Ocular Disease: anterior Flashcards
Which is associated with vitritis, choroiditis or retinitis
Retinitis
All posterior uveitis presents with vitritis, T or F?
F
Inflammation of the retina
Breakdown of blood retinal barrier, resulting in WBCs in the vitreous. Patients may complain of floaters and/or decreased vision
Vitritis
Inflammation of the choroid
Does NOT affect the blood retinal barrier and will NOT present with vitritis
Most common cause of posterior uveitits
Toxoplasmosis
Pathophysiology of toxoplasmosis
Parasitic infection caused by toxoplasma gondii, an obligate intracellular parasite. May be congenital or acquired
Which is the most common form of toxoplasmosis
Congenital
In what ways can congenital toxoplasmosis occur
Only if the mother contracts it during pregnancy. If she has it before pregnancy, it will not transfer to the fetus
Of congential toxoplasmosis, what are the possible outcomes
90%-baby will be fine, recurrence in early adulthood with chorioretinal scar at birth
10% mentally handicapped: triad of convulsions, CEREBRAL CALCIFICAITON, and retinochoroiditis
How do you get acquired toxoplasmosis
Inhalation of the parasite in cat feces and/or through eating undercooked meat
Typical characteristics of toxoplasmosis
- young health patient with redness, photophobia, floaters, uveitits, vitritis, and decreased vision
- focal, fluffy, yellow-white retinal lesion adjacent to an old inactive scar with an overlying vitritis (Headlights in the fog)
Headlights in the fog appearance
Toxoplasmosis
Difference between toxoplasmosis and histoplasmosis
Histoplasmosis: FUNGAL infection that causes CHOROIDITIS that does NOT lead to vitritis. Results in multifocal “punched out” lesions in the periphery with associated peripapilllary atrophy and maculopathy, including CNVM
Toxo: retinovitritis, parasite, univocal, young and healthy, vitritis
Less common causes of posterior uveitits
Sarcoidosis
Syphilis
CMV
Posterior uveitis in sarcoidosis
Granulomatous panuveitis Retinal vitritis (cotton ball opacities) Retinal vasculitis (candle wax drippings)
Ocular findings in sarcoidosis
- Chronic dacryoadenitis
- dry eye disease
- chronic, bialteral, anterior granulomatous uveitits
- CN VII palsy
- retinal vasculitis
- vitritis
- optic nerve disease (unilateral optic disc edema, papilledema)
CMV: posterior uveitis
- most common ocular infection and cause of blindness in AIDS
- white patches of necrotic retina with hemorrhagic retinitis and vascualr sheathing
When does someone get CMV retinitis in AIDS
CD 4 counts less than 50
Difference between CMV retinitis and toxoplasmosis
CMV has more intravitreal hemorrhages and less vitritis than toxo
Difference between PORN and CMV
PORN has minimal amounts of vitritis (similar to CMV) and hemorrhages (less than CMV)
Causes of iris coloboma
Incomplete closure of the embryonic fissure
Most common place of iris coloboma
Inferior nasal
Iris coloboma associations
Coloboma of
- CB
- zonules
- choroidal
- retinal
- ON
What layer are iris melanomas found
Stroma
Iris melanoma is an abnormal proliferation of
Melanocytes in the iris stroma
Signs of iris melanoma
Pigmented or amelanotic Iris stromal tissue Inferior quadrant Feathery margins >3mm in diameter
Iris lesions in younger patients (<40)
Any iris lesion found in younger patients (<40 years of age) with high risk characteristics, including associated hyphema, ectropion uvea, angle involvement, inferior iris location, and diffuse feathery edges, should be evaluated for potential iris melanoma
Dellen
◦ An area of the cornea that wets poorly, leading to stromal dehydration and corneal thinning, with resulting pooling of NaFL within the affected area; seen adjacent to areas of elevation such as pterygia, filtering blebs, tumors, and poor fitting RGP lenses
◦ Patients may be asymptomatic or complain of an occasional FB sensation and other dry eye symptoms
Exposure keratopathy
Due to abnormal CN 7 or orbicularis oculi function
CN 7 issues and exposure keratopathy
Bell’s Palsy (idiopathic CN 7 palsy), cerebrovascular accident, aneurysm, MS, HSV, HZV
Orbicularis oculi issues and exposure keratopty
eyelid surgery causing ectropion, thyroid eye disease, nocturnal lagophthalmos, floppy eyelid sybdrome
Number one cause of exposure keratopathy
Lag ophthalmos
Symptoms of exposure K
redness, FB sensation and burning; symptoms are typically worse in the AM
Signs of exposure K
vary from mild SPK (commonly in the inferior 1/3 or intrapalpebral region of the cornea) to corneal ulceration. Decreased corneal sensitivity is common
When is exposure K worse for the pt
AM
Most common cause of filamentary keratitis
Keratoconjunctivits sicca
What are the filaments composed of in filamentary keratopathy
Degenerated epithelial cells and mucous
Stain with NaFL
What generally causes filamentary keratitis
Chronic inflamamtion and friction
Early sign of filamentary keratitis
Coma shaped SPK
Treatment for filamentary keratitis
Acetylcistein (mucomyst)
Histroy of thygesons
Most common in the 2nd-3rd decade. Patients often have a history of recurrent episodes with similar symptoms. There is no sex predilection
Pathophysiology/Dx of Thygesons
unknown etiology although may be viral or AI. The condition has no known associations with ocular or systemic diseases
Symptoms of Thygesons
FB sensation, photophobia, tearing, and occasional blurred vision. Overal lthe eye is relatively quiet with no anteiror chamber reaction or conjunctival injections. Symptoms are typically chronic and almost always bilateral
Signs of Thygesons
bilateral (90%), small, multiple, asymmetric gray-white clusters of superficial intraepithelial raised corneal lesions (avg 15-20). The condition is characterized by periods of exacerbation of remissions without serious sequelae over a period of 10-20 years before It permanently resolves.
‣ Acute attacks (exacerbation)-last 1-2 months (if untreated) before resolving; lesions will stain lightly with NaFL. Exacerbations often recur within 6-8 weeks
‣ Remissions: periods of inactive disease in between acute attacks; lesions do not stain with NaFL during remission
Where are the corneal lesions in Thygesons
Intraepithelial
Pathophysiology of neurotrophic keratopathy
trigeminal nerve neuropathy (CN V1) that results from damage to sensor nerve supply anywhere from the trigeminal nucleus to the corneal nerve endings. This condition results in decreased corneal sensitivity and a subsequent decline in corneal regeneration and wound healing
Common causes of neurotrophic keratopathy
‣ Common causes that directly affect CN V1 include herpes simplex, herpes zoster, diabetes, LASIK, CL wear, conditions that cause chronic corneal epithelial injury, surgeries, and medications
Damage to CN 7 and neurotrophic keratopathy
‣ Damage to CN 7 can also results in neurotrophic keratitis due to impaired reflex tearing. Tumors, CVA, Bell’s palsy, surgeries or other conditions that damage CN 7 prevent reflex tearing, which results in chronic damage to the ocular surface and disruption of CN V1
Neurotrophic is damage to which nerve
Nasocilairy branch of V1
Symptoms of neurotrophic keratopathy
redness, tearing, decreased vision, FB sensation, and swollen eyelids. Corneal findgins are often worse than what the symptoms indicate
Signs of neurotrophic keratopthy
decreased corneal sensitivity (hallmark of the condition). Early signs include SPK with associated perilimbal injection. Late signs include a sterile inferior oval ulcer (often with an associated iritis) without signs of significant inflammation
‣ This condition is characterized by non-healing epithelial defects; if not treated appropriately, the corneal defects will ulcerate, which may lead to corneal perforation
Big ulcer, little pain
Neurotrophic keratopathy
When does RCE occur
In the morning upon awakening
Causes of RCE
Corneal abrasion (any trauma, especially from organic matter like wood or fingernails)
Corneal dystrophies, most commonly EBMD
Symptoms of RCE
recurrent episodes of acute pain that most often occur in the morning upon awakening. Additional symptoms include lacrimation, photophobia, and blurred vision.
What wavelengths cause thermal/UV keratitis
Below 300
What parts of the cornea absorb UV light below 300
Epithelium and bowmans
Pathophysiology of UV keratitis
recall that the epithelial and bowmans membrane absorb wavelengths below 300nm; excessive absorption of this short wavelength light can result in hyperactivation of K+ channels, with resulting loss of intracellular K+ and cell death
Symptoms of UV keratitis
ocular pain, photophobia, and blurred vision. Symptoms are typically worse 6-12 hours after the incident
When is UV keratitis the worst for the patient
6-12 hours after the incident
Signs of UV keratitis
SPK within the intrapalpebral region of the cornea that stains with NaFL
DEW dry eye def
according to the international Dry Eye Workshop (DEWS), dry eye is a “multifactorial disease of the tears and ocualr surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface.”
Who gets dry eye the most
Post menopausal women
Medications associated with dry eye
- Atropine, scopolamine, homatropine, cyclopentolate, tropicamide (STopACH)
- ANTIhistamines: diphenhydramine, brompheniramine, chlorpheniramine, promethazine
- ANTIpsychotics: chlorpromazine, thioridazine
- ANTIdepressants: TCAs (amitriptyline, imipramine), MAOI (phenelzine), SSRIs (fluoxetine, excitalopram)
- ANTIanxiety: diazepam
- Muscle relaxant: cyclobenzaprine
- Ipratropium (via muscarinic blockade)
When are dry eye symptoms typically worse
End of the day
TBUT and dry eye
<10s
Is tear osmolarity increased or decreased in dry eye
Increased
Aqueous deficient dry eye signs
thin tear meniscus (<0.2mm in height is abnormal), decreased Schrimer findings, and decreased phenol red thread test
Evaporative dry eye signs
‣ Decreased TBUT (<10s)
‣ Poor expression of the meibomian glands or toothpaste consistency of meibum, meibomian gland atrophy on meibography
Schirmer I testing
Performed without anesthetic. Measures the basal, emotional, and reflex tearing
Normal on Schirmer I
> 10mm wetting in 5m
Borderline: 5-10mm wetting in 5m
Abnormal: <5mm wetting in 5m
Schirmer II testing
Performed with anesthetic. Measures only basal tearing
Normal Schirmer II
> 5mm wetting in 5m
Normal phenol red thread
> 10mm of wetting after 15s
What do rose bengal and lissmine green stain
Dead and devitalized conjunctival and corneal cells, as well as cells that have lost their mucous covering.
Two mechanisms behind dry eye disease
Increased Tear osmolarity
Tear film instability
Increased tear osmolarity and dry eye
results in inflammatory cascade that damages the ocualr surface and releases inflammtory mediators into the tears. Aqueous deficient dry eye and evaporative dry eye can cause tear hyperosmolarity
TearLab
TearLab technology measures tear osmolarity and may become a new gold standard in the dx of dry eye syndrome because of its high level of sensitivity and specificity. A tear osmolarity >308 mOsm/L or >8mOsm/L difference between the eyes is considered diagnostic for dry eye disease
Tear film instability and dry eye
can arise secondary to tear hyperosmolarity, or can be the initiating event in the disease process (reduces lipid layer in meibomian gland disease)
How does aqueous tear deficient dry eye result in increased tear osmolarity
• Aqueous tear deficient dry eye results in increased tear osmolarity- even though water evaporates form the ocular surface at a normal rate, there is a reduces aqueous layer of the tears
What are the two main categories of dry eye
Aqueous deficient
Evaporative
What are the categories of aqueous deficient dry eye
Sjogrens
- primary: dry eye and dry mouth
- secondary: dry eye, dry mouth, and autoimmune disease (usually RA)
Nonsjogrens
- primary lacrimal gland deficiency (age related)
- secondary lacrimal gland deficiency (inflammatory disease, surgery, CL)
Types of evaporative dry eye
Intrinsic
-MGD, lid position disroders, low blink rate
Extrinsic
-ocular surface disease (vit A), CL wear,
Difference between MGD and posterior blepharitis
• Posterior blepharitis and meibomian gland dysfunction (MGD) are often used interchangeably in medical practice, but this is an incorrect use of clinical terminology. Posterior blepharitis is a general term that refers to inflammatory conditions of the eyelid and may be caused by several conditions. In the latera stages of MGD, if inflammatory signs are present, an MGD-related posterior blepharitis is the appropriate diagnosis.
Low blink rate and evaporative dry eye
A low blink rate resutls in poor expression of meibum from the meibomian glands. The terminal meibomian gland ducts hyperkeratinize=obstruction of the ducts=intraductal HTN due to build up of meibum=dilation of the ducts=meibomian gland atrophy
Vitamin A and dry eye
Vitamin A is essential for goblet cell and glycocalyx development. Vit A deficiency can also result in aqueous tear deficient dry eye as a result of lacrimal gland acinar damage. It is associated with Bitots spots on the conjunctiva.
