ectasia)

ƒ

  • Neovascularization
255
Q

Current Visual corrective SX

2 broad options

A

PRK

LASIK

256
Q

Optometrist role in corrective Sx USA

A

Patient Consultation & Education
ƒ Pre-operative exam
ƒ

Surgery (ODs can perform in some states)
ƒKentucky / louisianna / Oklahoma

Post-operative exam

257
Q

ƒ

Optom role

Determine Eligibility

A
  1. ƒ Age 18+
  2. Refractive Error: Amount meets FDA guideline -0.50 to -12.00 / +6.00 / -6.00 Astig
  3. Stability <0.50D change 1Yr
  4. VA (sc) < 20/40
  5. Ocular and Systemic

Medical History: Not contain any “absolute” contraindications

258
Q

Absolute (not a candidate) ocular contraindications

Refractive Sx

A

ƒ Diabetic retinopathy - accelerates
ƒ Glaucoma - Sx has IOP to 65mmHg / Need Steroids gtt post sx
ƒ Visually significant CAT - rather do CAT sx
ƒ Corneal ectasia Ie. Keratoconus
ƒ Active ocular herpes - Zoster Ophthalmicus / Herpes Simplex
ƒ Severe dry eye
ƒ Exposure Keratopathy Ie. Sjogren’s syndrome
ƒ

Monocular (actual or functional)

Amblyopia or Strabismus

259
Q

Relative Ocular Complications (Able to address)

A

Mild - Moderate Dry Eye
ƒ Blepharitis (all signs resolved)
ƒ EBMD(epi/base/mem/def) PRK only
ƒ Corneal scarring PRK vs. LASIK
ƒ Amblyopia(see specific guidlines)
ƒ Thinner Pachymetry than average corneal pachymetry

260
Q

AMBLYOPIA considerations corrective SX

A

ƒ

Mild- ( 20/40+ may be okay
ƒ Worse than 20/40, px considered monocular (contraindication)

ƒ Pre-laser BCVA= Post-laser BCVA
ƒ (may gain 1-2 lines)could improve BCVA
ƒ Help in patients with Anisometropia

261
Q

AbsoluteSystemic Contraindications

A

ƒ Auto-immune disease
ƒLupus Erythematous (SLE), Rheum Arthritis, Thyroid Disease
ƒ Increased risk of inflammation
ƒ

Immune Suppression
ƒ Increased risk of infection
ƒ (HIV+ is relative contraindication, if immune system is intact & stable, likely one eye at a time)
ƒ Pregnancy
ƒ Must wait 4-6 months* after giving birth/nursing

ƒ Any Illness affecting wound healing
ƒ Medications – MANY!
ƒ Systemic steroids, Plaquenil, Amiodarone, Imitrex, Accutane
ƒ Pacemaker

262
Q

Relative Systemic Contraindications

A

Diabetes (Type I & II)

Diabetic retinopathy is a systemic disease and contra indicated
ƒ Active Atopy (Eczema, Psoriasis, Dermatitis)
ƒFirst control

Epilepsy (no episode in the past 12 mo)

263
Q

Occupational Regulations

Millitary

A

ƒ NASA Astronauts- intralase LASIK only

ƒ Navy & Special forces- PRK only
ƒ

Army/Air Force- Either LASIK or PRK

264
Q

PRE OPPERATIVE EXAM

A

VA:

ƒ Uncorrected Visual Acuity

  • Best Corrected Visual Acuity

ƒ Entrance Testing:
ƒ Confrontation fields, EOMs, BV/Cover Test, ocular dominance

Pupils: Photopic Scotopic (Prevent glare)
ƒ

Refraction
ƒ Dry vs Cycloplegic
ƒ Push plus & maximize magnitude of astigmatism
ƒ 1% Cyclopentolate or 1% Tropicamide
ƒ

Binocular Vision Assessment
ƒ Slit lamp exam
ƒ IOP
ƒ Dilated retinal exam

265
Q

PRE OPPERATIVE EXAM

Slitlamp

A

Lids/lashes

  • ƒ Blepharitis
  • ƒ Lagophthalmos
  • ƒ Incomplete blink
  • Meibomian gland dysfunction

ƒ Cornea(Dry eye)

  • ƒ Quality of tear film
  • Superior punctate erosions or keratitis
  • ƒ EBMD

ƒ

Manage Dry Eye FIRST
ƒ Aggressive artificial tears supplementation
ƒ Occlusive punctal plugs
ƒ Topical cyclosporine (Restasis)
ƒ Topical Steroid (pulse dose)
ƒ

Oral supplements:
ƒ Omega 3 fatty acids (1000mg BID)
ƒ Doxycycline (50-100mg BID)

266
Q

Dilated Fundus exam and IOP

A

Rule out any lenticular, vitreous or retinal disease
ƒ Thorough examination of dilated media, posterior pole and
peripheral retinal exam

Baseline IOP (Post lasik art lowered)
ƒ
ƒ

267
Q

Aditional tests for possible corrective Sx

A
  • *Corneal Topography**
  • *ƒ Pentacam**
  • ƒ Topography vs. Tomography
  • ƒ “Belin-Ambrosio” scans
  • ƒ Global pachymetry

ƒ Aberrometry-Wavefront analyzers

  • ƒ Objective refractive error
  • ƒ Higher order aberrations
  • ƒ Measures pupil size
  • ƒ Pachymetry
268
Q

Corneal TOPOGRAPHY

38-49D K-reading preferred

A

ƒ Rule out abnormal corneal contour
ƒ Normal Cornea:
ƒ Prolate shape + Uniform in appearance
ƒ Approx 42-46D at the center
ƒ

Abnormal Cornea:

  • ƒ Inferior steepening, lobster-claw/kissing dove pattern
  • (Pallucid marginal degeneration)
  • ƒ Rule out Contact lens related abnormalities
  • ƒ Serial topography may be needed
  • ƒ Verify post-operative results
269
Q

PACHYMETRY

A

ƒ Ultrasonic pachymetry is standard of care
ƒ Will determine whether patient is a suitable candidate
ƒ

More important for higher refractive errors
ƒ Average corneal thickness ~ 535-545um
ƒ Must have enough corneal tissue for healthy residual stromal bed
ƒ

Thinner corneas= relative contraindication* - need room for
enhancement
ƒ Consider PRK/LASEK if not enough corneal tissue for LASIK

270
Q

RESIDUAL STROMAL BED

Stromal tissue remaining “untouched” after LASIK

A

ƒ LASIK Residual Stromal Bed (RSB)

= Corneal Pachymetry Treatment depth –LASIK flap thickness
ƒ According to the FDA,
ƒ LASIK RSB must be >250µm
ƒ Most surgeons prefer 300µm
ƒ

PRK Residual Stromal Bed (RSB)= Corneal PachymetryTreatment depth
ƒ PRK RSB must be >350µm stromal tissue + ~50um
(epithelium)= 400um

271
Q

RESIDUAL STROMAL BED CALCULATION

1 Diopter = 15 microns (µm) of corneal tissue

CUT OFF most SURGEONS

300qm

A

LASIK RSB=Corneal Pachymetry -Treatment depth[(sph +cyl)x15µm]—lasik flap thickness

272
Q

What causes post laser Ectasia

A

Corneal Ectasia: progressive instability and weakening of
corneal integrity,
resulting in a significant increase in the
posterior and anterior corneal curvature.

