Lids Lashes Adnexia Flashcards
Function of eyelids
- Prevent ocular desiccation (Drying of eye)
- Protects the globe
- Grandular secretion - maintain pre-ocular tear film
- Spontaneous blinking (10-15/min at near 5/min)
- Reflex blinking - responce to irritants
- Closure during sleep
Lid Coloboma (Incomplete closure of tissue)
- 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
Lid coloboma
- Ocular complications
- Management
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
Epicanthal folds
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
Epicanthal folds
CT + variation
Reversed epicanthal fold - only bottom lid has fold
Cover test: Norm Hirsberg 0.5mm nasal of midline
Every 1/2mm = 11 pd
Distichiasis
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
Blepharophimosis
Hereditary - Autosomal dominant
Narrowing of lid fissure Horizontally and vertically
Ddx - Epicanthal folds and Ptosis
RISK - Amblyopia
MX - Sx
Alcohol Fetal symdrome
caused 1st + 2nd trimester
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
Ectropion
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
Ectropion
Classifications (causes)
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
Bell’s Palsy
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
Entropion
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
Trichiasis
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
Blepharochalasis
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
Dermatochalasis
Common in older px /
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
Ptosis
Features + Signs
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
Congenital Ptosis
Cause and Signs
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)
Acquired Ptosis
Findings and causes
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
Treatment and Grading of PTOSIS
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)
LID EXCURSION TEST (explain)
levator muscle
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
Turning in of lashes
Trichiasis
small, focalized area of eyelash loss
Madarosis (missing)
Can be caused by chronic blepharitis (most common cause) or injury (the lid structure is changed which could leave scar tissue)
complete loss of hair/eyelashes
Alopecia (alles uit)
chemotherapy + other causes
whitening of the eyelashes
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
abnormal rows of lashes coming out of Meibomian orifices
Districhiasis
lashes coming out of Meibomian orifices
usually misdirected eyelashes
thickening of lid margins
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
Lid Nevus / Nevi
flat and uniform Benign
- Slightly darker/more concentrated pigmentation
- Usually congenital
- born but noticeable until puberty
~8 to 10 mm in size
Papilloma
space between lesions / Rasberry surface
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
○ Avascular ○ Raised surface
○ Well defined/textured lesions
Type of Papiloma ?
Sessile
■ Broader base
■ Dome-shaped
■ Slightly bumpy
Type of papiloma?
and Mx
Pedunculated
- ■ Smaller base
- ■ Very narrow in shape
- ■ Raspberry-like bumps
MX:
Treatment Papilloma
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)
Xanthelasma
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
Treatment and Management
- 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)
Sudoriferous Cyst
○ 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
Identify
Treatment and Management
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
Sebaceous Cyst
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
Identify
Treatment and Management
Sebaceous Cyst
- Excision with drainage
- Should “lance”/cut the cyst directly across and allow for drainage
Malignant lid lesions
ABC
● “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 ulceration ○ Skin 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
Basal Cell Carcinoma
- 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
Basal Cell Carcinomas
Risk Factors?
- Age (>60 years of age)
- Vocation (outdoors during sunlight)
- Exposure to UV radiation
- Race (Caucasian or more fair-skinned)
Types of Basal Cell Carcinomas
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
Identify, Treatment and Management
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
Moth’s Technique
- 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
Acute and Chronic Staphylococcal Blepharitis
Bacteria Involved?