What staining is used in dry eye
Lissamine green
-inferior and 3 and 9 o’clock
When does keratoconnus start
Puberty
Inheritance of keratoconnus
Sporadic but can be AD
Pathophysiology of keratoconnus
non-inflammatory progressive and degenerative disease of unknown etiology that initally damages bowmans membrane. The condition results from the following
‣ Stromal collagen fibril displacement due to a loss of adhesion between fibrils, which resutls in corneal thinning and protrusion due to degradation of the fibrils by MMPs
What is keratoconnus associated with
Eye rubbing
Atopy
CL wear
Ocular and systemic diseases
Ocular conditions that may be assoacited with keratoconnus due to eye rubbing
Allergic causes
-VKC, AKC, floppy eyelid syndrome
CT abnormalities
-fuches ED, PPMD, granular dystrophy, lattice dystrophy
Hereditary causes (poor vision causing eye rubbing)
-aniridia, RP, Lebers, ROP, cone dystrophy
Systemic conditions associated with keratonncus
T-DOME
- Turners
- Down’s syndrome
- Osteogensis imperfecta
- Marfans
- Ehlers-Danlo’s
Also atopic dermatitis and mitral valve prolapse
Which corneal Ectasias can have hydrops
All three of them
Signs of keratoconnus
classical clinical signs include inferior, central, or paracentral stromal thinning that is typically bilateral, asymmetric, and progressive. As the condition progresses, irregular astigmatism occurs and is poorly corrected with glasses or SCL
Early signs of keratoconnus
Fleischer’s ring (iron deposits at the base of the cone that is best seen with a cobalt blue filter (appears dark)), scissors reflex on retinoscopy, irregualr mires on keratometry, and inferior steepening on topography
Late signs of keratoconus
Vogt’s striae (vertical lines in deep stroma), Munson’s sign (lower lid protrusion on downgaze), RIzzuti’s sign (conical reflection on the nasal cornea when a light is shown from the temporal side), and hydrops (tears in descemets membrane that result in edema and rupture of the epithelium). 53% of patients with moderate to severe keratoconnus develop corneal scarring in one or both eyes
Mild keratoconus
Less than 48D
Moderate keratoconus
48-54D
Severe keratoconnus
> 54D
When does PMD present
Early adulthood
Pathophysiology of PMD
unknown; researches believe collagen abnormalities result in a thin, weakened area of the cornea in a crescent shaped distribution inferiorly. IOP causes the cornea to protrude right above the area of thinning (not WITHIN the area of thinning, as with keratoconnus)
Signs and symptoms of PMD
patients typically do not experience pain. Characterized by bilateral, inferior corneal thinning (4-8 o’clock) 1-2mm from the limbus that leads to high amounts of ATR astigmatism. Classic corneal topography findings include “kissing doves” or “Crab claws”
Difference between PMD and keratoconnus
PMD vs Keratoconnus: unlike keratoconnus, there is no cone, no Flieshcers ring, not Vogt’s striae found in PMD. However, patients in PMD can develop sudden vision loss from hydrops (although it is less common than keratoconnus). Corneal scarring is also more common in keratoconnus
When does keratoglobbus present
Birth
Pathophysiology of keratoglobus
associated with Ehlers-Danlo’s syndrome, blue sclera, and Leber’s congenital amaurosis
Signs of keratoglobus
diffuse corneal thinning most concentrated in the periphery, resulting in a globular appearance. Can result in acute corneal edema due to rupture of Descemet’s membrane; corneal perforation can occur with only minor trauma
What are the anterior corneal dystrophies
EBMD
Meesmans
Reis-Bucklers
Pathophysiology of EBMD
Excess basement membrane
Inheritance of all EBMD
AD
Signs of EBMD
characterized by negative staining of map-lines, dots, and/or finger prints of the corneal epithelium (best seen with retro)
EBMD and RCE
10% of patients with EBMD develop RCE. 50% of patients with RCE will have EBMD
Signs of Meesmans dystrophy
Anteiror corneal dystrophy
characterized by extensive (100s), bilateral, clear intraepithelial cysts that are diffusely spread across the entire cornea (most dominant in the intrapalpebral region)
Reis Buckler Syndrome
Anteiror corneal dystrophy
Reports pain early in life
Bowmans replaced with collagen
RCE that decreases with age
Signs: bialteral, symmetric, sub-epithelial Gray reticular opacities that are most concentrated in the central cornea and spare the peripheral cornea; these opacities typically get worse with age
What is the most severe stromal dystrophy
Macular dystrophy
Which stromal dystrophy is AR
Macular dystrophy
Symptoms of macualr dystrophy
Stromal dystrophy
progressive vision loss and episodes of irritation and photophobia (secondary to RCE); severe vision loss occurs by the age of 20-30
Signs of macular dystrophy
characterized by diffuse, superficial, central haze between 3 and 9 years of age. Progression results in diffuse stromal opacification (cloudy cornea), stromal thinning, and multiple gray-white opacities (mucopolysaccharide deposits) with irregular borders that are present in all layers of the cornea and extend to the limbus
What accumulates in macular dystrophy
Mucopolysaccharides
What accumulates in granular dystrophy
Hyaline
Signs/symptoms of granular dystrophy
small, snowflake granules (hyaline deposits) in the central stroma. The deposits eventually spread towards the epithelium and deep stroma, becoming confluent and resulting in decreased visual acuity. RCE are rare
Rare variant of granular dystrophy that is characterized by granular and lattice deposits within the central stroma
Avellino dystrophy
What accumualtes in lattice dystrophy
Amyloid
Signs and symptoms of lattice dystrophy
anterior stromal haze with branching, refractile, lattice-like lines (amyloid deposits). Patients typically report decreased acuity (in 3rd decade) resulting from significant corneal scarring and haze. RCE common
What are granular, lattice, and avellino dystrophies assocaited with
mutation in the transforming growth factor beta 1 (TGFB1) gene
What accumualtes in schnyders dystrophy
Cholesterol
Pathophysiology of schnyders dystrophy
the condition has a strong association with hyperlipidemia, xanthelasma, and corneal arcus, and is typically non-progressive
How to remember the types of deposit in the corneal stromal dystrophies
Marilyn Monroe Got Hers in LA
- Macular=Mucopolysaccharides
- Granular=hyaline
- Lattice=amyloid
-Schnyders=cholesterol
What are the posterior corneal dystrophies
Fuchs
PPMD
Epidemiology of Fuchs
AD inherited condition. Female predilection, mroe common in patients over 60 years old (post menopausal women). 30% of patients have a positive family histroy of the condition
Pathophysiology of Fuchs endothelial Dystophy
recall that descemets membrane consists of an anterior lamina (produced in the embryo) and a posterior lamina (secreted by the endothelium throughout life). In Fuch’s dystrophy, the posterior lamina is produced in excess and is seen as clumps (guttata) of BM on Descemet’s membrane with an assoacited decrease in endothelial cell density (hallmark of Fuch’s)
Symptoms of Fuchs endothelial dystrophy
most patients remain asymptomatic until later in life; progression resutls in blurred, hazy vision that is worse in the AM with pain and glare
Signs of Fuchs endothelial dystrophy
often apparent early in life. Characterized by decreased endothelial cell density associatd with pleomorphism (shape) and polymegathism (size), endothelial guttata that have a “beaten metal” appearance, and thick pachymetry findings
Primary concern in Fuch’s endothelial dystrophy
The primary concern in this condition is stromal edema, which develops when the endothelial cell pumps are no longer able to maintain the proper osmotic balance. Stromal edema most commonly occurs when endothelial cell counts are less than 500 cells/mm2. As the condition progresses, stromal edema can spill over into the epithelium, leading to painful bullae (within the epithelial layer of the cornea) and scarring
What kind of pumps does the endothelial have that get lost in Fuchs endothelial dystrophy
NAK
Cataract surgery and Fuchs endothelial dystrophy
Cataract surgery can increased endothelial cell loss and accelerate the condition, especially in cell counts <1000 cell/mm2.
Kids endothelial cell count
3000-4000 cells/mm2
Endothelial cell count age 80
1000 cells/mm2
What is the minus number of endothelial cells needed to prevent corneal edema
Between 400-700 cells/mm2
Epidemiology of PPMD
AD inherited condition that occurs within the 2-3rd decade of life, although it may manifest as a cloudy cornea at birth.
Symptoms of PPMD
typically slowly progressive or non-progressive and most patients are asymptomatic; thus most patients with PPD are not identified with the condition until 30-50 years of age. Decreased vision secondary to cornea edema is the most common symptom in patients with PPD
Signs of PPMD
characterized by bilateral, but often asymmetric, findings that occur at the level of Descemet’s membrane and the endothelium. Findings include subtle patches of vesicle (hallmark), band lesions (linear “Tran track lesions”) and diffuse opacities. In severe cases, corneal edema and bullae lead to painful vision loss
What is the main concern in PPMD
PPD results in metaplasia of endothelial cells and an epithelial like endothelium. These endothelial cells have the potential to spread over the iris and angle architecture, resulting in angle closure glaucoma from PAS formation. ALWAYS DO GONIO FOR PPD
What layer of the cornea is being effected in PPMD
Descemets (and endothelial)
Megalocornea
Males Bilateral Diameter >13mm Highly myopic Glaucoma
Microcornea
Unilateral or bilateral
Diameter <10mm
Hyperopic
Risk of angle closure
Cornea plana
- cornea and sclera equal curvature (pathognomonic)
- assocaited with sclerocornea and microcornea
- bilateral flat corneas (<38D)
- hyperopia, shallow angles, increased risk of angle closure glaucoma
Aniridia
Bialteral
Partial or complete
Associated with corneal lesions, lenticular changes, post seg abnormalities
Haab’s striae
- congenital glaucoma
- horizontal cracks in descemets (forceps trauma are vertical)
Axenfeld-Rieger syndrome
Condition characterized by a continuum of disorders, including posterior embryotoxon, axenfeld anomaly, Rieger anomaly, and Rieger syndrome. They suffer from anterior segment developmental abnormalities that affect the AC angle. Appx 50% of patients with axenfeld-Rieger syndrome develop glaucoma
Posterior embryotoxon (PE)
anteriorly displaced Schwalbes line. Hallmark of Axenfeld-Rieger syndrome
Axenfeld anomaly
PE + angle anomalies + increased glaucoma risk
‣ Angle anomalies include prominent iris processes that travel to the level of the PE, often obscuring the scleral spur
Rieger anomaly
PE + angle anomalies + increased glaucoma risk + iris stromal abnormalities
‣ Iris stromal abnormalities include a displaced pupil (corectopia) and iris hypoplasia with resulting holes within the iris tissue (polycoria)
Rieger syndrome
PE + angle abnormalities + increased glaucoma risk + iris stromal abnormalities + systemic abnormalities
‣ Systemic abnormalities include mental retardation, dental, craniofacial, genitourinary, and skeletal abnormalities
Peters anomaly
- Rare condition in which patients are born with central white corneal opacities (leukoma) with iris adhesions. 80% of cases are bialteral
- Although some consider the condition to be part of axenfeld-Riger syndrome continuum, peters anomaly rarely occurs in conjunction with these disorders; it is best to consider the condition separately. 50-70% develop secondary glaucoma. Patients may also develop corneal edema and cataracts
Limbal dermoid
Normal dense CT with hair follicles and sebaceous glands that is displaced to an abnormal location; most commonly located at the inferotemporal limbus
Sclerotic scatter
Corneal clarity
Naked eye
Optic section
Angle depth
Conical beam
Dark adapted
Cells and flare
Specular reflection
Endothelium
Angles of incidence
Indirect illumination
Adjacent
EBDM
Cobal blue filter + NaFL
Better visualization of corneal and tears film integrity. Use the filter without NaFL to see iron rings appear black (Fleischer rings in Kones)
Which is worse, red or white eye with chemical Brian
White
Limbal blanching not good
Which is worse, alkali or acidic burns
Alkaline
Alkali burns
Alkali injuries are more dangerous than acidic injuries; calcium hydroxide is they most common cause of alkali burns. Remember, limbal blanching is an indicator of inschemia and is most common in alkali burns
Basic Burns Bad
Penetrate faster and deeper to cell membrane
White chemical burn us bad=ischemia
Hydroxide=base
Why do we use doxycycline when there is injury to the cornea
Decrease MMPs=increased healing
What can a patient get once they have a healed injury on their cornea
RCE
Signs of ruptured globe
full thickness laceration, severe conjunctival hemorrhage, EOM restriction, leakage of intraocular contents, low IOP, positive Seidel’s sign, hyphema, commotio retinae, choroidal rupture, and tractional retinal detachmen
Siedels test
◦ Siedel’s test is used to determine if a wound leak exists. If a leak exists (a positive seidels sign), the NaFL dye will appear as a black stream (diluted by the aqueous) within the green dye of the tears; cobalt blue filter should be used
Pathophysiology of hyphema
condition typically results from trauma to the iris and/or CB
What should you not do to someone with a hyphema
DO NOT perform gonioscopy or scleral depression on these patients until 1 month post injury to avoid rebleeding. Rebleeds tend to be worse than the principal presentation.
Microhyphema
RBCs suspended in the AC that can only be viewed with a slit lamp
Signs of hyphema
Additional signs include iris sphincter tears, iridodialysis, cataract, lens subluxation, pigment ring (Vossius ring) on the anterior lens capsule, commotio retinae, and angle recession
Iridodialysis: truama, iris root (thin) is pulled from CB
Vossius Ring: trauma, back of iris hits the lens, pigment on the front surface of the lens
Trauma is the number one cause of subluxatio
Number one cause of lens subluxation
Trauma
Idiopathic hyphema
In idiopathic hyphema, always inquire about the use of blood thinners (aspirin, reversible NSAIDs, warfarin, clopidogrel) and consider ordering a CBC, PT/PTT, and sickle cell screen. Sickle cell and/or clotting diseases should be considered in these cases, especially in AA and Mediterranean patients.
Idiopathic-think sickle cell and NSAIDs
IOP and hyphema
Increases bc TM getting blocked by RBCs and debris
Patients should elevate their head (30 degrees), allowing RBCs to settle inferiorly
FBs that cause significant inflammation
iron, steel, copper, or vegetable matter
FBs that do not cause a lot of inflammation
Glass, stone, precious metals, and plastic are inert materials and may stay in the eye for prolonged periods of time without causing inflammation
Most common site of orbital fracture
Orbital floor
Maxillary bone is the weakest (posterior medial)
Things to look for in orbital fracture
In orbital wall fractures, look for a trapped inferior rectus or inferior oblique (limiting upgaze, downgaze, or both), damage to the infraorbital nerve (causing hypoesthesia of the cheek), positive forced ductions, and peripheral crepitus
What not to do after orbital fracture
Do not perform gonio or scleral depression until 4 weeks after the trauma, patients should not blow their nose within 48 hours of trauma in order to limit the risk of an orbital infection
Forced duction test and orbital fracture
Orbital floor fractures are associated with a positive forced duction test. Remember that during forced duction testing, the clinical attempts to move the anesthetize eye in the direction of gaze of the affected EOM by using forceps to grasp the conj
‣ Positive: eye cannot be physically moved. EOM restriction
‣ Negative: can be physically moved. Cranial nerve muscle palsy
Pathophysiology of commotio retina
trauam causes disruption of the RPE and PR outer segments. Although the condition usually resolves without sequelae within 3-6 weeks, permanent vision, VF loss may occur
◦ Vitreous smacks into the PR outer segments. Gone in 72 hours
Symptoms of commotio retina
Usually asymptomatic
Berlins edema
Macular edema in commotio retinae
• disinsertion of the iris root from the CB ; appears as a peripheral iris hole that’s is best seen with retroillumination
Iridodialysis
Carefully monitor for angle recession glaucoma
Vossius ring
• a pigment ring on the anterior lens surface that retuslt from contact with the posterior pigmented iris epithelium during trauma
Associated with acute chest compressing truama and acute pancreatitis
Purtchers retinopathy
Chorodial rupture
- occurs in 5-10% of cases of blunt ocular trauma. Most commonly appears as a single area or multiple areas of subretinal hemorrhage, usually with the temporal posterior pole, with crescent shaped tears concentric to the optic nerve head. Choroidal rupture is assocairted with a long term risk of development of CNVM at the margins of the tear, occurring in an estimated 5-10% of patients
- Rupture always between the disc and the macula
What should be performed when there is a conjunctival or corneal laceration
Siedels test
ONH and trauma
Optic neuropathies can also resutls from trauma, disc pallor often takes weeks to appear
Pathophysiology of preseptal cellulitis
Infection anterior to the orbital septum Most commonly from -ocular infection (horeodlum) -systemic infection -skin trauma
Signs of preseptal cellulitis
eyelid edema, erythema, ptosis, warmth, no pain to mild tenderness, hard bump on eyelid. WILL NOT see signs of orbital congestion, as in orbital cellulitis
One of the leading causes of exophthalmos in kids
Orbital cellulitis
What to ask about when a kid has orbital cellultiis
Fever, recent dental infections or recent trauma
Pathophysiology of orbital cellultiis
an infection posterior to the orbital septum. Most commonly results from the following
◦ 1. Sinus infection-specially ethmoid sinusitis (the infection can easily spread through the very thin lamina papyracea)
◦ 2. Orbital infection - dacryoadenitis, dacryocystitis, progression of preseptal cellulitis
◦ 3. Orbital fracture
◦ 4. Dental infection
Most common bacterial culprits of orbital cellultiis
Staphylococcus aureus=adults
haemophilis influenzae=kids
Symptoms of orbital cellulitis
red eye, pain, decreased vision, HA, fever, general malaise, reduced color vision, an afferent pupillary defect (APD), proptosis, and diplopia with pain on eye movement due to EOM restrictions
Prognosis of orbital cellulitis
◦ Orbital cellulitis is a serious infection that can results in a cavernous sinus thrombosis, brain abscess, and/or meningitis if not caught early and managed appropriately
◦ Diabetics and immunocompromised patients with orbital cellulitis can develop mucormycosis, an aggressive fungal infection that can be life threatening; these patients have a characteristic “black eschar” (black necrotic tissue) in their mouth and nose
Preseptal vs orbital cellulitis
◦ Preseptal vs orbital cellulitis: patients with preseptal cellulitis will NOT have decreased vision, proptosis, fever, pain on EOM, or EOM restrictions, all of which are common in orbital cellulitis
What is something that can occur with TED
MG
What is the strongest risk factor for the development of TED
Cigarette smoking (2-9x greater)
Pathophysiology of TED
autoimmune disorder characterized by thyroid stimulating (TSH) receptor ABs directed against the EOMs and orbital tissue, causing fibroblast proliferation and significant inflammation and thickening of the EOMs that results in ON compression in the last stage of the disease
◦ Abs may also affect the thyroid gland, most commonly causing hyperthyroidism. TED occurs in 30-70% of patients with Graves’ thyroid disease
Symptoms of TED
prominent eyes, chemosis, FB sensation, tearing, photophobia, pain, diplopia, decreased vision, and color vision loss (non exhaustive list)
Signs of TED
unilateral or bilateral (often asymmetric) proptosis, upper lid retraction, Elemis erythema and edema, conjunctival/ caruncle injection and edema, decreased color vision, EOM restrictions, and an APD. IOP may be elevated in primary and upgaze
Most common cause of unilateral OR bialteral proptosis in middle aged patients
TED
NOSPECS grading system for TED
◦ N: no signs or symptom
◦ O: only signs but no symptoms. Examples include upper lid retraction (stare appearance); this is referred to as Dalrymple’s signs
◦ S: soft tissue involvement such as lid edema and conjunctival chemosis
◦ P: proptosis
◦ E: EOM involvement, resulting in diplopia; inferior rectus is typically affected first, followed by the medial, superior, and lateral recti (IMSLOW)
◦ C: corneal involvement (SPK, SLK, ulceration)
◦ S: sight loss due to ON compression
What is the greates threat to vision in TED
Compression of the ON
◦ Enlarged EOMs and inflamed orbital fat at the orbital apex can compress the ON, causing optic disc edema, and APD, reduced color vision, and visual field loss. ON compression is the greatest threat to vision due to thyroid eye disease, and occurs in 5% of patients
Von graefes sign
Upper eyelid lag during downgaze
TED
Kochers sign
Globe lag compared to lid movement when looking up
Dalrymple’s sign
Lid retraction resulting in stare appearance
Dx for TED
◦ forced duction to detect EOM restrictions
◦ CT/MRI to detect enlargement of the EOMs (tendons will be spared)
◦ Exophthalmometry to measure proptosis
◦ VF to detect ON compression
◦ Blood work (T3/T4/TSH) to measure thyroid function
Normal exophthalmometry
‣ 12-22mm for caucasians
‣ 12-18mm for Asians
‣ 12-24mm for AA
‣ Abnormal titer if higher OR presence of >3mm asymmetry. Make sure to record the base
Carotid Cavernous Fistuals result from
Abnormally communication between the AV systems
Most common cause of cavernous sinus fistula
◦ Most commonly results from closed head trauma (77% of cases). CFFs may also develop spontaneously (classically from a ruptured ICA aneurysm) or from cavernous sinus pathology
Signs of cavernous sinus fistula
◦ High pressure blood from the carotid artery builds up in the cavernous sinus and impedes the return of venous blood back to the cancerous sinus; this leads to a build up of pressure posterior to the globe and the unique classic triad of chemosis, pulsatile proptosis, and an ocular bruit.