CAUSES
ƒ

  • <250um RSB
  • Corneal thinning dystrophies (pre operative
  • subtle/subclinical KC)
  • Thick corneal flaps
273
Q

PX Education and Counseing

A

ƒ Review Informed consent:
ƒ Surgical site to provide
ƒ Discuss risks and temporary side effects (risk of blindness, dry eye, glare & haloes etc.)
ƒ

Discuss Goals and Limitations of the procedure

  • ƒ Mild Spec RX for night-time driving
  • ƒ Reading glasses for Presbyopia
  • ƒ Enhancement for high refractive errors

ƒ Pre-operatively

  • ƒ D/C CL wear
  • ƒ No restrictions on eating
  • ƒ D/C eye make up x minimum 3 days prior to surgery day
  • ƒ Review intraoperative procedure details
  • ƒXXXX Review Pre/Post-OP Medication schedule
  • ƒXXXX Topical antibiotic QID 1 day prior to surgery date
274
Q

RISKS of REFRACTIVE SX

A

May still require eye glasses for Distance or Near activitiesÆ No vguarantees
ƒ Under-correction or over-correction

A lessening or increasing effect of the surgery over time

Infections
ƒ Dry eyes - generally treatable (greatest until 3mo then back to baseline) May be permanent

Anisometropia

Loss of BCVA
ƒ Injury or perforation of the cornea - loss of vision
ƒ Thinner than 250 micron RSB increases risk of complications

275
Q

CONTACT LENS PX’s

How prior to SX to DC

Discontinue contact lens wear to achieve accurate corneal
measurements:

A

ƒ Soft spherical daily/extended wear: 1 week
ƒ Soft toric wear: 2 weeks
ƒ

Rigid gas permeable Corneal RGPs, Scleral lenses, ortho-keratology:
Minimum of 1 month
1 month per decade of wear
(ex 20 years of wear needs to be out for 2 months)

276
Q

LENGTH of PROCEDURE

Laser Sx

A

Length of procedure:
ƒ Quick: 10-15 min in Laser suite
ƒ Actual procedure time: <5 min
ƒ Actual time spent in office: up to 2-4 hours

  • Lids/lashes prepped
  • ƒ Sedative/Anxiolytic, PO
  • ƒ Driver needed
277
Q

How long does Recovery take

Is it Painfull

A

Visual Recovery:
ƒ LASIK (faster)
ƒ Day 1 usually see 20/25-20/20!
ƒ Upto 3 mo for full visual recovery
ƒ

PRK (Slower)
ƒ Fluctuations in vision upto 5-7 days
ƒ Day 5- expect 20/25-20/20 vision
ƒ Upto 6 mo for full visual recovery

Painfull

LASIK
ƒ pressure with suction cup
ƒ slight “scratchiness/FB sensation” day 1-5 post op

ƒ PRK
discomfort while epithelial layer regenerates
“scratchiness/FB sensation” upto 2-5 days post-op
ƒ Bandage contact lens in place x 5 days

278
Q

Post - Sx

Complication

A
  • Mostly temporary

ƒ Pain or discomfort (upto 48 -72hours)
ƒ FB sensation

  • ƒ Increased sensitivity to light
  • ƒ Glare and haloes around lights

ƒ Upto 3 mo- LASIK
ƒ Upto 6 mo- PRK

  • ƒ Haze or fluctuating vision
279
Q

LASIK

2 Types of flap methods

A
  • *MOST COMMON** 85% Mainly due to 2 reasons:
  • FAST recovery
  • MINIMAL discomfort/pain post-operatively

Flap Creation:
Blade: Microkeratome
Laser: Intralase=Femtosecond laser
“Bladeless”
Laser Ablation (refractive correction)
Standard/Conventional
Custom

280
Q

Flap creation MICROKERATOME

A

ƒ2 components - Cuts circular corneal flap
ƒ Cutting head
ƒ Oscillating blade

Suction ring
ƒ Attaches to globe for stability of cutting head
ƒ Raises IOP to at least 65mmhg
cornea upwards & firms cornea no movement with cutting blade
suction ring determine flap size

281
Q

Flap Creation FEMPTOSECOND

Thinner Flap Possible

A

Wavelight FS200: Intralase - programmed specific depth
IOP elevated, then laser causes “photodisruption”
Air bubbles seaparate corneal layers flap created
ƒ

ADVANTAGES

  • ƒ Uniform Flap thickness
  • ƒ Planar/thinner flaps - less (neurotrophic) dry eye
  • ƒ Programmable depth
  • ƒ Wider range and higher Refractive errors
  • ƒ Thinner corneas
  • ƒ less flap complications and irregularities
  • ƒ Less risk of irregular astigmatism

ƒ DISADV
ƒ More post-op cornea edema (intralase) due to more energy

282
Q

Eximer Laser

sufficient energy to break
intermolecular bonds within the cornea

”photoablation”

A

Myopia: flattens central cornea
ƒHyperopia, indirectly steepens central cornea by
removing tissue from periphery

2 Modalitiesƒ

Conventional: Spherocylindrical only
ƒ Less predictable
ƒ Ablates central vs peripheral corneal differently - Higher order abberations
ƒGlare/haloes/contrast sensitivity post-operatively
ƒ

Custom:
ƒ _Wavefront-error measurement t_echnology
ƒ Ablation profile customized with Wavefront scan

refractive map of the entire visual system across the pupillary zone
ƒ A prescription at each and every point of the cornea
ƒ Incorporates both high and low order aberrations
ƒ Low-order aberrations: Sphere (myopia/hyperopia), Cylinder
ƒ High-order aberrations: Coma, Trefoil, Spherical aberration, etc

283
Q

IRIS registration

Eximer Laser

A
  1. Measure and compensate for ocular cyclotorsion
  • Significant Astigmatism
  • eliminates human error marking
  1. Confirm the patient’s identity and eye being treated
    * Iris is Unique to an Idividual
  2. measure and compensate for pupil center shift
  • compensate
    for differences in pupil size between wavefront capture
    and laser delivery
284
Q

LASIK PROCEDURE

A

mild oral sedative (ex. Xanax) approx 30 min prior
ƒ

Once in the surgery suite:

  1. ƒ Topical anesthetic drops instilled
  2. Skin is prepped with povidone iodine (antiseptic)
  3. Eyelids/eye lashes may taped. Lid speculum for microkeratome but not intralase
  4. Femtosecond Laser flap creation:~6 seconds
  5. Pt transfer from Femtosecond laser to excimer laser: ~7 s
  6. Excimer laser treatment of ex -5: ~Approximately 7 seconds

ƒ Specific sounds/smells during procedure

285
Q

Px instruction Post

LASIK

Dont’s

No rubbing or squeezing eyes x 7 days

A
  • ƒ No showering x 24 hours
  • ƒ No swimming (lake or pool)/hot tubs x 2weeks
  • ƒ No eye make-up x 7day
  • ƒ No exercise/heavy lifting x 7 days
  • ƒ No gardening x 7 days
  • ƒ No scuba diving x 1 month
  • ƒ Avoid dry/dusty environments
  • ƒ Wait 3 months = kickboxing, karate, skydiving
  • ƒ Consider PRK
  • ƒ Limit travel/vacation for 1 week / To be cleared for Drving