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
Acute Staphylococcal Blepharitis
Hx , signs and Symptoms
- ○ 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
Identify, Treatment and Management
Px Entance test expected results
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
Chronic Staphylococcal Blepharitis
Features
- 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
Chronic Staphylococcal Blepharitis
SIGNS
- 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)
Identify and full treatment / Management plan
CHRONIC
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
Seborrheic Blepharitis
Symptoms and Signs
- 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
Seborrheic Blepharitis
Signs
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
Identify
Treatment and Management
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
Angular Blepharitis
Features and Symptoms
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
Angular Blepharitis
Signs
- In the lateral canthus area, there could be redness/hyperemia
- Dermatological findings
- Excoriation → “cracked” skin
- Maceration → “softened” skin
Identify
Treatment and Management (2 variations)
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
Meibomian Gland Dysfunction (Meibomianitis)
Features
- 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
Meibomian Gland Dysfunction (Meibomianitis)
Symptoms and Diagnosis
Symptoms Variable if their tear film is unstable complain
Dryness ○ Blurriness ○ Blinking irritation ○ Tired eyes ○ Burning 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
Identity
Treatment and Management
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
Meibomian gland dysfunction classification
2 types
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
External Hordeolum
Features and Symptoms
- 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”)
External Hordeolum
Signs
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
Identify
Treatment and Management
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
Internal Hordeolum
Features and Symptoms
Acute onset and infection
○ Staphylococcal infection to Meibomian glands
○ Infection will involve **more surface area of the tarsal area **
○ Infection leads to acute inflammation ■ Redness ■ Tenderness/pain in the area ■ Swelling/edema ■ Warmth
● 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)
Internal Hordeolum
Signs and considerations
○ 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
Identify
Treatment and Management
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
Identify
Treatment and Management
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
Identify
Treatment and Management
○ 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
Chalazion
Features and Symptoms
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
Chalazion
Signs
Signs/Objective Findings
- Elevated focal lesion
- Dome-shaped
- Not tender/painful to touch!
- Not warm to touch!
Identify
Treatment and Management
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
Demodex
Features and Symptoms
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 sensation ○ Crusting on lid margins and lashes ○ Bilateral ○ Chronic
Demodex
Signs
○ 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
Identify
Treatment and Managment
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 days ● After 10 days, use 1x a day for another 10 days
Phthiriasis Palpebrarum
Features and Symptoms
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
Identify
Treatment and
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
Phthiriasis Palpebrarum
Signs
- 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
Phthiriasis Palpebrarum involves other necessary steps
- 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
Molluscum Contagiosum
Features and symptoms
○ 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
Molluscum Contagiosum
Signs
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
Identify
treatment and Management
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
Verruca
Signs and Symptoms
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
Identify
Treatment and Management
VERUCCA
May regress with time
- Cauterization when no longer active
- After many months, if no growth is occurring, can cauterize or laser
Contact Dermatitis
Features and symptoms
○ 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 adnexa ○ Increased lacrimation (if close to lid margin) ○ Adnexa swelling
Contact dermatitis
Signs
○ Redness to skin surface
○ Edema (swelling of lid adnexa)
○ Maybe bilateral or unilateral
○ Excessive tearing
○ Flaking of the skin surface
Identify
Treatment and Management
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!
Conjunctival Follicles
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)
Follicular conjuctivitis
Signs + Causes
Appearance
○ Elevated ○ Clear/milky/translucent centers ○ Blood 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!