◦ Additional signs include episcleral venous congestion, periorbital tissue swelling, elevated IOP, diplopia secondary to CN 3,4, or 6 palsies, and loss of lid /face sensation on the affected side due to a CN 5 palsy
Most common benign orbital tumor in children. Almost all cases are diagnosed by 6m of ge
Cap hemangioma
What can cap hemangioma cause
proptosis and deprivation amblyopia if the visual axis is blocked. Characterized bu rapid growth and spontaneous involution (70-75% of lesions gradually involuted by age 7)
Most common benign tumor in adults
Cavernous hemangioma
40-60 year old females
Signs of cavernous hemangioma
progressive, painless, unilateral proptosis as the tumor most commonly arises posterior to the globe within the muscle cone
Dermoid cyst
commonly located within the superior/temporal quadrant.l often congential and diagnosed in early childhood as a result of noticeable proptosis. A CT scan will show a well defined mass
Neurofibroma
a benign, yellow-white tumor of astrocytes that is most common in young to middle aged adults. A CT scan shows a well defined mass that is usually located int he superior orbit it can be isolated, multiple, unilateral, or bilateral. May be associated with NF
Neurolemmoma (scwhannoma)
a benign tumor of the Schwann cells that is mot common in young to middle aged adults. Typically located in the superior orbit, as the tumor develops within the first division of CN 5. Patients report a gradual onset of painless, progressive proptosis
Most common intrinsic tumor of the optic nerve
Optic nerve glioma
Usually in the first decade of life. Associated with NF1
Most common benign brain tumor
Meningiomas
Sphenoid meningiomas are the most common intracranial tumor to invade the orbit
Malignant orbital tumors
Rhabdomyosarcoma
neuroblastoma
Lymphoma
Most common primary pediatric orbital malignancy
Rhabdomyosarcmoa
Rapid bone destructing tumor thar causes progressive unilateral proptosis with an average age of 7
Rhabdomyosarcoma
Most common secondary pediatric orbital malignancy
Neuroblastoma
Where does a neuroblastoma arise from
The abdomen, they may have horners
Orbital lymphoma
most common in patients 50-70 yo. Characteristic signs include an APD and insidious progressive proptosis and vision loss. 30-50% of patients have orbital disease develop systemic involvement, of which 60% have a 5 year survival rate
Most common problems that result from orbital tumors
Progressive vision loss
Proptosis
Diplopia
APD
Who gets orbital pseudotumor
Young to middle aged patients
Pathophysiology of orbital pseudotumor
Idiopathic inflammatory process that can impact any soft tissue component of the orbit
Symptoms of orbital pseudotumor
Acute onset of unilateral pain, red eye, diplopia, and or decreased vision. Bilateral involvement may occur in kids. 50% of kids will have additional symptoms of fever, nausea, vomitting
Signs of orbital pseudotumor
‣ Lid ptosis ‣ Periorbital swelling ‣ Lacrimal gland enlargement ‣ Conjunctival chemosis ‣ Reduced corneal sensation (due to CN V1 involvement) ‣ Increased IPO on the involved side ‣ ON swelling (if posterior) ‣ EOM restrictions (causing external ophthalmoplegia) and proptosis due to inflammation of the orbital contents
If someone has chemosis unilaterally and not associated with allergies
Be certain to include idiopathic orbital inflammation in the list of differentials
Difference between TED and orbital pseudotumor
TED will not have EOM tendon inflammation and orbital pseudotumor will
Rare type of idiopathic orbital inflammation that can affect the cavernous sinus and the superior orbital fissure
Tolosa hunt syndrome
Patient presentation of tolosa hunt syndrome
Acute and painful exophthalmoplegia and diplopia due to ipsilateral palsies of CN 3,4,6,V1,V2
Loss of sensory innervation to V1 and V2 areas as well
What nerves pass though the cavernous sinus
3,4,6,V1,V2
Bilateral orbital pseudotumor in adults
Raise suspicions for systemic vasculitis (wagners, polyartertitis nodosa) or lymphoma
shrinkage and atrophy of the globe as a result of trauma, infection ,surgery, and advanced disease. Typically associated with inflammation, hypotony, and a blind eye
Phthisis Bulbi
absence of ocular tissue within the globe; primary cases are very rare
Anophthalmos
small globe, congential in nature
Microphthalmos
retraction of the globe within the orbit; often results from ocular trauma
Enophthalmos
Removal of the globe
Enucleation
Removal of inner contents of the eye; scleral and other orbital contents remain
Evisceration
Exteneration
Removal of all contents of the orbit, including EOMs and orbital fat
Who gets ocular rosacea
most common in middle aged adults of norther European ancestry. Women are affected more than men, but men often have more severe disease. Affects appx 10% of the population, including an estimated 50% with acne rosacea
Pathophysiology of ocular rosacea
condition affects the sebaceous glands (including meibomian glands of the eyelids), resulting in chronic ocular surface disease
Symptoms of ocular rosacea
redness, burning, FB sensation, ocular irritation
Signs of ocular rosacea
characterized by papules on cheek and forehead with telangiectasia, rhinophyma, and facial flushing
‣ Facial flushing with rosacea is associated with triggers such as alcoholic beverages, exertion, spicy food, caffeine, and increased sun exposure
What can ocular rosacea lead to
lid diseases (inspissated meibomian glands, blepharitis, hordeola, chalazion), which results in ocualr surface disease (phlyctenules, staph marginal keratitis, SPK, corneal neo (greatest inferiorly), and dry eye syndrome
What type of HS reaction is contact dermatitis
Type 4 HS reaction
What causes contact dermatitis
‣ Cosmetics: makeup, shampoo, soaps, hairspray, fingernail polish, perfumes, jewelry, poison ivy, CL solutions
‣ Medications: aminoglycosides (gentamicin, tobramicin), trifluridine, cycloplegic/mydriatics, glaucoma meds, preservatives
Symptoms of contact dermatitis
acute periorbital swelling redness, itching, tearing
Signs of contact dermatitis
unilateral or bilateral erythema and crusting of the lid and periorbital tissues and significant conjunctival chemosis.
Who gets ocular cicatricial pemphigoid
rare condition that affects females more than males. The average age of Dx is 65y; a significant number of these pateitns develop bilateral blindness an estimated 10-30 years after dx
Pathophysiology of ocular cicatricial pemphigoid
chronic AI idiopathic mucous membrane disorder that most commonly affects the oral and ocular mucous membranes (conjunctiva, mouth, esophagus, and less commonly the vagina and skin). Recent research suggests OCP is caused by a type II HS reaction involving auto Abs directed against the conjunctival BM. OCP can also be drug induced from timolol, epinephrine, and pilocarpine.
What type of HS reaction is ocular cicatricial pemphigoid
Type II HS
What is a common drug that can cause ocular cicatricial pemphigoid
Timolol
Symptoms of ocular cicatrial pemphigoid
sub-acute onset of nonspecific symptoms including redness, dryness, FB sensation, and/or decreased vision
Signs of ocular cicatricial pemphigoid
conjunctival fibrosis and scarring (seen as a fine white striate), bilateral symblepharon, ankyloblepharon, and stretched inferior fornices due to shortening of the conjunctival tissue.
Prognosis of ocular cicatricial pemphigoid
progression of the diseases results in the destruction of the goblet cells, meibomian glands, and the glands of krausse and wolfring, and the ducts of the main lacrimal gland, resulting in severe ocular surface disease. Additional late stage findings include entropion and trichiasis, with resulting corneal ulceration, neo, and keratinization
Pathophysiology of SJS
SJS is a severe progression of a type 3 or type 3 HS reaction that affects mucous membranes (typically oral and ocualr mucous membranes). It is most commonly drug induced (sulfonamide) or from an infectious agent
Acute signs and symptoms of SJS
systemic prodrome of fever, malaise, HA, nausea, vomitting. The prodrome is followed by the development of skin lesions ( diffuse erythema, classic target or bulls eye lesions, and papules on the palms of the hand and soles of the feet). Ocular lesions also occur in this phase and include
‣ Severe, bilateral, diffuse conjunctivitis associated with pseudomembranes
‣ Bacterial conjunctivitis can progress to endophthalmitis in severe cases
Chronic signs and symptoms of SJS
‣ Eyelid pathology: entropion, ectropion, trichiasis, meibomian gland damage
‣ Conjunctival pathology: symblepharon, foreshortening of the fornices, conjunctival keratinization, and limbal stem cell damage, which leads to subsequent corneal pathology
‣ Corneal pathology: ulcers, neo, scars, and in some cases, perforation
- common condition in the elderly. It is characterized by redundant upper eyelid skin that results from a weakened orbital septum, often causing eyelid ptosis, pseudoptosis, and a loss of typical distinct eyelid creases.
- Advanced cases may cause an apparent superior VF loss
Dermatochalasis
Two types of blepharitis
Staph and seborrheic
Symptoms of blepharitis
• Patients are often asymptomatic, but may report vision loss that clears after blinking, burning, itching, FB sensation, tearing, crusting (especially in the AM), and mild discharge.
Seborrheic bleph is assoacited with
Seborrheic dermatitis
Seborrheic blepharitis
◦ Seborrheic blepharitis is assocaited with less lid inflammation, more oily, gresasy scales with flaking, and more eyelash loss (madarosis) and/or misdirected growth compared to staph blepharitis
Anterior and posterior lids are separated by
The gray line (muscle of riolan)
Who gets chalazion
often have a history of similar recurrent lesions. Ask about acne rosacea and seborrheic dermatitis
Pathophysiology of chalazion
chronic, localized, sterile inflammation of a meibomian gland due to retention of normal secretions. 25% of chalazion resolve spontaneously without treatment
Signs and symptoms of chalazion
characterized by a hard, painless, immobile nodule without redness that is most commonly located on the upper eyelid. Patients are typically asymptomatic
Recurrent chalazia
warrant an evaluation for possible malignancies (sebaceous gland carcinoma
Difference between hordeolum and chalazion
◦ Both chalazia and internal hordeola affect the meibomian glands. Internal hordeola are caused by infection, and chalazia are caused by non-infectious inflammation
Who gets hordeolum
often have a history of similar recurrent infections (similar to chalazia) that are successfully self treated. As with chalazia, ask about acne rosacea and seborrheic dermatitis
Pathophysiology of hordeolum
An acute staph infection of the eyelid glands
Internal hordeola
Meibomian glands
External hordeolum
Affects the glands of zeiss and moll. Also known as a stye
Signs and symptoms of hordoelum
Tender, red, warm area of focal swelling on the lid
• benign lesions that develop from the epithelium of the epidermis and dermal tissues and are often associated with the meibomian, sebaceous, and sweat glands of the eyelids
Eyelid cysts
• Does not affect VA or cause pain, unless rupture of the cyst leads to an inflammatory reaction. The most common patient complaint is poor cosmesis
Decreased vitamin A
Bitot spots
Decreased B1
Thiamine
Wernicke-Korsakoff syndrome
a congenital or acquired lesion (secondary to trauma or surgery) found on the lid and surrounding adnexal tissue that often appears white due to the accumulation of kertinous debris
Inclusion cyst
acquired lesion found on the lid and the surrounding adnexal tissue that may appear white and is due to occlusion of sweat pores or pilosebaceous follicles
Milia
a congenital lesion that is firm and immobile and usually located on the superior temporal or superior nasal eyelid
Dermoid cyst
characterized by retention of fluid int he glands of zeiss or retention of debris in the meibomian glands. They are usually solitary, smooth lesions that are yellow or opaque
Sebaceous cyst
eversion of the Lid away from the globe of the eye. The most common cause is age related (involutional) loss of muscle tone of the orbicularis oculi muscle. Other causes include mechanical, cicatricial, paralytic, and congential.