Eye shields x 7 nights
ƒ Usually provided by the laser center
ƒ Sunglasses x 24 hours –every waking hour and then x 7days
when outdoors

ƒ No rubbing or squeezing eyes x 7 days

286
Q

Post op meds and follow up shedule

LASIK

A

Schedule:
ƒ 1-day
ƒ 5-day or 1-week
ƒ 1-month
ƒ 3-month

Anual check up (free augmentation)

287
Q

DAY 1

Post op LASIK

A
  1. Visual acuity : Expect mild hyperopia (over comp)
  2. Flap Check - alignment and clarity
  3. Cornea - SPK signs of infection and inflammatio
  4. Subconjuntival hemorrhages Reassure patient
  5. SPK - Increase dose lubrication
  6. Foreign body sensation, check for
    epithelial defect and flap striae
  7. Usually no pain
288
Q

DAY 5 / 1 Week

Post LASIK

A
  1. Visual acuity + Refraction (Hyperopia)
  2. Possible asthenopia - Give Readers
  3. Flap check - infection/inflammation Rule out: Diffuse Lamellar Keratitis (DLK)

After 7 nights:
eye make-up + discontinue wearing shields at night

289
Q

Post Sx 1 & 3 month evaluations

A

Month 1
ƒ Confirm vision is progressing normally
ƒ Flap intact
ƒ Rule out: epithelial in-growth
ƒ IOP check (Check if STEROID Responder)

Month 3
ƒ Confirm uncorrected visual acuity is stable
ƒ Flap intact

290
Q

LASIK

Complications

A

ƒ Interface opacities (debris/lint fibers) ƒ

No risk for infections ƒ

Do not need to be removed ƒ

Can be seen as early as Day 1 post-op

RBC - From neo at edge of flap, get trapped under flap

291
Q

LASIK

Compications

A

ƒ Epithelial defects

  • edge of the flap 1st few days post opƒ

Monitor for signs for signs of epithelial ingrowth
Poor corneal epithelial adherence EBMD
ƒ Heal within 24 -48 hours

292
Q

Micro-keratome flap complications

A

FLAP BUTTONHOLES “island” of uncut cornea
ƒ

Causes:
ƒ Steep cornea (>46D)
ƒ Loss of suction
ƒ Reduction of IOP

FREE CAP: = hinge detaches

Causes:
ƒ Flat corneas (K<39D)
ƒ Poor suction
ƒ Improper settings
for the microkeratome blade

INCOMPLETE FLAP: Incomplete termination

ƒ Interference of the forward movement of the microkeratome
ƒ Lid speculum, lids/lashes, conjunctiva or drapes
ƒ Loss of suction

293
Q

Post Operative Flap complications

Microstraie - No effect on VA

A

MACROSTRIAE

Gross linear folds caused by misalignment of flap to
stromal interface

ƒVA reduction dt optical aberrations & irregular astigmatism
ƒ

Treatment
caught early (1-4 weeks)- easier to lift, stretch and
smooth flap Surgical Sponge
ƒ May need to suture

294
Q

DRY EYE

Post LASIK Sx

A

ƒNEUTROTROPHIC DRY EYE

Decreased corneal sensation
ƒ Decreased tear secretion
ƒ Decreased blink reflex
ƒ Delayed epithelial healing
ƒ SPK staining
ƒ Increased risk of infection/inflammation
ƒ Fluctuating vision

POST OP dry eye:

  • Damage to goblet cell function dt suction ring - mucin deficiency

ƒ *less pressure w Femtosecond laser vs Microkeratome blade
ƒ

Corneal curvature alterations
ƒ Interrupts wetting / Tear film uneven causing tears to
stagnate
ƒ

Epithelial toxicity
ƒ Artificial tears (preserved)
ƒ Medications

295
Q

POST SX

Dry Eye management

3-6months improve

A
  • Preservative-free Artificial tears (x 1 mo)
  • ƒ Gel ointments (as needed)
  • ƒ Cyclosporine 0.05% (Restasis) BID
  • ƒ Topical Steroids
  • ƒ Punctal plugs
  • ƒOral Doxcycline

Environmental modification

  • ƒ Personal humidifier
  • ƒ Good hydration
  • ƒ Fish Oils
296
Q

Diffuse Lamellar Keratitis

DLK

sands of Sahara

A

Non-specific sterile inflammatory response to a corneal
insult
ƒ Incidence: 1/200-1/500
Should be checked for DLK D1. - D7
ƒ white sand underneath the flap

Causes
ƒ Bacterial toxins from sterilizer
ƒ “outbreaks/sequential patients”
ƒ Meibomian secretions
ƒ Machine cleaner/oils from microkeratome
ƒ Excessive femtosecond laser energy (intralase)

297
Q

DLK

Signs + Symptoms

TX

: Topical prednisolone 1% every 1 hr while
awake. Follow up within 24 hours

A

Symptoms
ƒ Initially mild photophobia/sandy-gritty sensation
ƒFeels like dry eye / VA decreases

ƒ Signs
ƒ Diffuse haze at the flap interface
ƒ Begins peripherally or para-centrally migrates centrally
ƒ Appears “wave-like”
Progresses, coalesce, into clumps of inflammatory material
ƒNO AC reaction
ƒ Although rare- if left untreated, flap melting can occur

298
Q

DLK Treatment

Prevention

ƒ Managing blepharitis pre-operatively
ƒ Meticulous cleaning, sterilizing and drying of instrumentation

ƒ Adjusting level of femtosecond intralase laser

A

detected early —good prognosis

  1. ƒ treat with aggressive steroid therapy even at day 1
  2. Pred Forte is instilled hourly for the first 24 hours.
  3. If improvement in 24 hours, PF taper at QID until the
    * *inflammation has** resolved.

ƒ Taper steroid 2-3 wks IOP (STEROID RESPONDERS)
ƒ IOP’s must be closely monitored
ƒ Change to a “or add ocular hypotensive

299
Q

EPITHELIAL INGROWTH

A

ƒEpithelial cells growing under the flap edge
ƒ “pearls or nests” of epithelium that are translucent white/gray in color
ƒ Progresses centrally from edge of the flap
ƒ
ƒ Higher with enhancement or trauma
ƒ *less common with Intralase
ƒ Graded in stages – 1, 2, 3
ƒ Typically seen @ 1month

300
Q

EPITHELIAL INGROWTH

Grading and TX

A

Grade 1+
ƒ limited to within 2mm of flap edge
ƒ no associated flap edge changes

Self –limiting
ƒ

Grade 2+
ƒ ingrowth extending >2mm past flap edge
ƒ slight flap edge erosion/thickening/melting
ƒ Should be lifted and cells removed
ƒ

Grade 3+
ƒ Flap erosion and melting
ƒ Flap lifting and cell removal.
ƒ They are at risk for corneal melt if left untreated