Causes ○ Toxins: irritants to patient’s eye cause patient to develop hypersensitivities ○ Examples: Molluscum contagiosum, chemicals, viruses
Folliculosis
○ 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
Papillae
General
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)
Papilae
Signs and Causes
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
Retention Cysts
● 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
Gross Anatomy of the lacrimal system
Drainage pathway
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
Jones Test 1 + 2
Explain
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
Regugitation test
Explain
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
Common Disorders of the lacrimal system
list
S / ECT / EN
★ 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 lid → eversion of the puncta
Nasolacrimal Duct Obstruction
Features / MX & TX
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
Dacryocystitis
Features / Symptoms
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
Dacryocystitis
Signs
Signs
- Red focal elevated lesion
- Tearing
- Inner canthal area to lacrimal sac involved
- Firm nodule
- If infection spreads further, complications like preseptal cellulitis
Identify
Treatment and Management
Dacryocystitis
- Warm compresses
- Topical antibiotics - Broad spec. Polytrim / Gentamycin
Tobramycin QID 1 week
- Oral antibiotics 1 week
DRY EYE
Definition
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
DRY EYE
Approach
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
Overview of Lacrimal system
- 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
Tear Film Lipid Layer
Defects of lipid Layer
- ○ 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
Aqueous Layer tears
Defects of Aqeous layer
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
Mucin layer of tears
Defects of Mucin Layer
- 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
Mucin layer Glycocalyx
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
Tear film Structure
Traditional & Contemporary
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
What is tear Osmolarity, how does it affect dry. eye
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
DRY EYE
GENDER / AGE
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
DRY EYE
Environmental & Lifestyle
● 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
DRY EYE
Systemic Med HX and Systemic Drugs
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
Risk factor for dry eye specific to the ocular HX , MX used and Ocular Sx
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
Underlaying CAUSES of dry eye - 2 Primary causes
Broad 1st tier devision
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 /
2n tier of dry eye Causes following the Primary AQUEOUS DIFFICIENT and EVAPORATIVE DRY EYE
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
DRY EYE
Symptoms
● 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
Anterior segment diseases Causing
DRY EYE
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
SIGNS to look for in DRY EYE
★ 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
Evaluate Blinking Paterns and Drainage system
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
How to measure TEAR VOLUME
5 Options
- Tear MENUSCUS Height
- Schirmers 1 and 2
- Strip Meniscometry
- Phenol Red Thread
Tear Meniscus HGT
Schirmirs 1 + 2
explain + Norms
● 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
Phenol Red Thread
Strip Meniscometry
Norms and explanation
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)
Variations of tear film Stability
TBUT & New TBUT
● 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
Corneal Staining
Different Agents Used
What stain which defect better
- 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
Identify Condition and what to use to diagnose
● 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
★ Mucocutaneous Junction
Line of Marx (LOM)
○ 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
Lid Wiper Epitheliopathy (LWE)
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
Bio Marker analysis, Norms
Meibomien Gland Evaluator ?
Inflamatory Marker MMP
important for which patients?
Use for Sjorgens Syndrome Px
Rapid Pathogen Screening
Elevated protein in tears, Only tests for Matrix Metalloproteinse
MMP-9
What 2 test can be done with a trans illuminator
related to Dry eye
Meibography
To view the anatomy of the meibomian glands / Usually done with Infra Red
KORB-Blackie method to check for lid seal
Posterior Embryotoxon
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.
PANNUS
2 types
Normally superficial limbal vessels do not extend onto the cornea for more than 1mm
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
Dellen
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.
Identify and also stain used
Herpes Simplex
Rose Bengal stains dead devitalized cells very well
Identify and what should be considered
NEGATIVE staining
Consider: Possible recurrent corneal abrasion / Erosions
Identify
SPK
Superficial punctate Keratistis (DRY EYE)
FB scar, 2nd NaFl diffused into epithelium at site of injury after some time
Cornea
Functions
Parameters
Layers
- Stay Transparent
- Refractive – 75% of refractive power
- 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
Corneal Epithelium
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
Basement Membrane
Bowmans Membrane
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
Stroma
+ dua
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.
Decements Membrane
Endothelium
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
Cornea Innervation
&
Blood Supply
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.
Palisades if Vogt
- 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.
Loss of Corneal Clarity
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.
Epithelial Edema
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.
Important factors to consider when taking the HX of CORNEAL Edema
- 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
Possible CAUSES of
Corneal Edema
- 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
Signs and Symptoms of
Corneal Edema
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
Treatment for
Corneal Edema (Epithelial)
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
Stromal Edema
- 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
Causes of
STROMAL EDEMA
- 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
Signs and Symptoms
Stromal Edema
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
Treatment of
Stromal Edema
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
Surgical interventions at Endothelial layer
Prevent Corneal Edema
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.
How IOP influences which part of the Cornea swells
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
Corneal Scarring
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.
Stages of Wound healing
CORNEA
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