• Signs/symptoms: exposure keratopathy, epiphora, brow ptosis
Ectropion
inversion of the eyelid against the globe, causes include age related (involutional) (most common), cicatricial (trachoma), and congenital. Can result in pseudotrichiasis
Entropion
eyelashes grow posteriorly from their site of origin
Trichiasis
a second row of eyelashes arises from the meibomian gland openings
Distichiasis
Signs of entropion
range from mild punctate keratitis to corneal ulceration and pannus (in chronic and severe cases)
Blindness due to trachoma are due to
corneal ulceration secondary to entropion and trichiasis
Who gets floppy eyelid syndrome
most common in obese men with obstructive sleep apnea
Pathophysiology of floppy eyelid syndrome
associated with significant reduction in elastin within the tarsal plate; this occurs predominantly in face down sleeping and is thought to result from mechanical trauma to the tarsal plate from chronic lid to pillow contact
◦ During sleep, spontaneous lid eversion exposes the superior tarsal subconjunctival to the bedding, causing a papillary conjunctivitis due to friction
◦ Systemic disease associations include obstructive sleep apnea, diabetes melliutus, hyperthyroidism, and HTN
Symptoms of floppy eyelid sybdrome
chronic, bilateral red eyes in the morning upon wakening, often with mild mucus discharge
Signs of floppy eyelid sybdrome
chronic papillary conjunctivitis with loose upper eyelids that every easily; punctate epithelial keratopathy (50%) and keratoconnus are noteworthy corneal associations
Ocular conditions that most often cause red eye in the AM
floppy eyelid syndrome, RCE, and exposure keratopathy
Who gets BEB
most common in ages 50-70, with a mean age of onset of 56 years. Women are affected 2x more commonly than men
Symptoms of BEB
involuntary, sustained, repetitive bilateral twitching and/or forceful closing of the eyelids that is less common during sleep
Signs of BEB
spasm of the orbicularis oculi, procerus, and corrugator musculature
Pathophysiology of BEB
most commonly idiopathic, although can be a result of corneal or conjunctival irritation. 78% of patients with BEB initially Jane random episodes of increased blinking that last seconds to minutes, with eventual progression to involuntary spasms with eyelid closure
◦ Over 50% of patients have an ocular surface disorder (most commonly dry eye) that may be exacerbating the spasms
Meige’s syndrome
characterized by BEB AND lower facial abnormalities (difficulty chewing, and opening the mouth, jaw spasms, jaw pain, etc) appx 50% of patients with BEB have Meige’s syndrome
Overview of BEB
Bilateral Idiopathic 3 muscles involved -orbicularis -procerus -corrugator
Myokimia
- characterized by unilateral twitching (NOT eyelid closure) of the orbicularis oculi; does not affect the procerus or corrurgator muscles
- Commonly caused by sleep deprivation, too much caffeine, or stress
Overview of myokimia
One eye
One muscle (orbicularis)
Triggers
List of malignant eyelid tumors from most deadly to least concerning
Melanoma
SGC
SCC
BCC
This is also the order from rarest to most common
BCC epidemiology
the most common skin cancer in the US. Affects males more than females. BCC is the most common eyelid cancer, accounting for over 90% of all eyelid malignancies. It is asooiciated with fair skin and UV exposure, especially in the UV-B range. Patients often report a chronic lesion that occasionally bleeds and will not heal
Pathophysiology of BCC
malignancy of the basal cell layer of the epidermis. Increases sun exposure in childhood and adolescent years is a critical risk factor for the development of BCC later in life
‣ BCC is minimally invasive; the incidence of metastasis is less than 0.1%
Signs of BCC
varies in appearance. Most commonly presents as a shiny, firm pearly nodule with superficial telangiectasia. If not recognized and treated at an early stage, progression occurs and central ulceration develops (“rodent ulcer”). Most commonly located on the lower eyelid (50-66%) and the medial canthus
Shortened version of BCC
Telangiectasia
Early pearly
Late=rodent ulcer
Epidemiology of SCC
more common in males. SCC is the second most common eyelid cancer, but it is 40-50x less common than BCC
Pathophysiology of SCC
malignancy of the stratus spinosum layer of the epidermis. Associated with UV exposure (especially in the UV-B range of 290-320nm), actinic keratosis, fair skin, prior radiation, burn scars, chemical exposure (smoking), and other forms of chronic irritation
Main differnece between SCC and BCC
SCC has NO telangiectasia
Most common precancerous skin lesions and is a precursor to SCC
Actinic keratosis
-It is an elevated, commonly pink or red, scaly lesion on sun exposed skin that does not heal. 25% of cases of actinic keratosis develop into squamous cell carcinoma
Signs of SCC
variable presentation; often appears similar to BCC but WITHOUT surface telangiectasia. Classically described as an erythematous plaque that appears rough, scaly, and/or ulcerated, and may be flat or elevated. Most commonly located on the lower eyelid or lid margin
What range of UV light causes malignant eyelid tumors
UV-B
SCC and BCC
‣ SCC and BCC are both associated with chronic exposure to sun light; they can appear very similar, but SCC rarely contains surface vascularization
Keratoacanthoma
usually found in sun-exposed areas and has an early appearance (often a central plaque or ulcer) that is similar to BCCs and SCCs. Keratoacanthoma tumors grow very quickly to a large size (1-2 cm) before they slowly shrink and often sponataneously resolve
Who gets SGC
rare, with a similar incidence to SCC. More common in elderly females. Patients may have a History of chronic unilateral blepharitis or recurrent chalazia
Pathophysiology of SGC
neoplasm of the sebaceous glands of the eyelids (meibomian glands and glands of zeiss) that may be assocaited with prior radiation therapy. Sebaceous gland carcinoma has a poor prognosis; if the lid lesion is greater than 2cm, the mortality rate is 60%. If symptoms have been present longer than 6 months, the mortality rate is 38%. The overall mortality rate is 10%
Signs of SGC
varies. The tumor is often hard and yellow. It is associated with madarosis, thickened and red lid margins (most common on the upper eyelid), and lymphadenopathy
Epidemiology of malignant melanoma
rare (<1% of all eyelid malignancies) but most lethal primary skin cance r
Pathophysiology of malignant melanoma malignancy of melanocytes, the cells that produce pigment within the skin. Risk factors include age, skin color, family Hx, repeated irritation, and sun exposure
malignancy of melanocytes, the cells that produce pigment within the skin. Risk factors include age, skin color, family Hx, repeated irritation, and sun exposure
Signs of malignant melanoma
characteristics that increase suspicion for a malignant melanoma include the following: ‣ A: asymmetry ‣ B: border irregularity ‣ C: color differences (uneven) ‣ D: large diameter ‣ E: elnalrgement of the lesion
Most important prognostic factors for malignant melanoma
Depth of invasion and size of the lesion
Who gets dacryoadenitis
more common in children and young adults. Ask if acute or chronic symptoms and if there is any history of a recent fever or systemic infection
Pathophysiology of dacryoadenitis
inflammation of the lacrimal gland that can be acute or chronic in nature
‣ Acute infections: most commonly a result of an infection by bacteria (staphylococcus aureus, neisseria gonorrheae, streptococci) or viruses (mumps, mono, influenza, HSZ)
‣ Chronic infections: more common than acute infections. Results from inflammatory disroders including sarcoidosis, TB, graves, and idiopathic orbital inflammation; 25% of patients with idiopathic orbital inflammation will have lacrimal gland involvement
Signs and symptoms of dacryoadenitis
swelling of the outer 1/3rd of the temporal upper eyelid region (near the lacrimal gland). Signs may vary in acute and chronic presentations
‣ Acute: classically presents with a S shaped ptosis, temporal upper eyelid pain, redness, and swelling, preauricular lymphadenopathy, an occasional fever, and an elevated WBC count
‣ Chronic: presents as temporal upper eyelid welling with less redness, swelling, and pain. May have inferonasal globe displacement
Pathophysiology of canaliculitis
inflammation of the canaliculi that can be caused by bacterial, viral, or fungal infections. The most common culprit is actinomyces israelii (streptothrix), which is characterized by yellow sulfur granules after expression of the canaliculi
‣ Other culprits include staphylococcus aureus, Candida albicans, aspergillus, nocardia asteroides, HSV, HZV
‣ Canaliculitis May also occur after surgery, trauma, and secondary to neoplastic disorders
Most common cause of canaliculitis (bacteria)
Actinomyces Israelis
Symptoms of canaliculitis
smoldering, unilateral red eye that is often unresponsive to abx treatment; often misdiagnosed as recurrent conjunctivitis
Signs of canaliculitis
tenderness over the nasal portion of the upper or lower eyelid, a swollen puncta (pouting puncta), dacryoliths, and mucopurulent discharge that occurs with palpation over the lacrimal sac region
Epidemiology of dacryocystitis
ask about concomitant ear, nose, or throat infections
Pathophysiology of dacryocystitis
lacrimal sac infection that occurs when the lacrimal drainage system is obstructed (NLDO) resulting in a back flow of bacteria from the nasolacrimal duct into the lacrimal sac
‣ Common causative agents include staph aureus, staph epidermidis, pseudomonas, and H. Influenzae in kids
‣ Characterized by swelling below the medial canthal tendon: note that swelling ABOVE the medial canthal tendon should raise suspicion for a lacrimal sac tumor
Chronic cases of dacryocystitis
should raise suspicion for epithelial carcinomas and malignant lymphomas, unfortunate pathology that are often overlooked; carcinomas can express blood into tear film with palpation of the lacrimal sac
Symptoms of dacryocystitis
pain, often with crusting and tearing, occasional fever
Signs of dacryocystitis
prominent edema and tenderness over the lacrimal sac area
Differnece between dacryocystitis and canaliculitis
Dacryocystitis has more swelling, tenderness, and pain
Treating dacryocystitis
‣ DO NOT refer for surgery or attempt to irrigate the lacrimal system during an acute dacryocystitis infection. Treatment should be initiated first
Punctal stenosis
◦ Acquired punctal stenosis is defined as a narrowing or occlusion of the puncta of the upper or lower eyelids. It is commonly associated with older age, where progressive narrowing and occlusion of the puncta occur
Symptoms of punctal stenois
◦ The most common symptom is epiphora, although patients may also report nonspecific complaints of ocular irritation
NLDO
Congenital or acquired, more common in females
Older patients; NLDO
Involutional stenosis most commo ncause
Young patients: NLDO
Most commonly caused by membranous blockage of the valve of hasner, occurs in 5-30% of newborns. Spontaneous opening occurs 1-2 months after birth. Gentle massage
Symptoms of NLDO
unilateral tearing, discharge, crusting, and recurrent conjunctivitis
Signs of NLDO
epiphora, mucus reflex from the puncta after compression of the lacrimal sac, medial lower eyelid erythema, and mild to no redness to tenderness around the puncta
Secondary dacryocystitis in cases of congenital NLDO
‣ A secondary dacryocystitis is not uncommon in cases of congenital NLDO due to the stagnant tears in the lacrimal sac
Tests to evaluate the ability of the tears to pass through the lacrimal drainage system
Jones I and II
Jones I
Tests the patency of the system
- NaFL in 5minues
- positive=patent. Confirmed by the presence of NaFL in the back of the patient’s throat or by having them blow theirn nose and seeing NaFL on the tissue
Jones II
Irrigation with saline following a negative jones I
◦ Reflex of fluid through the same punctum indicates an obstruction within the upper and lower canaliculus (proximal to the common canaliculus)
◦ Retrograde flow though the opposite canaliculus and punctum indicates nasolacrimal blockage (obstruction distal to the common canaliculus)
◦ If the patient tastes the saline, performs a gag reflex, or if the fluid is recovered from the nose, the obstruction has been cleared
◦ If the Jones II test fails to open the nasolacrimal drainage system, a DCR is the best treatment option
A common benign, fluid filled (typically clear) sac on the conjunctiva that may cause irritation. Also referred to as an inclusion or retention cyst
Conjunctival cyst
Superficial, white yellow deposits of mucous secretions and epithelial cells in the palpebral conjunctiva. Conjunctival concretions are also known as ocular lithiasis
◦ Patients are typically asymptomatic, but may experience a FB sensation
Conjunctival concretions
Conjunctival nevus
◦ Rare benign proliferation of melanocytes that presents around puberty or early adulthood (within the first two decades of life). During puberty it is not uncommon for the size and darkness of the nevi to increase
◦ Conjunctival nevi are typically unilateral, solitary, flat, freely mobile, and are occasionally non-pigmented. Inclusion cysts within the lesion ar diagnostic for a conjunctival nevus
◦ The most common location for a conjunctival Venus is the juxtalimbal area, followed by the plica and caruncle
PAM is a precursor for
Malignant malanoma of the conjunctiva
PAM
◦ Unilateral acquired pigmentation with indistinct margins that is more common in elderly white patients
◦ The patches, which can be located anywhere on the conjunctiva, are usually flat with indistinct margins. Although PAM can be benign, it also has premalignant potential; 30% of cases progress to malignant melanoma. Nodular lesions with increase vascualrity and/or increased growth are suspect for possible malignancy. A biopsy is warranted to determine whether the lesion is malignant.
Conjunctival melanoma
◦ Secondary to the uncontrolled proliferation of melanocytes. They are found almost exclusively in whites and usually develop around age 50
◦ Malignant melanomas of the conjunctiva can be pigmented or non pigmented and most commonly arse from PAM (50-75% of cases), less commonly from a pre-existing nevus (33% of cases), and rarely be novo
◦ The most important prognostic indicator for progression to malignancy is the thickness of the lesion. The most common site of metastasis is the liver.
Conjunctival intraepithelial neoplasia (CIN) is a precursor for
SSC
CIN
◦ Although rare, CIN is the most common conjunctival neoplasia in the US. It is also known has Bowen’s disease or conjunctival squamous dysplasia
◦ CIN is a unilateral, premalignant condition that can progress to SSC (although the risk is low as the BM most often remains intact). Risk factors for development include UV-B exposure, smoking, exposure to petroleum derivatives, fair skin, xeroderma pigmentosa, HIV, and HPV.
◦ Presentation can vary, but the most common appearance is an elevated, gelatinous mass with neovascularization; appx 10% of cases exhibit leukoplakia (keratinization) 95% of cases are found at the limbus within the interpalpebral fissure. CIN can progress onto the cornea.
◦ Studies have suggested that toluidine blue 0.05% staining may be used as a diagnostic tool for benign vs malignant or premalignant lesions, although the PPV is only 41% and the NPV is 88%. It does not distinguish between premalignant and malignant conjunctival lesions.
◦ A pedunculated, benign, red, vascular lesion of the palpebral conjunctiva that results from trauma, surgery, a chalazion, or other sources of chronic irritation.
Pyogenic granuloma
Inflamed area (white, yellow, translucent, brown) located within the conjunctival stromal tissue that results from retained FB, surgery, trauma, infections, or associated systemic conditions Patients may be asymptomatic or complain of ocular irritation and FB sensation
Conjunctival granuloma
Simple bacterial conjunctivitis culprits
- kids
- H influenza most common in kids, S epi and S aureus most common in adults
Symptoms of simple bacterial conjunctivitis
acute onset of redness that usually begins in one eye and becomes bialteral. Additional symptoms include FB sensation and eyelid stuck together upon wakening. Symptoms typically subside in 10-14 days, even without treatment
Signs of simple bacterial conjunctivitis
variable discharge (typically moderate to severe) that is often initially serous before becoming mucopurulent (most common) or purulent. Corneal signs and preauricular lymphadenopathy are rare.
What is the most commonly isolated organism in simple bacterial conjunctivitis
S aureus
Pathophysiology of gonococcal conjunctivitis
neisseria gonorrhoeae is the most common causative agent. The Thayer Martin agar (chocolate agar) is used for diagnosis. Gram stain for N. Gonorrhea will show gram negative intracellular diplococci
Thayer martin (Chocolate agar)
Neisseria gonorrhea and Haemophilus influenzae
Hershey’s and Nestles CHOCOLATE
Symptoms of gonococcal conjunctivitis
characterized by hyperacute onset of severe purulent discharge. Aspirational symptoms include redness, FB sensation, and eyelids that are stuck together upon awakening; condition usually begins in one eye and becomes bilateral over time
Signs of gonococcal conjunctivitis
severe purulent discharge, conjunctival chemosis (often with pseudomembranes), a severe papillary reaction, marked preauricular lymphadenopathy, and tender, swollen eyelids. remember that N. gonorrhea can invade an intact corneal epithelium and may result in peripheral corneal ulceration in severe cases.