May need to suture flap to prevent recurrence/further growth

301
Q

POST LASIK

EBMD

A

Very rare, Months to heal

Cells damage during procedure

302
Q

Post Lasik

Corneal Ectasiaƒ

Keratoectasia

Patients need to be followed every 3 – 6 month

PRK for moderate risk Px

A

Risk Factors:
ƒ Steep K-values (High Myopia)
ƒ Thin/asymmetric pachymetry
ƒ Asymmetric, progressive, irregular, high astigmatism
ƒ Decentered corneal apex
ƒ Abnormal topography
ƒ Patients with or FHX of Keratoconus, Pellucid marginal degeneration,forme fruste KCN
ƒ +atopy/eye rubbing

303
Q

Corneal Ectasia

Keratoectasia

A

Signs:
ƒ Inferior Corneal Steepening
ƒ Corneal thinning
ƒ Progressive myopia
ƒ Irregular or oblique astigmatism
ƒ Loss of BCVA
ƒ Treatment:
Rigid gas permeable

Corneal Intacs
ƒ Corneal crosslinking
ƒCorneal Transplants

304
Q

LASIK

Enhancements

Criteria – UCVA 20/40 or worse and -1.00D or worse refraction

A

4+months for Myopic patients
ƒ 6+months for Hyperopic patients
ƒEnough corneal stromal tissue RE-Cut flap
ƒ Enhancements if regression is significant and cornea adequately healed
ƒ Criteria – UCVA 20/40 or worse and -1.00D or worse refraction
ƒ Benefits must outweigh risks!

305
Q

PHOTOREFRACTIVE KERATECTOMY

PRK

  1. Epithelial layer removed
  2. Excimer laser treatment is applied to
    stromal bed
A

Thin corneas
Irregular corneas (abnormal topography/tomography)
EBMD, RCE
Corneal scarring
Anatomical issues- fissure size/orbital depth
Enhancements
Armed services
ƒ Contact sports/occupations
ƒ Football player/athletes
ƒ Flap fear!

306
Q

PRK

Advantages and Disanvantages

A

ƒ Advantages:
ƒ Improved outcomes for thinner or irregular corneas
ƒ Avoids complications of a corneal flap (LASIK)
Less overall tissue manipulated

No suction ring (LASIK)
ƒ

Disadvantages

Higher risk of infection/inflammation

Post operative discomfort / Re-epithelialization 1wk

Slow visual rehabilitation - several weeks before BCVA is achieved
ƒ Risk of stromal scarring

307
Q

PRK

Procedure

A

Epithelium is removed

  • Chemical debridement (5-25% Alcohol or 4% Cocaine)
  • Mechanical debridement- rotating abrasive brushes or manual w a brush/spatula
  • Laser debridement (with or without manual debridement)

Excimer laser (same as used for LASIK) ablates underlying stroma

Bandage CL placed on cornea

  • *Epithelium** to grow back (~5-7 days)
  • *Remove BCL** once epithelium is 100% healed
308
Q

PRK

Procedure Additions

MMC 0.02%-0.05%

Silicone Hydrogels

A

Mytomycin- C (anti-tumor, antibiotic activity)
ƒ MMC 0.02%-0.05% is used for ~20 seconds after ablation
ƒ Reduces post-op corneal haze and scarring
ƒ Especially useful for higher RX corrections

Risks of MMC - Delay re- epithelialization / Longer discomfort
ƒ

BCL - Silicone Hydrogels

Acuvue - Oasys

Air optix N&D

309
Q

PRK

Re-Epithelialization

A

Re-Epithelialization

  1. 4-6 days (BCL stays until 100% epithelialized)

ƒ Peak discomfort @ 2-3 days postop
ƒ Visual decrease @ 3-4 days postop
ƒ Followed DAILY until BCL removed

310
Q

PRK

Reducing Scarring

Recovery Time

A

ƒ Ways to minimize scarring:
ƒ Intra-operatively use Mytomycin-C
ƒ Intra-operatively use Chilled BSS (balanced saline solution)
ƒ Oral Vitamin C (1000mg)- start pre-operatively
ƒ

Reduce sunlight exposurepost operatively
ƒ Steroid use x 1 mo post operatively

Recovery Time

Vision is good in about a week, great in about a month
ƒ Day 1:
UCVA is normally20/40 to 20/80
Day 3-5: UCVA
may be aslow as 20/200-20/400
Day 7: UCVA
normally20/20 to 20/40
ƒ Recovery dependent on:
ƒ
Level of activity Individual physiology, healing pattern
ƒ Age
ƒ Level of refractive error

311
Q

PRK

MEDICATIONS USED

A

Orals Meds
ƒ Tylenol (acetaminophen) or Advil (ibuprofen)
ƒ Take as needed with food, do not take in addition to Vicoden
OR
ƒ Vicodin (acetaminophen + hydrocodone)
ƒ
ƒ Vitamin C- 500mg BID 4mnths pre + 4Months Post
ƒ

312
Q

PRK

DO’s Dont’S

A

NO makeup, swimming, use of hot tubs, gardening, dry/dusty
environment for 1 week
ƒ

NO exercise or strenuous activity x 1 week
ƒ

OK to shower @ Day 1 but keep eyes closed
ƒ

Driving when vision improves to 20/40 +

313
Q

PRK

POST-OP Shedule WK1
ƒ Expected epithelium healing:
ƒ Day 1- 30-60% healed
ƒ Day 2- 60-90% healed
ƒ Day 3-5 100% healed

A

Days 1-5 (until epithelium is 100% healed)
ƒ Assess UCVA / Worse 3-5days epi healing
VA clearing week 1 and considerably by weeks 3-4
First 5 days:ƒ

Patient should be wearing a bandage contact lens
ƒ DO NOT stain/remove CL
ƒ Assess Fit- ensure lens is in place/not moving excessively
ƒ Rule out infections/corneal infiltrates/tight lens

Document % healed Daily

314
Q

PRK

POST-OP

Removing BCL

A

Copious amounts of topical lubricant - float lens
Drag inferiorly or temporally(Px Nasaly) FORCEPS
ƒ BE CAREFULL TO NOT PULL THE NEW EPITHELIUM OFF

ƒ D/C Antibiotic next day, Continue steroids
ƒirritated/discomfort for an additional 1-2
day after CL removed
ƒ CONTINUE lubrication

315
Q

PRK

POST-OP WK2 - 6MTHS

A

2 week

  1. UCVA
  2. Manifest Refraction ~+/- 1.00D for regression
  3. IOP* (Steroid Response)
  4. IOP less - Thinner Cornea

ƒMonth 1, 2, 3, 4, 5, 6

  1. UCVA
  2. Refraction and BCVA = pre-op BCVA
  3. IOP
  4. Corneal Evauation clarity
316
Q

POST-OP complications

RECTICULAR CORNEAL HAZE

GRADED

A

ƒ Diffuse corneal reticular haze is a normal part of healing
ƒ Onset @ 2 weeks
ƒ Peaks @ 3 months
ƒ Clears @ 6 months
ƒ

Risk of permanent haze
ƒ 1%- mild to moderate Myopia
ƒ 2-5% - severe Myopia

317
Q

POST-OP complications

RECTICULAR CORNEAL HAZE

GRADED

A

ƒ Sub-epithelial
ƒ Qualitative and Quantitative reduction in BCVA
ƒ Significant haze without reduction in VA
ƒ