Systemic complications and gonococcal conjunctivis
- Men: purulent urethral discharge that occurs after 3-5 day incubation period
* Women: discharge is less common; appx 50% of patients are asymptomatic
All patients with a gonococcal conjunctivitis should be tested for
Chlamydia
What kind of bacterial conjunctivitis causes preauricular lyhmpadenopathy and pseudomembranes
N gonorrhea
Hallmark of adenoviral conjunctivitis
Follicles
Pathophysiolgoy of adenoviral conjunctivitis
most adenoviral infections result from upper respiratory tract or mucosal infections. Appx 1/3 of serotypes are associated with ocular infections. Transmission occurs from direct contact (e.g. respiratory or ocular secretions, contaminated towels, equipment) and is highly contagious for 12-14 days. Classic adenovirus syndromes include acute nonspecific follicular conjunctivitis, pharyngoconjunctival fever (PCF), and epidemic keratoconjunctivitis (EKC
What are adenoviral syndromes assocaited with
follicles, pseudomembranes, and diffuse conjunctival hyperemia and will follow from a systemic viral infection
Acute nonspecific follicular conjunctivitis
results from serotypes 1-11 and 19 and is the most common type of adenoviral infection
• Presents with a diffuse red eye, conjunctival follicles in the inferior fornices, tearing, and mild discomfort; corneal involvement is rare
No lymphadenopathy
PCF
results from serotypes 3-5 and 7. It is also referred to as “swimming pool conjunctivitis.” PCF more commonly affects chidlren and is highly contagious
• Diagnosis of PCF is based on a triad of acute follicular conjunctivitis (occasionally hemorrhagic), mild, low grade fevere, and pharyngitis. Corneal involvement is not common
Fever, follicles, pharyngitis
EKC
most serious form of adenoviral conjunctivitis and results from serotypes 8, 19, and 37. This condition is well known for pain and corneal involvement (80% of cases)
• Clinical symptoms classically occur 8 days after initial exposure to the virus. Superficial keratitis is common during the acute phase (1-2 weeks), while subepithelial infiltrates (SEIs) commonly occur after the 3rd week, after the active portion of the disease has subsided (patient no longer contagious)
• Preauricular lymphadenopathy is almost always present in EKC patients. They may also have pseudomembranes.
Lymphadenopathy, pain, corneal invovlemt
Rules of 8 for EKC
caused by serotypes 8, symptoms occur 8 days after exposure, and SEIs occur 8 days after the onset of symptoms.
Symptoms of adenoviral conjuncgitis
rapid onset of redness, tearing, mild discomfort, and preauricular lymphadenopathy. The condition typically starts in one eye before spreading to the other
Signs of adenoviral conjunctivitis
acute follicular conjunctivitis (follicles are most common in the inferior fornices), marked conjunctival injection, pseudomembrane formation, preauricular lymphadenopathy (classic for EKC), and diffuse keratitis (particularly in EKC)
What is virtually always pathognomonic for EKC
Palpable node in a patient with suspected adenoviral infections
Molluscum contagiosum
- areas of poor hygiene
- chronic infectious skin condition caused bu the DNA pox virus that is spread through direct contact. If multiple molluscum nodules RA present, consider HIV or other immunodeficiency conditions
- characterized by single or multiple dome-shaped, umbilicated, waxy nodules located on the loud or lid margin. Patients are usually asymptomatic but may complain of a mild mucus discharge. Rupture of the molluscum nodules may lead to an associated chronic follicular conjunctivitis and superficial pannus.
Viral conjunctivitis with unilateral follicular conjunctivitis with a watery discharge
Herpes simplex
Seasonal allergic conjunctivitis is a _____ hypresentivity reaction
1
Signs and symptoms of allergic conjunctivitis
conjunctival chemosis, papillae, itching, tearing, watery discharge
VKC
- very rare condition. Classically affects young males under the age of 10 that live in hot, dry climates. The condition occurs for 2-10 years before resolving around puberty
- VKC occurs in patients predisposed with atopic systemic conditions; 40-75% of patients with VKC have eczema or asthma, and 40-60% of patients have a family history of atopy. Seasonal outbreaks during the warm months are common, although patients may have symptoms year round.
- intense itching and photophobia (most common complaints), ptosis, thick mucus discharge. The initial outbreak is the most severe; symptoms decrease in intensity over time
- the classic sign is bilateral prominent papillae, either on the limbus (horners trantas dots) or the upper palpebral conjunctiva (cobblestone papillae). Can also have corneal involvement that begins with punctate keratitis that eventually coalesces into larger erosions, leading to plaque formation and localized ulceration (shield ulcer)
Classic signs of VKC
Cobble stone papillae
Shield ulcer
Horner trantas dots
VKC signs are predominantly in the
Conjunctiva and cornea
The eyelid margin and skin of the outer eyelids is rarely affected
AKC
- no asthma, not seasonal, chronic eczema on face, rubbing lids=Dennie’s lines, small papillae inferiorly
- atopic dermatitis
- type 1 and 4 HS
- bilateral itching of the eyelids (the main symptom). Other common associated symptoms include watery discharge, redness, photophobia, and pain
Signs of AKC
‣ Prominent outer eyelid (scaly, thickened, swollen) and periorbital involvement, including Dennie’s lines (an extra crease under the lower lid due to periorbital edema), and “atopy shiners” (bags under the eyes from constant eye rubbing)
‣ Papillae are classically more prominent inferiorly (as compared to superior papillae in VKC and GPC), although signs may be very mild, causing the inferior conjunctival to appear featureless
‣ Corneal neo, cataracts, and keratoconnus common
‣ Symblepharon formation of the inferior fornices may occur in severe cases and mimic ocular cicatricial pemphigoid
Atopic dermatitis
type of chronic eczema that starts in early infancy (within the first two years of life). 60% of patients are diagnosed within the first year of life. Hallmark signs include pruritis and a rash. An estimated 25-42% of patients with atopic dermatitis have ocular involvement. 10% of patients with severe AD develop a cataract between the ages of 15 and 30
Toxicity to topica;l medication or CL solutions can easily result in an ______ that is characterized by _____
Allergic conjunctivis
Follicular reactions
What conditions get follicles
CHAT Chlamydia Herpes Adenovirus Toxic (molluscum)
Conditions that get papillae
pABillae
- allergies
- bacterial
- non specific inflammation (friction)
GPC
can results from silicone hydrogel CL, exposed sutures, glaucoma filtering blebs, scleral buckles, and ocular prosthetics. Environmental factors are the second most common cause of GPC (severe allergies). Although GPC can occur with any type of CL, it is most commonly associated with extended wear SCL.
‣ Obtain a detailed CL histroy (replacement schedule, cleaning system, recent switch to silicone hydrogel lens?). Risk factors for hydrogel lenses include extended wear, high watyer0ionic lenses, higher modulus of elasticity, and poor replacement compliance.
‣ The average length of time with soft lenses before development of GPC is 8 months, although it may develop as early as 3 weeks depending on the type of lens wearing schedule, etc,
Pathophysiolgoy of GPC
Friction causing inflammation
Symptoms of GPC
itching, scant mucus discharge (early), ropy mucus discharge (late), decreased Cl wearing time, photophobia. Symptoms are often more severe after removing CL
Signs of GPC
mild to severe papillae of the upper (tarsal) conjunctiva and eyelid, ptosis, and mucous throughout the eye and/or on the CL
‣ GPC is characterized by papillae > 0.3mm in diameter. Giant papillae (>1mm) form when neighboring papillae break down septa’s and coalesce together after prolonged inflammation
CL solutions hypersensitivity/toxicity
patients may have very subtle complaints and no signs to very obvious signs and symptom that most commonly occur after a recent switch to a new CL cleaning system. Severe reactions are most often in reasons to solutions containing chlorhexidine or thimerosol, although newer solutions may also cause reactions
• Symptoms: redness and burning upon CL insertion after cleaning, solution change weeks to months prior with chronic redness and discomfort, reduced CL wear time due to dryness or discomfort
• Signs: follicular conjunctivitis, diffuse conjunctival injection, and diffuse SPK
If a previously asymptotic patients complains of increased dryness throughout the day, and no signs or symptoms of dryness are present without the CL,
Remember to ask about a recent change in CL solution
Corneal neo and CL
results from chronic hypoxia; watch for superior pannus. According to the FDA, corneal neo larger than 1.5mm is abnormal and or course; stromal scarring and hemorrhage are uncommon but can occur
Corneal warpage
alteration in corneal shape due to the CL material that is classically seen in long term PMMA wearers o GP wearers with poor fitting CL; in rare cases it can be seen with SCL
‣ Initially, patients often report that vision is clear in CL but blur in classes. They also note ghost images and diplopia
‣ Irregular astigmatism, which can mimic keratoconnus, is evident on topography. A high riding CL classically causes inferior steepening of the cornea over time.
Corneal warpage vs keratoconnus
corneal warpage will not have other corneal findings consistent with keratoconnus and will improve with discontinuing/refitting of the CL
SLK due to CL
CL hypersensitivity or a poor CL fit
‣ Signs include: superior bulbar and upper tarsal conjunctival injection. Papillae reaction and corneal filaments are uncommon, unlike SLK in thyroid disease
Causes of SLK
CL
Thyroid
Dry eye
Contact lens deposits
common in CL abusers who are not replacing lenses on schedule or who are not cleaning their lenses properly.
‣ If deposits are located on ONLY the back surface of the CL, the patient may be digitally cleaning the lenses incorrectly. Re-instruct the patient to use the finger and palm of the hand for digital cleaning
‣ A stronger cleaner or a weekly enzyme cleaner should be considered for diffuse deposits on GP contact lenses
Deposits on HP will be ______ deposits on SCL will be ______
Plaques
Jelly bumps
Tight lens syndrome
occurs when a CL is fitting too tight, resulting in poor movement with the blink (appears stuck on to the cornea)
‣ More common in high myopes (>-8D), CL that are fit too steep, or an abnormally small (<13mm) or large (>15mm) OAD. It is less commonly seen in hyperopes and aphakes
‣ symptoms: redness that worsens after the CL is removed, hazy vision, halos, dryness
‣ Signs: injection or indentation around the limbus and distorted keratometry mires that clear with blinking
• Severe cases may result in mild to severe corneal edema or corneal blebs and an AC reaction
• A corneal abrasion may occur when the CL is removed from the eye
3 and 9 staining with CL
the most common implication associatd with GP CL wear
‣ Classically due to low riding GPCLs that do not adequately cover the cornea, resulting in poor spreading of the tears across he exposed corneaal surfaces
‣ Patients may be asymptomatic or complain of horizontal redness
‣ Chronic 3 and 9 staining may lead to dellen formation, pseudopterygia, and corneal vascularization
Classic complication of a CLthat ride too high is ____ and too low ____
Corneal warpage
3 and 9 staining
SEAL
characterized by an arcuate shape of superior corneal staining within 1mm of the limbus
‣ SEAL most often occurs secondary to tight extended wear hydrogel CL. Loose CL that chafe or contact lenses with poor wettability may also cause SEAL
‣ An estimated 30% of cases are symptomatic. Symptoms include FB sensation, irritation, and corneal subepithelial infiltrates
Dimple veiling
characterized bu small depression within the cornea that pool NaFL. Caused by small gas bubbles that become trapped underneath a CL (most often GCL
Chlamydia-adult inclusion conjunctivitis pathophysiolgoy
adult inclusion conjunctivitis is the ocular manifestation of urogenital disease and is caused by chlamydia serotypes D-K. It is most commonly spread via direct inoculation, although there have been reported cases of tranmission through contaminated swimming pool water or shared cosmetics; ocular manifestation begin appx 5-14 days after inoculation. 54% of men and 74% of women will have an active genital infection
Symptoms of chlamydia conjunctivitis
acute follicular + papillary conjunctivitis that becomes chronic (this prompt patients to seek medical attention); most infections begin unilaterally, but bilateral involvement often develops. The infection can persist for 3-12 months if not treated
Signs of chlamydia conjunctivitis
follicles (limbal or palpebral) AND papillae that are most concentrated in the inferior palpebral conjunctiva and fornices, preauricular lymphadenopathy, scant mucopurulent discharge, and matting of the lids. Corneal involvement occurs in 30-85% of patients and includes punctate keratitis, superior pannus, and subepithelial infiltrates (more peripheral in location compared to EKC)
Leading cause of ophthalmia naonatorum in US
Chlamydia
Trachoma epidemiology
most prevalent between the ages of 1 and 5. Trachoma is the leading cause of preventable blindness worldwide (3rd most common cause of blindness worldwide after cataract and glaucoma). The primary risk factor is living in a community with poor hygiene. Most infections spread directly from eye to eye, but fomites, flies, and shared cosmetics are other routes of transmission
Pathophysiolgoy of trachoma
caused by chlamydia serotypes A-C. Presentation begins in early childhood with a follicular and papillary conjunctivitis of the superior tarsal conjunctiva that ultimately spreads throughout the entire conjunctiva. It is almost always bialteral
Signs and symptoms of trachoma
‣ Early: follicular conjunctivitis predominantly on the superior tarsal conjunctiva, mucopurulent discharge, lymphadenopathy, and mild superior pannus
‣ Late: Artl’s Lines (white scarring of the superior tarsal conjunctiva) and Herbert’s Pits (depression on the limbal conjunctiva after resolution of limbal follicles); progressive tarsal conjunctival scarring can lead to distortion of the eyelids and subsequent corneal ulceration from trichiasis
Things that cause preauricular lymphadenopathy
Gonorrhea Chlamydia EKC Parinauds Phthisis palpebrum
SLK epidemiology
uncommon condition that most often affects females with a mean age dx of 50. History likely to include recurrent episodes
Pathophysiology of SLK
chronic inflammatory reaction most commonly associated with keratoconjunctivitis sicca, thyroid disease, and CL wear. The exact etiology is unknown. SLK is characterized by flare ups and remissions that eventually cease over time
Causes of SLK
‣ Keratoconjunctivitis sicca-drying effect between the upper eyelid and bulbar conjunctiva enhances friction and creates an environment where natural turnover and replacement of mature superior bulbar conjunction cells does not occur
‣ Thyroid disease-may results from continual friction of the superior palpebral conjunctiva against the superior bulbar conjunctiva as a result of tight apposition from exophthalmos
‣ CL wearers and those with tight upper eyelids also have increased friction and thus have an increased risk of SLK
Symptoms of SLK
redness, FB sensation, frequent blinking, no discharge. Symptoms are often worse than the signs; in these cases, instillation of a vital dye (NaFL, rose bengal, lissmine) can reveal prominent staining and pathology that is otherwise difficult to visualize on clinical examination
SLK is best seen with
Lissamine green
Signs of SLK
characterized by thickened, red, superior bulbar conjunctiva that is most prominent at the limbus and is often bilateral, with adjacent SPK and inflamamtory keratitis. The upper tarsal conjunctiva can have a velvety appearance as a result of diffuse papillary hypertrophy
Friction on the cornea leads to
Papillae and filaments
Number one cause of phlyctenules
Staph
Epidemiology of phlyctenules
most common in teenage years with a higher occurrence in females. Ask if the patient has had simialr eye infections in the past and whether he/she has a histroy of TB
Pathophysiolgoy of phylectenules
most commonly a result of type 4 HS reaction to staphylococcus (blepharitis is the most common culprit), tubuerculoprotein, and acne rosacea
Symptoms of phlyctenules
tearing, FB sensation, and itching associated with conjunctival and corneal phylctenulea; significant photophobia is common with corneal phlyctenules
Signs of phlyctenules
phlyctenules can be located on the conjunctiva or cornea
‣ Conjunctival phlyctenules most commonly occur at the limbus and classically appear as pink, fleshy nodules with conjunctival injection
‣ Corneal phlyctenules most commonly occur near the limbus as a small, white (lymphocytic) nodule with adjacent conjunctival injection
When should a PPD test be read
48-72 hours
Ligneous conjucntiis
◦ Epidemiology/Hx: rare, starts during childhood
◦ Pathophysiology/Dx: ocualr manifestations of a systemic disorder; is associated with systemic plasminogen deficiency. May affect mucous membranes throughout the body
◦ Signs: thick, white, “woody” membranous plaques of the superior tarsal conjunctivitis
◦ Symptoms: chronic tearing, FB sensation, photophobia; constant discomfort and cosmetic concerns are typical in advanced disease
Plasmin
derived from plasminogen) catalyze the breakdown of fibrin, which drops unwanted clot formation within healthy vessels throughout the body
Parinaud’s oculoglandular syndrome
◦ Epidemiology/Hx: rare, ask about contact exposure to cats, dogs, rabbits, squirrels, and ticks
◦ Pathophysiology/Dx: common cause include the following
‣ Cat scratch fever (most common cause)-caused by bartonella henselae, which can be transmitted by a cat scratch to the eye or through cat flea bites to the eyes
‣ Tularemia-typically transmitted via ticks, rabbits, and squirrels
‣ TB and syphilis-other noteworthy causes
◦ Symptoms: red eye, FB sensation, mucopurulent discharge
◦ Signs: unilateral, granulomatous, follicular, palpebral conjunctivitis, visibly swollen preauricular/submandibular lymphadenopathy. May also have a fever and rash
Unilateral
Granulomatous
Swollen nodes
Phthiriasis palpebrum
◦ Pathophysiology/Hx: results from phthisis pubis, know as the crab louse, found in the hair follicles of the genital area. Infection of the eyelashes, eyebrows, and facial hair may occur trough direct contact with infected individuals or infected clothing or linen. May be unilateral or bilateral
‣ Differs from demodicosis, a common parasitic mite hair follicle infectio nassociated with blepharitis that classically causes sleeving of the base of the eyelashes
◦ Symptoms: range from mild itching of the eyelids to marked inflammation with resultant burning, itching, tearing, and blurred vision
◦ Signs: transparent lice and white nits (egg sacs) attached to the eyelashes, blood tinged debris on lids and lashes, mild to severe chronic follicular conjunctivitis, and preauricular lymphadenopathy
Subconjunctival hemorrhage
◦ Blood underneath the conjunctiva that typically results from valsalva, medications, hypertension, or a blood clotting disorder
◦ Remember to consider ordering a CBC, PT/PTT, and sickledex for idiopathic and recurrent cases, especially in patients of African or Mediterranean descent
Pterygium/pingeucula
◦ Epidemiology/Hx: associated with environmental exposure and UV radiation; common in individuals who work outdoors
◦ Pathophysiology/Dx: UV exposure (leading cause) and chronic dryness are believed to cause degeneration of collagen fibrils within the conjunctival stroma
◦ Symptoms: range from asymptomatic to irritation, redness, and decreased vision (depending on the location of the pterygium)
◦ Signs: both conditions are typically located at 3 and 9 o’clock
‣ Pingueculum: yellow-white (typically raised) deposit adjacent to the limbus (but not on the cornea)
‣ Pterygium-triangular fibrovascular growth of bulbar conjunctiva that extends onto the cornea, destroying Bowman’s membrane and often leading to WTR astigmatism due to flattening of the horizontal meridian. Stocker’s line (iron deposits) can be present at the anterior (leading edge) of the pterygium
Most common cause of pterygia/pingeula
UV radiation
Pterygium affects what layer
Bowmans
Sign of pterygium
Stockers line
Epicleritis
• epidemiology/Hx: most common in young adults (2nd-4th decade). History of frequent recurrences (60-67%) is common
• pathophysiology/dx: benign, self limiting inflammation of the episclera; often idiopathic, but can be associated with systemic diseases, including the following
◦ Collagen vascular/inflammatory diseases-RA, ulcerative colitis, crohn’s disease, reactive arthritis, ankylosing spondylitis, psoriatic arthritis
◦ Spirochetes- syphillis, Lyme
◦ Viruses- herpes zoster, herpes simplex, mumps
◦ Metabolic diseases- temporal arteritis, Wegner’s granulomatosis, Behcet’s diseases, polyarteritis nodosa
◦ Dermatological diseases- acne rosacea
• Symptoms: acute unilateral red eye, occasional mild pain
• Signs: injection that is typically sectoral (70%). The condition can be simple (80%) or nodular (20%); the nodule can be moves slightly with a cotton tip applicator (unlike scleritis)
What vessels are affected in episcleritis
ACA
Types of scleritis
Necrotizing
Nonnecrotizing
Necrotizing scleritis types
Inflammatory (worst kind) Non inflammtory (scleromalacia perforans)
Types of nonnecrotizing scleritis
Diffuse (#1) and nodular
Who gets scleritis
female predilection (peak incidence in the 4th-6th decades). Scleritis is much less common than episcleritis. Anterior scleritis occurs in 98% of cases (2% of cases are posterior). Anterior scleritis can be divided into non-necrotizing and necrotizing scleritis
Diffuse scleritis
Non necrotizing scleritis
60%): most common type of anterior scleritis and the most benign form of the disease; associated with the least severe systemic conditions. Characterized by diffuse hyperemia.
Nodular scleritis
Non necrotizing
25%): characterized by a deep, focal, painful, injected immobile nodule
Necrotizing scleritis with inflammation
5%): the worst form of scleritis, as 33% of patients may die within a few years as a result of severe AI disease. 40-82% of patients will lose vision; 60% have ocular or systemic complications, including anterior uveitis, scleroising keratitis, peripheral corneal melt, scleral thinning, cataracts, and secondary glaucoma
Necrotizing scleritis without inflammation
scleromalacia perforans) (10%): typically a result of chronic RA. The condition is characterized by almost complete lack of symptoms and minimal injection; asymptomatic, large, gray-blue patches of scleral thinning (due to exposure of the underlying uvea) my be seen
What type of scleritis is assocaited with the most severe ocular signs
Necrotizing scleritis
peripheral cornel melt, sclerosing keratitis, scleral thinning, anterior uveitis, cataracts, and secondary glaucoma
Pathophysiology of scleritis
granulomatous inflammation of the sclera in which 50% of cases are assocaited with an underlying systemic disease; 30% of the cases that result from systemic disease are caused by collagen vascular disease; RA is the most common, followed by Wegner’s granulomatosis.
Symptoms of scleritis
severe, boring ocular pain (hallmark for scleritis) that can radiate to the ipsilateral forehead, brow, or jaw and awaken the patient during the night. Additional symptoms include a gradual onset of redness and a decrease in vision (except for scleromalacia perforans!)
Signs of scleritis
sectoral or diffuse inflammation of the large, deep vessels that cannot be moved with a cordon swab. Edematous or thin sclera with a classic bluish hue under natural light. Signs are frequently bilateral (compared to unilateral signs of episcleritis)
Hyaline plaques
benign, oval shaped areas of scleral thinning that occur with age and allow underlying visibility of the uvea
What is associatd with scleromalacia peroforans
RA
Things that can cause severe pain in the eye
Corneal pathology
Antererio uveitis
Scleritis
Angle closure
Episcleritis vs scleritis
◦ Scleritis is typically gradual in onset, unlike the acute nature of episcleritis, but results in more significant ocular pain and more severe ocular complications
◦ Scleritis often has a characteristic bluish hue under natural light (due to scleral thinning), as compares to the red appearance of episcleritis
◦ 2.5% phenylephrine will result in conjunctival blanching in a patient with episcleritis. It will NOT blanch the deep episcleral vessels (scleritis will remain injected.
◦ Scleritis findings are frequently bilateral and diffuse injection is more common; episcleritis signs are typically unilateral and sectoral injection is more common
◦ Scleritis is much less common than episcleritis and is more commonly associated with an underlying systemic disease
a congenital anomaly characterized by a focal, pigmented, elevated area where the posterior ciliary nerve loops are visible in the sclera; can be painful
Axenfelds Nerve loop
Epidemiology of anterior uveitis
affects 15/100,000 per year; there are 45,000 new cases per year in the US. Anterior uveitis frequently occurs in young adults (peak incidence in the second-fourth decade of life); it rarely locusts in individuals older than 70 (common causes in this age group are toxoplasmosis and herpes zoster)
Blood aqueous barrier
Schlemms
Iris vessels
NPCE
Pathophysiolgoy of anteiror uveitis
uveitis occurs secondary to breakdown in the blood aqueous barrier. 50% of patients with acute anterior uveitis are HLA-B27 positive (70% if the condition recurs). 50% of new onset acute anteiror uveitis cases have an associated spondyloarthropathy; 80% of these patients have anylosing spondylitis
HLA-B27 conditions
UCRAP
Ulcerative Colitis, Crohn’s disease, Reactive arthritis, Ankylosing spondylitis, Psoriatic arthritis
Terminology for anterior uveitis
acute, chronic, or recurrent, and classified by cell type (granulomatous vs non), location (anteiror, intermediate, posterior, pan), and laterality
◦ 75% of uveitis cases are anterior (iritis, iridocyclitis), 8% are intermediate (pars planitis), and 17% of cases are posterior or panuveitis
Acute anteiror uveitis definition
self limiting disease of less than 3 months duration; it may b characterized by recurrent attacks. Chronic uveitis persists for more than 3 months; it may have periods of exacerbation, but nerve fully resolves
Symptoms of anterior uveitis
pain, redness, photophobia, lacrimation, and mildly decreased vision (especially with CME). Patients with chronic anterior uveitis may be asymptomatic or report blurred vision or a dull ache
What is the pain from in anteiror uveitits
congestion and irritation of the anterior ciliary nerves
Grnaulomatous antieror uveitis causes
Sarcoidosis
TB
Nongranulmatous causes of anteiror uveitis
Idiopathic (70%)
UCRAP (30%)
Signs of anterior uveitis
diagnosed based on the presence or absence of white blood cells in the anterior chamber (or elsewhere for other locations of uveitis)
◦ Main threats to vision include posterior synechiae (PS), peripheral anterior synechiae (PAS), CME, and cataract formation (most commonly PSC and assocaited with chronic cases)
◦ Other prominent anterior segment signs include flare, hypopyon, circumlimbal injection of the conjunctival vessels, decreased IOP in the involved eye (in early stages), and keratic precipitates (collection of white blood cells) on the endothelium
‣ Note that although IOP is decreasing during the early stages of uveitis due to ciliary body inflammation, IOP may also be elevated in the later stages from a variety of factors (e.g. the eye getting better, trabeculitis, PS (Leading to acute angle closure), PAS (leading to chroninc angle closure), significant inflammation, topical steroid use, chronic TM damage)
◦ Fine KPs are characteristic of non granulomatous etiology
◦ A granulomatous etiology, in comparison to non granulomatous, is more commonly infectious (TB, syphilis) and chronic in course with an increased predilection for the posterior chamber. Mutton Fat KPs and iris stromal nodules (Koeppe, Bussaca) are highly suggestive of a granulomatous etiol
Cyclitic membranes and uveitis
• Cyclitic membranes may be present in chronic uveitis; they are fibrovascular membranes that extend from ciliary body into the posterior chamber and may involve the lens
Types of KPs
Mutton fat -granulomatous Fine -nongranulomatous (UCRAP) Stellate -herpes and fuches
Koeppe nodules
Collection of WBC located on pupillary margin
Granulomatous and non granuloamtous
BUsacca nodules
WBC on any part of the iris stroma expect the pupillary margin
Most common corneal findgin of antieror uveitis
KPs
Inflammatory bowel disease
usually bilateral with a posterior uveitis component. Characterize by chronic intermittent diarrhea with alternating episodes of constipation. Uveitis is rare in Crohn’s disease, but is more common with ulcerative colitis
Acute non granulomatous anterior uveitits
Reactive arthritis
young makes with urethritis, polayarthritis, and conjunctivitis
Acute anterior non granulomatous uveitiis
Ankylosing spondylitis
more commonly affects males in the 3rd decade. Characterized by lower back pain; symptoms improve with exercise
Acute, anterior non granulomatous uveitis
Psoriatic arthritis
characterized by asymmetric, peripheral, small joint pain and psoriatic lesions on the knees, elbows and scalp
Acute antieror non gran uveitis
Behçet’s disease
most common in young males of middle eastern and Asian descent. Characterized by acute, recurrent hypopyon iritis and mouth and genital ulcers. May also be assocaited with retinal vasculitis, cataracts and glaucoma
Acute anteiror nongran uveitis
Lyme disease
patients may have a history of tick bites, a skin rash, and/or arthritis. Note that Lyme disease may be assoacited with non-granulomatous or granulomatous uveitis
Glaucomatocyclitic crisis
Posner-Schlossman syndrome. Unilateral condition characterized by mild iritis with recurrent, self limiting episodes of elevated IOP (30-40) secondary to trabeculitis, fine KPs, and open angle.
rare to mild cells in the AC, normal corneal sensitivity, absence of a vesicular rash, normal angle anatomy (no NVA or PAS)
Unilateral iritis, increased IOP, trabeculitis
3 major conditions that will present with unilateral cells in the AC with acutely elevated IOP (30-50mmHg)
poster-schlossman syndrome
HSV or HZV trabeculitis
Fuch’s heterochromic idirocyltiis
HSV or HZV trabeculitis
reduced corneal sensitivity, concurrent corneal edema, concurrent dendrite or psuedodendrite, vesicular rash along dermatome that respects vertical midline
Unilateral cells in the AC with acuity elevated IOP
Fuch’s heterocyclic iridocyclitis
Unilateral cells in the AC with acute elevated IOP
rare to mild cells in the AC, normal corneal sensitivity, NVA is often present on gonio, significant iris atrophy and cataracts.
Chronic granulomatous anterior uvetiis mate be assocaited with the following conditions
Sarcoidosis
TB
HSV/HZV
Syphilis
Sarcoidosis and anteiror uveitis
Chronic, granulomatous
-more common in females and AA. Uveitis is typically bilateral and may be posterior or panuveitis. Patients typically have an abnormal chest radiograph and increased ACE (angiotensin converting enzyme) levels.
TB and anteiror uveitis
Chronic granulomatous
positive PPD test, abnormal chest X ray, night sweats. May have posterior or panuveitis.
Number one symptom or TB
Night sweats
HZV and HSV uveitits
Chronic granulomatous OR nongranu
associated with increased IOP in the involved eye. May have stellate KPs, corneal edema, and/or epithelial defects. Zoster will present with vesicles along the affected dermatome
Syphilis and uveitis
Chronic and can be gran or non gran
may have an associated interstitial keratitis. Characterized by a maculopapular rash (on the palms and soles), a positive VDRL or RPR, and a positive FTA-ABS or MHA-TP
‣ Interstitial keratitis is a stromal inflammation without primary involvement of the epithelium or endothelium.
• IK is characterized by acute stromal inflammatory edema and neo. Progression results in diffuse stromal neo that often spares the line of sight
• During the late stages of IK, stroma vessels may partially clear, leading to ghost vessels, corneal scarring, and irregular astigmatism.
stromal inflammation without primary involvement of the epithelium or endothelium.
Interstitial keratitis
• IK is characterized by acute stromal inflammatory edema and neo. Progression results in diffuse stromal neo that often spares the line of sight
• During the late stages of IK, stroma vessels may partially clear, leading to ghost vessels, corneal scarring, and irregular astigmatism.