Predisposing Factors:
ƒ High Myopia
ƒ Previous refractive surgery

Treat only if significant

ƒ Steroids:
ƒ Ex 1% Prednisolone Acetate (PRED FORTE) Q1-2H x 2-3 week
ƒ If improvement - - taper

318
Q

POST-OP PRK complications

A

Open wound higher risk of:
ƒ Inflammation 1/1000
ƒ Infection/Infiltrates: 1/1000
ƒ Scarring/Haze: 1/100
ƒ Pain: 1/10
ƒ Risk of regression is higher

Corneal edema from tight lens
ƒ
May see folds in Descemet’s membrane
ƒ Requires contact lens removal and antibiotic ointment “patch”

319
Q

POST-OP PRK complications

STERILE CORNEAL INFILTRATE (BCL -Cause)

Small
Periphery of cornea
Not in the ablation zone
*****Related to BCL/hypoxia if lens too tight****
No ant chamber reaction
Mild discomfort

A

POST-OP PRK complications

Infectious CORNEAL INFILTRATE

Larger
Central cornea
Larger defect IN ablation zone - Confluent Ulcer
Ant. Chamber reaction
Progress with time/increase in size
More discomfort

320
Q

Infectious Corneal infiltrate

Causes And Treatment

A

Bacteria 90% are gram+

flora on the ocular surface Mycobacteria, Acanthomoeba
instruments, solutions, tap water, swimming pools,

TREATMENTƒ

4th generation fluoroquinolone
ƒ Vigamox/Gatifloxacin Q15min x 6 hours, then decrease to Q1H
(waking hours)

ƒ Fortified antibiotics
ƒ May need to culture*
ƒ DON’T WAIT TO REFER TO SURGEON

321
Q

LASER SX

MRSA

Methicillen Resistant Staph Aureus

Fortified oral Vancomycin & topical fluoroquinonole

A

MRSA keratitis
LASIK and PRK
ƒ Eye-lid cultures - patient is a carrier? re-infection
ƒ Pre-OP treatment of blepharitis
ƒ Prophylaxis: Use of 4th gen Fluroquinolone or bacitracin
ƒ Monocular treatment in known carriers
ƒ
ƒ Treatment
ƒ Fortified oral Vancomycin & topical fluoroquinonole

322
Q

SMILE

A

SMILE: Small Incision Lenticule Extraction
ƒ No flap
ƒ Femtosecond laser only
ƒ FDA approval 2016
ƒ -1.00 to -8.00 sph, upto -0.50 astigmatism
ƒ Correction of myopia only
ƒ Patient must be 22yr +

323
Q

Inflamation of the Conjunctiva

A

Inflammation is defined as localized:

  • Heat (Warm to Touch)
  • Swelling CHEMOSIS (more pronouced at limbus)
  • Redness
  • Pain Tender to touch

• Inflammation is a result of:

  • Irritation
  • Injury
  • Infection
324
Q

CONJUNCTIVITIS Self Limiting

Definitions

Pathogenicity:
ability of organism to cause disease
• Virulence:
ability to exhibit pathogenicity even in small numbers
• Invasiveness:
ability to invade, multiply and spread
Toxigenicity:
ability to elaborate toxic substances

A
  • blinking reaction and flushing of tears
  • lysozymes, lactoferrin provide protection from micro-organisms
  • epithelial glycocalyx prevents bacterial adherence to corneal surface
  • mucous aids in trapping bacteria preventing corneal penetration
325
Q

LAB Testing for Conjunctivitis

  • Conjuc - Cultures
  • Smear
  • Scraping

Mandatory for:

A
  • *Hyperacute** conjunctivitis
  • Neonatal conjunctivitis
  • post-operative infection

Intra introit injections

  • routine treatment has failed
  • corneal ulcer: central
326
Q

Conjunctival lab cultures

Conjunctival Smears

Conjuctival Scrapings

A

Cultures - Incubated / Sensitivety tested /

Conjunctival smear for analysis of white blood cells
(cytological testing)

neutrophils -Bacterial
eosinophils - Allegic
basophils - Allergic

leukocytes - Viral

Conjunctival scraping - Aneastetic - Kimura spatula

Better than smear

327
Q

CLinical evaluation of a RED EYE

HX: FOLDAR + Vocation + Allergies + CL wear

Subjective exam:

A

VA, pupils. EOM

  • Pre-auricular adenopathy – feel nodes in front ear
  • lids for blepharitis, Meibomian gland orifices
  • Lower fornix for discharge + conj inflamation
  • Follicles and papilla: lower and upper palpebral conjunctiva
  • Chemosis (Ridge at limbus)
  • Cells and Flare (Before Dye)
  • Qaulity of Tear film -Dry EYE
  • Observe cornea for staining patterns, infiltrates, ulcers: stain with Fl. and Rose
    Bengal or Lissamine green (Conj)
  • Posterior synechiae near pupil margin (stuck to lens)
    IOP after anterior chamber evaluation
    Observation of optic nerve and macula evaluation necessary at minimum for a problem specific examination.
328
Q

Clinical Features

Conjunctival

Infection / Inflamation

A

Hyperemia (redness/injection)/Hemorrhage

Diffuse / circumlimbal and nasal fornix

Chemosis (swelling) Allergies

Discharge

Bacteria Muccus / Viral Serrous

Papillae / Very red bv at surface

Follicles / BV at base, fluid filled

Membrane/Pseudo-membrane - Caused by fibrin in discharge

329
Q

Bacterial Conjunctivitis

+ cornea - Keratoconjunctivitis
+ lids - Blepharoconjunctivitis
+ lids and cornea -
Blepharokeratoconjunctivitis

A
  • muco-purulent type discharge
  • exogenous pathogens
    • Staphlococcus aureus
    • Staphlococcus epidermidis
    • Streptococcus pneumonae
    • Haemophilus Influenzae
  • Fundamental tissue changes
    • hyperemia
    • edema
    • discharge
  • Mono - Binoc - Incr in intesity first few days
330
Q

Pre-auricular lymphadenopathy

A
331
Q

Acute Bacterial

Conjunctivitis

A

Bulbar Conjunctiva

Hyperemia (meaty red)

  • circumlimbal area is usually clear
  • hyperemia greater towards the fornices

Palpebral conjunctiva
Papilla (Superior lid)

Cornea involvement Dt exotoxins

- PAN

+ PMN

332
Q

MX & TX

Acute Bacterial Conjunctivitis

A
  • Lid hygiene – warm compressors and lid scrub
    • QID 10min commercial
  • Lavage - BD reduce mucus in eye
  • Antibiotic
    • Polysporin qhs / Polytrim QID 1week
    • Cyloxin QID
  • Disgard cosmetics
  • non-resolvingpatients - after 48 hours
  • consider cultures and sensitivity
  • consider a second opinion or secondary site of infection.
  • confirm compliance
  • consider non-bacterial microbial infections
333
Q

Hyperacute Bacterial Conjunctivitis
Acute purulent conjunctivitis.