The most common cause of IK
Congenital syphilis
Acquired syphilis and IK
Not common
Congenital syphilis triad
Hutchinson’s teeth (small widely spaced teeth), deafness, and interstitial keratitis. Additional signs of congenital syphilis include saddle-nose deformity and frontal bossing (prominent forehead)
Chronic non gran anterior uveitis
JIA
Fuchs heterochromic iridocyclitis
JIA and anteiror uvetiits
Chronic non gran
most common known caused of uveitis in chidlren. Classic presentation is a bialteral uveitis in young girls. Patients typically have a negative RF and positive ANA
Fuchs heterochromic iridocyclitis and antieror uveitis
Chronic non gran
more common in patients with blue eyes. Characterized by a unilateral mild uveitis with fine, stellate KPs, angle neo, and iris heterochromia. Assocaited with glaucoma (15%) and cataracts (70%); patients are often asymptomatic
a chronic intermediate uveitis characterized by inflammation over the pars plana (known as snowbanking) and peripheral retina; it is NOT associated with systemic conditions
Pars planitis
Risk factors for corneal infectious keratitis
CL wear, dry eye, exposure keratopathy, neurotrophic keratopathy, trauma, lid abnormalities, and bullous keratopathy
Epidemiology of bacterial keratitis
bacterial keratitis is the most common etiology for infectious keratitis. Cl wear, especially extended wear, is a commmon predisposing factor for bacterial keratitis. Consider bacterial etiolgoy first with any corneal infection associated with Cl wear
‣ The most common microbes invovled are pseudomonas aeruginosa, stap epi, staph aureus, haemophilus influenzae, and moraxella catarrhalis
Pseudomonas and keratitis
Pseudomonas is the most common gram negative pathogen found in severe bacterial keratitis. It is characterized by significant thick mucopurulent discharge (often green in color), hypopyon, and dense stromal infiltrates, and rapid progression )can perforate the cornea within 48 hours)
Pathophysiolgoy of bacterial keratitis
remember that most bacterial rewuire an epithelial defect for invasion and subsequent infectious corneal ulceration. Noteworthy bacterial that can invade an intact corneal epithelium
‣ “Canadian national hockey league”-Crynebacterium, Neisseria gonorrhea and meningitis, Haemophilus influenzae, and Listeria
Bacterial that can invade an intact corneal epithelium
Canadian national hockey league”-Crynebacterium, Neisseria gonorrhea and meningitis, Haemophilus influenzae, and Listeria
Symptoms of bacterial keratitis
severe pain, rede eye, photophobia, and decreased vision
Signs of bacterial keratitis
a corneal stromal infiltrate with and overlying epithelial defect (infectious corneal ulcer
Corneal infiltrate
sign of your body’s immune system attacking an antigen via Ab. An infiltrate without an overlying epithelial defect is an immune mediated repsosne and is NOT a sign of infection
Corneal ulcer
corneal infiltrate with an overlying epithelial defect. Cornal ulcers may be infectious or non infectious. A non infectious (sterile) corneal ulcer may result from a sterile infiltrate that erodes through the corneal epithelium, leading to a small overlying epithelial defect
Infectious corneal ulcers
NaFL staining are to lesion ratio of 1:1. They classically present with moderated to severe pai nwith a mild anterior chamber reaction and diffuse conjunctival injection
Sterile corneal ucler
NaFL staining area to lesion ratio of less than 1:1 with less pain and injection compared to an infectious corneal ulcer. (Staph marginal keratitis)
Sterile infiltrate
NOT stain with NaFL (there is no overlying epithelial defect); they commonly present as multipl leasions with mild pain, sectoral conjunctival injection, and no anteiror chamber reaction
Epidemiology of fungal keratitis
the most common type of corneal ulcer after traumatic corneal injury, especially from vegetable matter.
Pathophysiology of fungal keratitis
‣ 1. Candida infections often occur in eyes with chronic corneal disease or in immunocompromised patients
‣ 2. Aspergillus and Fusarium species are more commonly the culprit after vegetable matter trauma
‣ Culture of fungi should be performed on a Sabaroaud’s agar
What kind of culture is used for a fungal infection
Sabarouds agar
When is candid harmful
Immunocompromised
Signs of fungal keratitis
‣ 1. Aspergillus/Fusraium: classically prestn as an epithelial defect with an underlying gray white corneal infiltrate with feathery edges and possible surrounding satellite infiltrates
‣ 2. Candida classically presents with a similar appearance as a bacterial corneal ulcer
‣ Additional signs include an aC reaction and hypopyon
Epidemiology of acanthamoeba keratitis
rare parasitic infection associated with inadequate CL hygiene
Pathophysiolgoy of acanthamoeba keratitis
acanthamoeba is one of the most common Protozoa found in soil and is also frequently found in water and within the oral cavity of humans. Compromise of the corneal epithelium allows acanthamoeba to invade the corneal epithelium and stromal tissues. Infections progresses slowly and are often misdiagnosed early in management. Culture should be performed with a non nutrient agar with heat killed E. coli.
Signs of acanthamoeba keratitis
‣ Early=punctate or pseudoendritic epithelial defects (may be confuse with HSV) associated with severe pain out of proportion to the signs
‣ Late=radial keratoneuritis(inflammation of the corneal nerves) and patchy anterior stromal infiltrates that progress to ring ulcer
Gram stain
Bacterial
KOH or Giemsa
Fungi and yeasts
Sabarouds
Fungi
Chocolate agar
Haemophilus and N gonorrhea
Thioglycate
Aerobic and anaerobic bacteria
Non nuretient agar with E. coli
Acanthamoeba
Epidemiology of HSV
DNA virus that is mot common in young patients. Ask about previous history of cold sores
Primary exposure of herpes simplex
occurs in young kids age 6m to 5 years. Patients are mot commonly asymptomatic but they may experience mild virus-type symptoms
Recurrent HSV infections
resutls from reactivation of a latent infection in the trigeminal ganglion. Can be triggered by physical or emotional stress from sun exposure, fever, and immunosuppression
Pathophysiology of HSV
tissue damage in HSV occurs either by direct invasion from the virus, neurotrophic mechanisms, or by immune system repsosne to HSV
Symptoms of HSV keratitis
decreased corneal sensitivity is common in these patient
Primary exposure of HSV reuslts in
‣ 1. Blepharitis-focal vesicular lesions with crusting located not he eyelids and periorbital area (usually UL if dendrite is present)
‣ 2. Conjunctivitis-acute unilateral follicular conjunctivitis with watery discharge and preauricular lymphadenopathy
Recurrent HSV infections reuslts in
Epithelial disease
Neurotrophic keratitis
Stromal disease
Endotheliitis
Epithelial disease from HSV
• Includes corneal vesicles, dendritic ulcers, geographic ulcers, and marginal uclers. Due to direct invasion of the corneal epithelial cells by HSV
◦ Corneal vesicles-small epithelial lesions often referred to as punctate epithelial keratopathy. Represent the earliest epithelial sign of reactive HSV
◦ Dendritic ulcers-most common presentation of HSV keratitis. The edges of the HSV dendrite (active viral cells) stain well with rose bengal; the center of the ulceration stains well with NaFL
◦ Geographic ulcers: similar to a dendritic ucler but wider in appearance; assocaited with previous use of topical steroids
◦ Marginal ulcers: located close to the limbus; presents as a stromal infiltrate with an overlying epithelial defect and assocaited limbal injection
Neurotrophic keratitis from HSV
• Reuslts from reduced corneal innervation (V1) and decreased tear secretion, leading to poor wound healing (big ulcer, no pain)
◦ Occurs in patients who have had infectious epithelial keratitis; unique because etiolgoy is not immune mediated or infectious
◦ A neurotrophic ucler appears as an oval defect with smooth borders, it is often preceded by punctate epithelial erosions that then progress to form an ulcer
Appearance of neurotrophic keratitis
Neurotrophic ulcers are typically inferior in location and oval in appearance with smooth borders, geographic ulcers result in irregular epithelial defects with scalloped borders
Stromal disease (interstitial K) from HSV
Accounts for only 2% of initial epidoses of ocular HSV disease but 20-40% of recurrent ocular HSV disease. There are several types of stromal disease in HSV keratitis
◦ Interstitial keratitis (IK)-characterized by an infiltrate with diffuse neo, an immune rings (Wesley ring), stromal thinning, and subsequent scarring
‣ In herpetic disease, IK is thought to result from an Ag-Ab complement cascade against a live virus or viral antigen retained within the corneal stroma
‣ By definition, IK I stromal inflammation without primary injury to the epithelium or endothelium
◦ Necrotizing stromal keratitis-rare keratitis that results from direct virus invasion into the stroma. Results in severe stromal inflammation with necrosis that can lead to corneal thinning and perforation
Why is HSV interstitial keratitis concerning
it may lead to significant stromal scarring and decreased acuity
Endotheliitis from HSV
Secondary stromal edema due to an immune reaction against a viral antigen or live circus within the corneal endothelium
◦ Disciform endotheliitis-most common form of endotheliitis. Characterized by focal, disc shaped, sotrmal edema overlying KPs. Often accompanied by a mild to moderate iritis.
Differnece between IK and endotheliitis
stromal infiltrates and neo are not present in disciform endotheliitis
Additional findings in HSV K
Acute unilateral anterior granulomatous uveitis
Trabeculitis (unilateral mild to no cells in the AC with acutely elevated IOP and often concurrent corneal edema
Acute retinal necrosis
Epidemiology of HZV
varicella zoster virus (VZV) is the initial invading organism, affecting 95% of children by the age of5 in the US. After the primary infection (chickenpox), VZV is transported to the trigeminal ganglia and other neural cell bodies, where it becomes dormant. Older age, trauma, neurodegeneration, or immunosupression may contribute to reactivation of the virus and resulting herpes zoster infection
Who gets HZV most
‣ HZV primarily affects the elderly and is rarei n kids to young patients. If HZV occurs in patients younger than 50, consider a medical eval to determine if the patient is immunocompromised. HZV is contagious for those who have not had chickenpox
Signs of HZV
vary depending on invovlemt of the cornea. Symptoms are more severe in immunocompromised patients. HZV is unilateral and follows the affected dermatomes
Pre zoster
cluster of warning signs known as prodrome
Active zoster
vesicular rash that respects the dermatomes and does not cross the midline. Vesicles can form on the lid margin, resulting in blepharoconjunctivitis
HZO
◦ Activation along the ophthalmic branch of the trigminal ganglion leads to ophthalmic manifestations and is referred to as herpes zoster ophthalmicus
Eyelid signs of HZO
- Trichiasis
* Ectropion
* Entropion
* Madarosis
* Poliosis
Corneal signs of HZO
occur in 65% of patients with acute HZO and include • Punctate epithelial keratitis • Pseudodendritis keratitis • Anterior stromal keratitis • Interstial keratitis • Endotheliitis • Keratouveitis • Neurotrophic keratitis • Exposure keratopathy
How does HZV start on the cornea
begins with small, stellate lesions that can progress to pseudodenrites (tapered ends with no terminal bulbs) with a “stuck on” appearance. The entire lesion stains with rose bengal (compared to just the edges in HSV) HZV lesions DO NOT stain well with NaFL (unlike HSV)
Other eye findgins in HZO
‣ Episcleritis/scleritis
‣ Uveitis occurs in up to 40% of patients with acute HZO
• Can be granulomatous or non and typically assocaited with significant KPs, corneal edema, and PS
‣ Trabeculitis (acutely elevated IOP with minimal to no cells in the AC and likely corneal edema)
‣ Cataracts
‣ Acute retinal necrosis
‣ Optic neuritis
‣ Cranial nerve palsies
Hutchinson’s sign
• Hutchinson’s sign is a rash on the tip of the nose as a result of reactivation of the virus along the terminal branch of the nasocilairy nerve (V1). It indicates a high risk of ocualr involvement
Post zoster
characterized by PHN and depression
‣ PHN-defined as pain persisting beyond 1 month after rays onset or rays resolution. Most common complication of herpes zoster and affects 10-30% of patients
‣ Severe PHN affects about 7% of patients. The leading cause of suicide in patients over 70 years of age with chronic pain
Epidmiolgoy of mooren’s ucler
rare condition that is more common in men and older patients (40-70, although may occur at all ages). The classification of mooren’s ulcer
‣ 1. Benign (typical or limited) mooren’s ucler (75%)-unilateral, affects the elderly, mild to moderate symptoms, responds well to treatment
- 2. Malignant (atypical) Mooren’s ulcer-bilateral, affects younger patients (especially black males), severe symptoms, responds poorly to treatment, and progresses relentlessly
Pathophysiology of mooren’s ulcer
painful, progressive, chronic vasculitis of the limbal blood vessels that leads to ischemic necrosis and peripheral ulcerative keratitis
‣ Mooren’s ulcer is idiopathic in nature, but is likely autoimmune mediation. By definition, the condition occurs idendpent of any diagnosable systemic disorder that could be responsible for the progressive corneal pathology
‣ Associatd with systemic hepatitis C viral infection or hookworm infestation
Symptoms of mooren’s ulcer
the most common symptoms is pain, which is often severe. Additional symptoms include redness, tearing, and photophobia. Decreased vision can result from irregular astigmatism, associated iritis, or if the ucler is central in location
Signs of mooren’s ucler
the classic presentation is an unilateral peripheral crescent shaped gray infiltrate in an older patients that progresses to an ulcer. The ulcer is concentric to the limbus and has a unique overhanging edge. The ulceration may be self limiting Ir may spread circumferentially and/or centrally in the late stages of the condition
Epidemiology of staph marginal keratitis
Most common PUK
common condition. Ask about a similar recurrent acute episode
Pathophysiolgoy of staph marginal keratitis
type III HS response to staph aureus; typically occurs in patients with chonric staph blepharitis. Recurrences are common unless the underlying blepharitis is treated appropriately
Symptoms of staph marginal keratitis
patients may be asymptomatic or complain of acute photophobia, pain, tearing, redness, and decreased visio
Signs of staph marginal keratiits
corneal stromal infiltrates (usually multiple and bilateral) located in the periphery; classically occur at 2, 4, 8, and 10 o’clock positions where the lid margin makes contact with the limbus. Look for assoacited phlyctenules, signs of bleph, and/or acne rosacea. Residual thinning, superficial neo, and peripheral scarring are common
What is a corneal infiltrate
infiltrate is a sign of your patients immune system attacking the staph antigens via antibodies. In isolation, it is an immune mediated repsosne and not a sign of an infectio
Collagen vascular disorders (PUK)
◦ Recall that collagen vascular disorders such as RA, SLE, polyartertiis nodosa, and Wegner’s granulomatosis can cause peripheral corneal thinning and/or uclers
◦ Patients can be asymptomatic or may report significant pain, redness, and decrease in vision
◦ Corneal findings include peripheral corneal thinning/uclers with or without inflammation. The condition may be unilateral or bilateral. The uclers may progress to encompass the entire peripheral cornea. Corneal findings may be associated with scleritis, episcleritis, and keratoconjunctivitis sicca
Appearance of corneal deposits
may be pigmented, refractile, metallic, or non pigmented in color. They can occur within any layer of the cornea, from the surface epithelium to Descemets membrane
Whork K causes
seen in Fabry’s disease and with the use of chloroquine, hydroxychloroquine, amidoarone, indomethacin, tamoxifen
Fleischers ring cause
iron ring in the base of the cone in keratoconnus
Rust ring causes
Metallic FB
Hudson Stahli line
common in the elderly, iron deposits found at the junction between the middle and lower third of the cornea
Stocker’s lines
iron deposits on the leading edge of a filtering bleb
Kaiser Fleischer ring cause
accumulation of copper that occurs in patients with certain liver disorders, Wilson’s disease
Band keratophy cause
calcium deposits within Bowmans layer
Types of corneal degenerations
Terriens marginal degeneration Salzmanns nodular degeneration White limbal girdle of Vogt Band keratopathy Arcus senilis Crocodile shagreen Corneal farinata
Terriens marginal degeneration
Superior nasal thinning ATR Bilateral 30 yo male idiopathic non-inflammtory degeneration that reuslts in slowly progressive peripheral stromal thinning. Perforation occurs in appx 15% of cases
Symptoms of terriens
often asymptomatic, although progressing can lead to irregular astigmatism (classically ATR) and decreased acuity
Signs of terriens
characterized by superonasal, bilateral (asymmetric), slowly progressive peripheral thinning with an associated vascularized pannus. In most cases, there is no AC reaction, no conjunctival injection, and no overlying epithelial defects
Difference between mooren’s ucler and terriens
Mooren’s has an overlying epithelial defect and terriens does not
Salzmanns nodular degeneration
60 yo female Really bad dry eyes Blue gray nodules Bowmans Hyaline
Symptoms of salzmanns nodular
typically asymptomatic, although patients may experience pain if RCE develop in epithelial cells overlying the nodule; vision may be reduced if the nodule is located within the visual axis
Signs of salzmanns nodular
hyaline plaque deposits located between the epithelium and bowmans membrane that classically appear as midperoheral, elevated blur gray or yellow white nodular lesions. May be unilateral or bilateral and single or multiple in number. Nodules are often located within or adjacent to an old corneal scar or corneal pannus
White limbal girdle of Vogt
Older patients (common)
Bilateral chalk like linear opacities of nasal limbus
Asymptomatic
Base keratopathy pathophtysiolgoy
reuslts from the following
‣ Ocular conditions that cause chronic inflammation and ocular surface disease
‣ After trauma
‣ Systemic conditions that cause increased serum Ca++ or phosphorous levels, including gout, hypercalcemia, sarcoidosis, and renal failure
Symptoms of band keratopathy
patients are often asymptomatic because the calcium plaques are usually located in the periphery at 3 and 9 o’clock positions. Although uncommon, the plaques may move centrally and cause a FB sensation and decreased vision
Sign of band keratopty
calcium deposits on the anterior surface of Bowmans membrane or in the sub-epithelial space that appear as white splits with a Swiss cheese pattern; usually concentrated with in the intrapalpebral region of the cornea
Arcus senilis epidemiology
most common peripheral corneal opacity. Arcus is prominent in the elderly and affects almost 100% if patients over the age of 80. Higher incidence in males and AA
Pathophysiolgoy of arcus senilis
associated with aging and high cholesterol. Lipid deposition begins on descemets membrane and is subsequently deposited on bowmans layer before extending into the stroma
Signs of arcus senilis
usually bialteral and symmetric circumferential 1mm band within the peripheral cornea, with a clean zone of separation to the limbus
When is arcus concerning
‣ Arcus is typically of little concern, unless
• Unilateral arcus is rare and is assocaited with carotid disease on the side without the arcus
• Arcus in patients younger than 50 is assocaited with an increased risk of coronary artery disease; a lipid profile is warranted in these cases
Crocodile shagreen
bilateral, gray white, polygonal stromal opacities (Cracked ice) either near bowmans layer (anterior crocodile shagreen) or occasionally near descemets membrane (posterior crocodile shagreen). Opacities are caused by irregularly arranged folds of collagen
◦ Symptoms: usually asymptomatic and benign
Corneal farinata
◦ Bilateral flour dust deposits that are most commonly located in the central deep stroma. May be due to aging or an AD condition. Patients are typically asymptomatic
Corneal graft rejection
• type 4 HS reaction to the donor cornea. 30% of patients will have rejection within one year. Characterized by decreased vision, mild pain, redness, and photophobia
◦ Epithelial rejection: rare; appears as an elevated, irregualr epithelium
◦ Stromal rejection-assocaited with subepithelial infiltrates known as Krachmer’s spots
◦ Endothelial rejection line-characterized by WBCs on the endothelium that form a Khodadoust line
an elective procedure that modifies the refractive status of the eye by lenticular or corneal modifications.