OCULAR EMERGENCY

A

Hyperacute Bacterial Conjunctivitis
OCULAR EMERGENCY
• The intensity of the inflammatory changes with an
overflowing purulent discharge
- HYPERACUTE

Can penetrate the cornea 24hrs

Cause:

Neisseria Gonorrhoeae
Neisseria Meningitis

334
Q

Hyperacute Bacterial Conjunctivitis

Clinical maifestations

A

Subjective:

  • EXAGERATED Progression ofacute bacterial conjunctivitis
  • Tenderness and marked edema around adnexa - copious discharge
  • intermittent blurred vision

Objective:

  • Hyperemia lids margin
  • Marked - hyperemia of conjunctiva
  • Chemosis around adnexa
  • POS pre-auricular node
  • mucopurulent discharge
335
Q

TX & MX

Hyperacute Bacterial
Conjunctivitis

A

suspect N. Gonorrhea unless proven otherwise

Ocular emergency / LAB workup indicated

Treatment:

  • Topical & Systemic Antibiotics
    • BABY -Eurithromycin. / Silver nitrate
    • ADULT: 4th Gen Flouroquinelones Moxyfloxicine 1gtt 15min
  • Lavage
  • Refer
  • treatment needed for related systemic signs
336
Q

Chronic Bacterial Conjunctivitis

A

accompanies a chronic blepharitis
Variable symptoms

  • burning
  • Irritation,
  • Foreign body sensation
    • lids stuck together especially in the morning

Objective

Lid involvement

    • madarosis
    • tyalosis; poliosis
  • Evert he lids → Papillae. PMN.
  • recurrent chalazion, hordeoli
  • collarettes at the base of the lashes

Auto - immune rxn
- cornea involvement: sub-epithelial infiltrates SEI (Grey white lesions per cornea)

superficial punctate keratitis SPK

337
Q

MX & TX

Chronic Conjunctivitis

A

Short and long term management and treatment
Warm Compressors – tapered scheduled over time Lid scrubs –tapered scheduled over time
Topical Antibiotics –drops (day), ointment (night) - x 1 week or drops only
Artificial tears drops- several times a day
Avoid any make-up products/discard any recent use of make up products
Use of steroids
Use of oral antibiotics

338
Q

FOLLICLES

focal hyperplasia (new tissue)
formed by lymphocytes acc in conj.

Elevated, clear to milky centers, base of the follicle has blood vessels

localized cell mediated immune response

A

Causes

  • *TOXINS**: developed HYPERSENSITIVITIES.
    eg: Molluscum Contagiosum VIRAL,

chemicals ALLERGIES.

339
Q

FOLLICULOSIS

A
  • *NOT a disease**
  • *Children to young adolescents** - eye is very quiet
  • due to hyperactive lymphatic system
  • disappears with age
340
Q

PAPILLAE

non-specific response to irritants to conjunctiva
-fibrovascular in origin

Upper and lower lid

Giant papillae occur in Vernal conjunctivitis and Giant papillary conjunctivitis. GPC

A
  • Elevated, deeper red vascular, with a blood vessel at the core of the papilla
  • increased and polymorphonuclear neutrophils (PMNs); eosinophils.

Causes

-bacterial infections

  • contact lens wear
  • allergies
341
Q

Identify

A

Appearance: clear like vacuoles; spherical in shape

DT: Cellular degeneration on the surface of conj

Location: bulbar and palpebral conjunctiva 00

Signs And Symptoms : asymptomatic

TX & MX

Lubricating Gtt: QID 4-6wks Then taper

Lancing

342
Q

Identify

A

PINGUECULA(E)
Very common
Location
interpalpebral zone of the bulbar conjunctiva
Pathiophysiology: Fibrovascular degeneration
Causes →Environmental / Mechanical CL / UV

PX education

343
Q

Identify

A

Pingeuculitis

Inflamed Pinqeucula

344
Q

Identify

A

Pterygium

When it passes limbus destroys Bowman’s membrane replacing it with a fibro-vascular layer SCARRING

  • *Appearance: fleshy,** triangular growth that extends onto the cornea; apex points towards the pupil
  • *Growth pattern Varies**

Symptoms:

  • blurry vision monocular
  • diplopia dry eye
  • foreign body sensation red eye
345
Q

Identify

A

Stokers Line

At the edge of pterygium / No progression

Pterygium

Causes irregular astigmatsim / Dry Eye

MX

FML - BID Finish coarse

Art tears QID -6/pd As lomg as needed

Removal sx / Conjunctival Grafts

346
Q

Identify

A

CONCRETIONS / Lithiasis

Small yellow white deposits on upper or lower palpebral conjunctiva
• ~1-3mm in size
• representative of a degeneration (aging palbebral conjunctiva) or chronic allergies
• Instead degenerating epithelial cells and mucin secretion

347
Q

Idenify

A

Axenfeld loop
Bulbar conjuctiva

Cilliary nerve loops varaible amount of pigment

348
Q

Conjunctival pigmented variations

A

MELANOSIS:

CONGENITAL More Pigmented individuals
- diffuse pigmentation visible on sclera/conjunctiva

349
Q

Pigmented Conjunctival Variations

A
  • *NEVUS:**
  • if the pigmentation is grouped it maybe called nevus - may increase in pigmentation -document
  • usually flat
350
Q

Pigmented Conjunctival Variations

A

ADENOCHROME DEPOSITS

exogenous source. ie: medications

Dark pigment granuales Inferior Fornix

  • *-**usually occurred when patients are placed on
  • *epinephrine** medication for glaucoma treatment

**Pro-drug - Propine

Effects Reversed

351
Q

Pigmented Conjuctival variations

A
  • *MELANOMA:**
  • concerned about changing in size and if elevated
  • newly acquired pigmentation
  • from a nevus or spontaneously from sun exposed areas
352
Q

Subconjunctival hemorrhages

Spontaneous rupture of conjunctival capillaries
3 levels of BV
- bright red
- bulbar conjunctiva involved

A

TRAUMATIC - MUST Do fundus examination and Prelims

Good Hx to determine the frequency + Cause

NON-TRAUMATIC

spontaneous increase in venous pressure
* coughing fit * sneezing

- diabetic
* vomiting
* straining: mechanical lifting
picking up weights giving birth

* post- surgical
* medications: blood thinner eg. Aspirin
* some bacterial and viral conjunctivitis
* blood pressure
eg: Epidemic keratoconjunctivitis
BPA
severe or un-controlled

353
Q

Management of subconjunctival hemorrhages

A

* patient re-assurance always needed
* the hemorrhage will disappear depends on size approx. 7-21 days
dilate the pupil to check the anterior portion of the eye and the retina in traumatic cases

354
Q

Ocular Allergies

Signs And Symptoms

A

Ocular allergic conditions:

  • Type I: anaphylactic or immediate hypersensitivity
  • Type IV: cell mediated reactions
  • Type III: immune -complex reactions

SIGNS

  • Vasodilatation of blood vessels
  • Itching
  • Chemosis to lid area and conjunctiva
  • Mucous discharge (Eosinoplils IGE)
  • Conjunctival lab tests: eosinophils & basophils
355
Q

VERNAL KERATOCONJUNCTIVITIS

A
  • Hot And dry
  • Age group: ~3 to 20-25 years of age
  • Early onset before puberty Male > Female 3:1
  • Recurrent for ~4-10 years and then stops
  • IgE mediated hypersensitivity

Symptoms

  • *-intense itching**
  • photophobia
  • ropy, stringy mucous discharge -red eye
  • *-bilateral**
356
Q

Identify

A

Vernal Conjuntivitis

PALPABRAL FORM: Giant Papillae / Cobblestone

Forms Superior lids/ Pseudo ptosis

357
Q

Identify

A

Limbal form VERNAL Conjunctivistis

  • Gelatinous precipitates
  • Trantas Dots: Eosinopils + Mast Cells + Epithelial cells

Diffuse Hypereamia

Marked Chemosis

358
Q

Clinical Signs of

VERNAL CONJUNCTIVITIS

A
  • Neovascularization of cornea
  • Pannus (Fibrovascular tissue)
  • SPK superiorly and centrally
  • Can lead to ulcer (Shield formation over ulcer)
359
Q

Vernal Conjunctivitis

MX working

A

MX & TX

  1. cold compressors QID stops itching (Mask in fridge)
  2. Antihistamine and mast cell stabilizer ophthalmic
  • PATANOL BID OU 4-6WKS
  • PATADAY QD
  • ZADITOR BID
  1. LAVAGE 2 x per day
  2. Non preserved art tears 1gtt GID - 6pd

preparations
•Lavage 2✗perday
• Non preserved artificial tears drops

360
Q

Vernal Conjunctivitis

Severe Cases MX & TX

A

ADDITIVE MX

Steroids - side effects – cataracts, increase in IOP

QID -2 WKS STOP

PRED FORTE

LOTEMAX (Not affect IOP Expensive)

FML

361
Q

HAY FEVER

Atopic Conjunctivitis

Characteristics: airborne allergens (pollen, molds , perennial allergens)
Type 1 hypersensitivity

A

Symptoms

  • itching (Primary Complaint
  • eye lid swelling
  • mucoid to watery like discharge
  • red eye
  • bilateral

MX & TX

  • Cold compressors QID
  • Artificial tears drops
  • Antihistamine and mast cell stabilizers
    • PATANOL BID OU
    • ZADITOR BID OU
  • Lavage BID
  • Protective eye wear
362
Q

Identify + Causes

Bulbar: Chemosis

Palpabral: GPC

A

GPC

Giant Papillary Conjunctivitis

Contact lenses: (HIGH WATER + IONIC)

  • lens deposits abrade the conjunctiva epithelium, exposing the immune system to the antigen on lens
    • Decr wearing time
    • Exess Movement
    • Rubbing
    • Mucoud discharge
  • CHANGE TO AOSEPT / PEROXIDE SYSTEM
363
Q

Identify

TX & MX

A
  1. discontinue CL wear
  2. alternative CL
    1. RGP
    2. Dailies / RX
  3. cleaning regiment change - PEROXIDE
  4. GTT mast cell stabilizers with antihistamine
    1. Patanol / Pataday / Zaditor BID 4-6wks
    2. ADDITIVE FML LOTAPREDNOL
  5. Cold Compress
364
Q

MEDICAMENTOSA

(Secondary to Preservative)

A

Preservative not medication or drug itself

BAK / Sulphar Gtt / Thimersol

  • immediate reaction
  • redness

SIGNS:

  • Diffuse SPK
  • Stinging burning Sensation
  • Hypereamia

MX & TX

Supportive

Flush with saline / Unpreserved Tears 6xpd 1week

Avoid allergen

365
Q

Identify

Other Signs and Symptoms

A

FOLLICLES in

VIRAL CONJUNCTIVITIS (Pink Eye)

Symptoms:

  • tearing
  • diffuse conjunctival hyperemia
  • FB
  • one or both eye involvement

Signs

  • follicles
  • corneal involvement: Sub-epithelial infiltrates (SEI), Superficial punctate keratitis (SPK)
    • PAN
  • Discharge: usually watery/serous
  • Laboratory : cytological response -lymphocytes
366
Q

VIRAL Conjunctivitis

Sub- catagories

A

Adenovirus DNA virus / 6 sub-groups

B&D Occular infections - Attaches to Surf Proteins

  • * Pharyngoconjunctival Fever (PCF)
    • Type #3
    • Swimming pool
    • Eye + respitory secretions
  • * Epidemic keratoconjunctivitis (EKC)
    • ​Type B
    • Most severe - Survive on surfaces for a long time
    • Auto enoculation
367
Q

ADENOVIRUS

Pharyngoconjuctival Fever

A
  • Fever
  • pharyngitis
  • follicular conjunctivitis
  • superficial keratitis SPK
  • unilateral
  • +PAN
  • CHEMOSIS

MX & TX

very contagious

Self - limiting

  • avoid contact with others
  • stay away from work environment or schools
  • disinfection at office and home

TX - Palative

Unpre Art Tears with SPK 7-10 days QID+

368
Q

ADENOVIRUS

Epidemic Kerato-conjuctivitis EKC

Signs and Symptoms

A

Symptoms

extremely contagious

  • may have feeling of malaise (tiredness)
  • starts unilaterally and then becomes bilateral

FB sensation

Signs:

  • MARKED Follicles
  • +PAN
  • FB sensation - SPK (membrane caused)
  • copious discharge / White Water
  • Severe conjunctival chemosis
  • pseudo-membrane Sup >> Inferior
  • sub-conjunctival hemorrhages
369
Q

EKC

RULE OF 7

No - Work

Clean surfaces CHLOROX

Daiken Solution 9:1 Bleach 10/10

A

Week 1

TX

  • Lavage BID try and reduce membrane formation
  • Cold Compresses
  • SPK -Art Tears Unpreserved QID++
  • Remove Membrane Manually

OFF - LABEL (In office only) Need Px Consent

Betadine Opthalmic Solution

  • Aneastetic
    • Rinse Eye well (toxic)
  • Expect Significant SPK
  • Art tear Gell post
  • Can be repeated
370
Q

EKC

RULE OF 7 (Week 2)

No - Work

Clean surfaces CHLOROX

Daiken Solution 9:1 Bleach 10/10

A

Active Viral Shedding 10-14 days

Subepithelial elevated Areas

371
Q

EKC

RULE OF 7 (Week 3)

No - Work

Clean surfaces CHLOROX

Daiken Solution 9:1 Bleach 10/10

A

SEI - central

Sub-epithelial infiltrates

Antigen antibody reaction to Viral particles

AUTO-Immune

372
Q

SEI - central

Sub-epithelial infiltrates

Antigen antibody reaction to Viral particles

AUTO-Immune

TX

A

White grey feathery boundries

If not in pupil - Steroid use contraversial

Central - PRED Forte Gtt

8 - 1wk

6 - 2wk

4 - 3wk

taper to 1gtt for 1month

373
Q

ADENOVIRAL DETECTOR

RPS

A

RPS Adenoviral detector
2 Antigen specific antibodies capture the viral antigens/particles
RPS detector notes proteins within the adenovirus
The kit consists of 2 parts: collection of sample

Dab about 4-6 times and keep for additional 3 seconds

immunoassay testing
Takes about 10 minutes to obtain the results

374
Q

HERPES ZOSTER

Primary infection - VARRICELLA

Varicella - dormant Dorsal Ganglia

re-activation varicella - HZV

A

Herpes zoster or shingles

Immunocompromised Individuals more at risk

  • HIV / Transplant px / Chemotherapy
  • Stress
  • average age of onset >45 years
375
Q

HERPES ZOSTER

Primary infection - VARRICELLA

Clinical Manifestations

A

Symptoms:

  • Fever / Malaise / HA
  • Pins and Needles sensation
  • 1-4 days before skin surface affected / 1-3 Dermatomes in same region 1 sided
  • intensely painful vesicular eruption of a single sensory nerve. thoracic nerve
    • ​Macular rash small flat spots
    • papular rash Erythematous
    • Vesicles 24hrs Blister like fluid filled
  • Post herpatic Neuralgia - > 1 month extreme pain
  • 2-3wks crusts and acute phase subsides
376
Q

Ophthalmic nerve of the Trigeminal nerve

Herpes zoster ophthalmicus

A

Nasociliary involvement - Lesion on the side ofthe nose

  • *Hutchingson’s sign - ocular involvement**
  • If you see a vesicle, look to see if it respects the dermatome
377
Q

HERPES ZOSTER OPTHALMICUS +

Signs + MX 72hr window

  • -accelerated Healing
  • Limits severity and duration
  • Decr Occular complication
  • decr Vision loss
  • decr post herptic neuralgia
A

PSEUDO dendrites better stained with ROSE Bengal

Gancyclovir GTT HS

Oral Mx - Start 72hrs

Valacyclovir (Valtrex): 1000mg TID for 10 days

Longer treatment - BID x 2 then / qh 2wks

  • *Acylovir** (Zovirax):(safer)800mg 5x/day for 10 days
  • *Famciclovir - 500mg TID for 10 days**
378
Q

Herpes Zoster

Managment and Treatment (Preventative)

A

Zostavax vaccine - 2006

Live attenuated vaccine

CONTRA-INDICATION - Immuno compromised

Shingrix vaccine - 2017

Glycoprotein E and adjuvant system
2 doses
2 to 6 months apart
>90% reduction in HZ

379
Q

Herpes Simplex Keratoconjunctivitis

Ocular type 1 / Type 2 south

Latent in Trigeminal nerve

primary cause of corneal blindness in the US

dt Stromal Keratitis

A

Subjective:

watery discharge - Photophobia

  • *Corneal sensitivity dec at repeated=infection**
  • foreign body sensation -
  • red eye - unilateral

Objective

•SPK

• Dendrites with terminal end bulbs
• RISK of epithelial involvement becoming stromal

380
Q

Identify and TREAT

Stromal Involvement consider STEROIDS

A

HERPES SIMPLEX

  1. Debridement (Decr viral particles)
  2. • Topical antiviral: Viroptic solution (triflururidine)
    1. VIROPTIC 1 gtt 9x pd till healed - QID 1wk
    2. Acyclovir Gtt 5xpd till dendrites heal Then TID 1Wk
    3. ZIRGAN Gel 0.15% Gtt 5pd then TID 1wk
  3. Acyclovir 400mg -5x a day 7-10 days
    * Valacyclovir 500mg -3x a day 7-10 days*Famciclovir 250mg -3x a day 7-10 days​
381
Q

Trachoma Inclusion Conjunctivitis

Organism

Type 1: Adult Inclusion Conjunctivitis CHLYMIDIA

Type 2: Trachoma

cyclical stages: active and cicatricial stages

A

Gram negative obligate intracellular organisms

Need a system to replicate

Inhibited by antibacterial drugs

Life cycle in Conjuctival tissue

Detection - Cytology - Giemsa stain – inclusion bodies
Antigen testing – ELISA test
DNA detection – PCR testing

Chlamydia microbes can mimic viral besides bacterial features

382
Q

CHLAMYDIA

serotype: D through to K

+PAN

Signs

A

Clinical Signs

  • +PAN
  • usually unilateral presentation (most cases)
  • discharge - muco-purulent
  • lids “sticky feeling”
  • light sensitive – mild photophobic
  • foreign body sensation
  • ***Acute follicular conjunctivitis predominantly lower lid
    bulbar hyperemia
  • conjunctival chemosis
  • ***Pappillae on sup Tarsal plate
383
Q

Adult Inclusion Conjunctivitis CHLYMIDIA

Clinical Manifestations

MX & TX

A

Acute Follicular inferior lid RXN (balooned)

Nasal Fonix Follicles

Corneal - SPK superior cornea

SEI (Sub epithelial infiltrates) PERIPHERAL

MX

Systemic oral antibiotic: best way to manage and
prevent recurrences: “Tetracycline family”
1,000mg Azithromycin - single, one-day dose OR
(2-3) days

384
Q

TRACHOMA

Chronic Component - Causes visual loss

A
  • Due to poor sanitization
  • Living in crowded areas
  • Poor hygiene OUTHOUSE
  • Lack of running water
  • Dry, Dusty environment
  • Human face fly / Feeds on ocular secretions
385
Q

Trachoma

Clinical Manifestations

ACTIVE stage

A
  • Follicular Conjunctivitis Upper >> Lower lid
  • +PAN
  • 0.2-2.0mm Folicles with LIEBER CELLS(necrosis if present long term
  • Affects mucous menbranes

PROGRESSION

  • PAPILLARY Hypertrophy (papillae btw follicles)
  • Sup Tarsal Conj Thickening
  • VELVET appearance
  • Limbal Follicles HERBERT’s Follicles
386
Q

Trachoma

Clinical Manifestations

Later stages

A

Herbert’s follicles

– Limbal region

Herbert’s pits

  • Cicatrization (Scarring forming depressions)

of limbal follicles

387
Q

Trachoma

Clinical Manifestations

Active stages

A

Cornea involvement pre-dominantly

–upper cornea - - Pannus

Goblet cell destruction leading to dry eye and other related complications

Pathoneumonic

ARLT’S Line - Star Shaped

HERBERT”S Pits

388
Q

Trachoma

Clinical Manifestations

Advanced stages

A

- Entropion - trichiasis / Tyalosis
- Secondary corneal infections / ulcerations
Muco-purulent - discharge
Corneal scarring – blindness

389
Q

TRACHOMA

TREATMENT

A

S Surgery for entropion: advanced trachoma

A Antibiotics: single dose 1g Azithromycin / 30mg / Kg Childern

F Facial cleanliness (wash. daily Environmental improvement

E Environments Importance / Clean Water - Good Hygiene

390
Q

Fundus landmarks:

Equator:

Imaginary line drawn fronm the vortex ampullae

A

VORTEX VEINS

391
Q

Fundus landmarks:

Peripheral Retina

40% 3DD away

Anterior to the eqautor extending to the ora serrata

A

Long posterior ciliary nerves and arteties

  • 3 & 9 o’clock
  • Temporal retina artery runs below Nerve
392
Q

Fundus landmarks:

Peripheral Retina

40% 3DD away

Anterior to the eqautor extending to the ora serrata

A

Short posterior ciliary nerve

  • Vertical meridians with arteries (10-20)