Refractive surgery
Absolute contraindications for refractive surgery
‣ Younger than 18 with an unstable refractive error within the last year
‣ Unrealistic expectations-will reduce dependence on glasses (but NOT glasses free), will experience post op glare and dryness
‣ Keratoconnus, active herpes simplex keratitis, contact lens warpage
‣ Connective tissue disease, collagen vascular disease, immunocompromised disease
Relative contraindications for refractive surgery
‣ Blepharitis, DED, chronic eye rubbing, ocular surface disease, large pupils
‣ DM-fluctuating blood sugar levels can change the refractive error, which makes the amount of treatment needed unclear
‣ POAG (if not well controlled)-IOP elevates during placement of the suction cup during surgery, which could be dangerous if a patient already has uncontrolled or advanced glaucoma
‣ Pregnancy
‣ Retinal thinning/lattice degeneration May increase the risk of retinal tears during or after surgery. Although a clear link has not been establishes, caution should be taken
How long do spherical SCL wearers need to be out of CL before refractive surgery
3-14 days
How long do toric and RGP lens wearers need to be out of their CL before their refractive surgery
14-21 days
Radial keratotomy
- radial incisions are made with a diamond knife it flatten the perierhal corneal stroma; the normal IOP then pushes the weakened peripheral cornea outward, causing the central cornea to flatten to reduce myopia
- No longer performed due to better options. RK was difficult to titrate, caused significant instability in the refractive error, and led to progressive hyperopic shifts
PRK
- the corneal epithelium, Bowmans, and superficial stromal tissue are removed (no flap) and excimer laser is applied directly to the central cornea (for myopia) or mid periphery (steepens the cnetral cornea to correct for hyperopia)
- Treatment range: -8D to +4D, up to 4D of astigmatism
- 400um residual cornea is required after treatment
- PRK requires longer healing time (1-2 weeks) compared to LASIK because the entire corneal epithelium must regrow. Patients will experience extremely poor vision and pain (controlled with NSAIDs and BLC) in the immediate post op period
- The risk of stromal haze is greatest with higher Rxes and can be reduced by using MMC during the procedure
Benefits of PRK
◦ PRK is ideal for patients who are at risk of trauma because there is no risk of flap complications. PRK is also associated with less risk for corneal ectasia, less induction of higher order aberrationsm les post op dryness, requires less corneal thickness, and is cheaper compared to LASIK
LASIK
- an epithelial flap is made with a micokeratome, an excimer laser is applied to the anterior stromal bed, and the flap is then reattached
- Treatment range: -10D to +4D, up to 5D of cyl. Clear lens extraction can be performed on patients who exceed LASIK refractive error requirements
- LASIK patients heal faster (1-2 days), experience less pain, and have less post op corneal haze compared to PRK patients
Thickness requirements for LASIK
◦ 250um must remain under the flap to maintain a corneal integrity
◦ The flap itself is approximately 150um thick (determined by intraoperative pachymetry)
◦ Ablation depth is appx 12 um/Diopter
Total pachymetry for LASIK
‣ Total pachymetry minus the flap thickness (160-200um) minus the ablation depth (15um/diopter) should be at least 250um
Femtosecond laserflap for LASIK
the same procedure as LASIK but the flap is made with a femtosecond laser instead of a micorkeratome. A femtosecond laser flap is thinner, leaving behind more tissue to ablate. It also removes the risk of mechanical malfunction of the microekratome and is assoacited with less post op dry eye
LASEK
same procedure as LASIK, but the flap is made with dilute alcohol instead of a microkeratoma
Epi-LASIK
this is another version of LASIK where a blunt plastic blade is used to create the epithelial flap rather than a microkeratome
Conductive keratoplasty
- used to treat presbyopia, low hyperopia, and for treating residual astigmatism after previous surgeries
- Uses radio frequency energy to shrink the collagen fibers in the peripheral corneal stroma, allowing the central cornea to steepen. Regression is expected after about 2-3 years; the surgery can be repeated
- Treatment range: +0.74D-+3D with less than 0.75D cyl
Intratromal corneal rings
- PMMA rings are inserted into the peripheral stroma to flatten the cornea (shortens the corneal arc length); rings can be removed or exchanged
- Approved fro use with keratoconus
- Treatment range: -0.75D to -3D; does not treat hyperopia
Clear lens extraction
- essentially cataract surgery without a cataract. The IOL that is selected reduces the refractive error
- No residual accommodation remains unlesss a multifocal or accommodating IOL is used
- Large treatment range
Phakic IOL (implantable CL)
- intraocular lens implantation in a phakic eye. The lens implanted to alter the total power of the eye
- The IOL is angle supported, iris supported, or sulcus supported. Rewuire a peripheral iridotomy
- Can be used to treat a larger range of refractive errors compared to corneal surgery and the IOL is removable. Also preserves natural accommodation (unlike clear lens extraction)
Astigmatic keratotomy (AK)
• corneal incisions are made with a diamond blade to relax the cornea in the steepest meridian
Wavefront guided, custom corneal surgery
- reduces higher order aberrations in addition to correcting the refractive error.
- Can be done with LASIK or PRK and theoretically resutls in better quality vision with improved contrast and acuity and less glare
Refractive surgery success
In refractive surgery, success is generally considered 20/40 VA or better. In those with low refractive error, about 90-99% achieve this level. About 75% achieve 20/25 or better
Potential LASIK complications
- Pain in the first 24 hours
- Serious infection
- Flap complications
- Corneal ectasia
- Residual refractive error
- Glare
- Dry eye
- DLK
- Epithelial ingrowths
- . corneal haze
Serious infection after LASIK
◦ Typically occurs day 1-3. Can lead to corneal melting, irregular astigmatism, and scarring
◦ Bacteria are usually gram + or mycobacterium
◦ Risk with PRK=1/1000 to 1/35000
◦ Risk with LASIK=1/5000
Flap complications from LASIK
Free caps, button holes, flap folds, irregualr flaps, corneal perforation, and flap subluxation
Flap displacement is more common with keratome flaps than with femtosecond laser flaps and is usually due to accidental touch to the eye or eyelid. Dislodged flaps can be repositioned
Types of flap complications after LASIK
‣ Button holes (cap perforation, a hole in the flap) are more common with very steep corneas or deep et eyes. The steep cornea can buckle in the suction ring, causing a hole as the keratome moves across the cornea
‣ Free caps (no hinge made) are more common with very flat corneas and are the result of an inadequate amount of cornea in the ring, causing the blade to cut off the hinge
‣ Flap folds occurs in 56% of cases at day 1 (usually within the first hour), and 95% of cases within 1 week
Microstriae and macrostriae flap folds after LASIK
- Flap folds are called macrostriae if they are full thickness with undulating, parallel stromal folds; they result from slippage or malpositioning during surgery. They typically require treatment of the flap by lifting and reposition
- Microstriae are fine, irregular, multi0directional folds in bowmans layer that typically resolve on their own; they are treated only if they are visual significant
Corneal ectasia after LASIK
◦ Anteiror protrusion of the cornea due to thinning. Patients with high myopia, undetected keratonnus, or forme fruste keratoconnus are more at risk. Corneal ectasia may occur at any time following the surgery
Residual refractive error after LASIK
◦ Patients may be over or under-corrected or may have regression after surgery (more common if >8D)
◦ Patients can be fit with GPS or reverse geometry lenses after appx 8-12 weeks. Refractive surgery enhancement may also be considered
Glare after LASIK
◦ Worse glare is expected with small ablation zones, large pupils, monovision correction, and higher refractive errors
Dry eye after LASIK
◦ The most common side effect of LASIK; occurs in up to 33% of all refractive surgery patients
‣ Corneal nerves are severed during LASIK, resulting in decrease in corneal sensitivity resulting in decreased neural feedback to the lacrimal gland. Resolves 1-2 months
DLK after LASIK
rare, inflammtory non infectious reaction that occurs at the lamellar interface (between the corneal flap and stroma). It is characterized by fine, granular, sand like infiltrate that typically presents within 2-3 days after surgery. The etiology is poorly understood, but may be a response to toxins (glad debris). DLK is less common with dispoasalbe microkeratomes
maybe be asymptomatic or experience photophobia, blurred vision, FB sensation, and pain. Can lead to vision loss (from corneal scarring and corneal melt) if not properly managed
Epithelial ingrowths after LASIK
Rare, less than 3% of surgical cases
‣ Last pos op LASIK complication that is most commonly observed at the one month post op visit as a faint gray line or white, milky despots within 2mm of the flap edge interface
‣ The pattens is typically asymptomatic and the condition is not treated unless progression is documented, the visual axis is obstructed, greater than 2mm of ingrowth occurs from the flap edge, or resutls in corneal astigmatism
Most common complication associated with LASIK enhancement
Epithelial ingrowths
Corneal haze after LASIK
◦ The prevalence of lone term haze with LASIK is 0.1% and with PRK is 1% in those with refractive errors below 6D. The risk increases with higher refractive errors
◦ Remember, corneal haze is normally present for severeal weeks after PRK
Retreatment criteria for enhancement in refractive surgery
◦ The earliest time for retreatment is 3 months, but 6 months is preferred to allow the refractive error to stabilize. Criteria for enhancement include the following
‣ Astigmatism >0.75D causing symptoms
‣ RE> or equal to 0.75D from target in an unhappy patient
‣ Uncorrected VA of 20/30 or worse in an unhappy patient
Long term management of LASIK
◦ IOP realigns will always be falsely low due to thin corneas
◦ Gonio and retinal evals are still necessary in patients with a history of high hyperopia and myopia, respectively
◦ Patients should wear eye protection during contact sports to avoid dislodging the corneal flap and to block UV radiation
AOA definition of cataract
opacification of the lens that leads to measurably decreased VA and/or some functional disability as perceived by the patient. An estimated 20.5 million Americans older than 40 have them
Nuclear sclerosis
most common aging cataract. Typically causes myopic shift, elderly patients often report “second sight” because of thei improved abiltiy to read without spectacles
Cortical cataract
radial spoke like opacities that commonly induce a hyperopic shift
Anteiror subcapsular cataracts
located directly underneath the anterior lens capsule
Posterior subcapsular cataracts
located directly in front of the posterior lens capsule; often affects near vision more than distance vision and is commonly a result of systemic or topical steroids and X rays.
Mild PSC
can cause significant reduction in acuity and are typically associated with worse glare compared to other cataracts
Infant cataracts
associated with galactosemia and rubella. The most common type of congenital or infantile cataract is a lamellar (zonular) cataract that consist of a lens opacity that surrounds the embryonic nucleus
Cerulean cataract
type of congenital cataract that rarely affects VA. It appears as tiny dot like or flake like white or bluish green opacities
Presenile cataracts
assoacited with DM, myotonic dystrophy (PSC Christmas tree), Wilson’s disease, hypocalcemia, and atopic dermatitis
Traumatic cataract
rosette cataracts, also look for a Vossius ring
Toxic anterior subcapsular cataract
chlorpromazine (stellate cataract), amiodarone (deposits), miotics (vacuoles), and gold salts (gold deposits)
Toxic posterior subcapsular cataract
Corticosteroids
Secondary cataract
common causes include chronic anterior uveitis (most common), high myopia, retinitis pigmentosa, and gyrate atrophy
Epicapsular stars
‣ Residual remnants of the tunica vasculopathy lentos and appear as small, star shaped, pigmented deposits on the anterior capsule of the lens
Testing for catracts
PAM
BAT
A scan
B scan
PAM
can help determine how much the lenticular changes are impacting acuity in order to better predict post op VA
BAT
asses glare disability
Axial length for catracts
A scan or IOL master; axial length and keratometry measurements are used to calculate the appropriate IOL power based on the desired final refractive error
B scan and cataracts
helps to determine if posterior segment abnormalities are present when cataracts are so dense that the fundus cannot be viewed
Axial length and IOL power
‣ The average axial length us 24mm; a 1mm error in axial length measurement corresponds to a 3D error in the calculated IOL power
If the cataract is monocular
before referring for surgery consider the age of the patient’s and whether lens removal would impact accommodation status and post op refraction
If the patient is monocular, before cataract surgery
consider the severity of the cataract and discuss the risk/benefit ratio with the patient’s
Preop by PCP before catract surgery
◦ Each patient’s should have a careful preop eval by their medical doctor prior ro cataract surgery; medications should also be reviewed carefully-anticoagulants, A blockers, and PGs are of particular concern
Alpha blockers for BPH and cataract surgery
‣ Flomax is an alpha blocker that can cause floppy iris syndrome, which is characterized by poor preop pupil dilation, iris billowing and prolapse, and progressive intraoperative miosis. This occurs in up to 90% of pateitns who are currently on the medication or have been at any time in the past
Ocular conditions to consider before cat sx
◦ Ocular conditions should be considered prior to referral, including history of acute or chronic uveitis, severe bleph, Fuchs endothelial dystrophy, and pseudoexfoliation
Types of cataract surgeries
intracapsular cataract extraction (ICCE)
Extracapsular cataract extraction (ECCE)
Phacoemulsifcation
Femtosecond laser
Intracapsular cataract extraction (ICCE)
◦ the entire lens and capsule is removed, requiring large incision
◦ Resulted in aphakia and the need for cataract glasses (+12D) with caused distortion of images, secondary IOLs could be implanted with a second surgery
◦ ICCE was associated with a higher risk of RD. It also required a surgical peripheral iridotomy to prevent vitreous prolapse and pupillary block
◦ This surgery has been replaced by newer and safer techniques
◦ ICCE=ICE age, not done anymore
Extracapsular cataract extraction (ECCE)
◦ The lens is removed by the lens capsule remains. The incision must still be large because the lens is removed as a while. An IOL is typically inserted into the capsule
Phcaoemulsification
◦ A form of ECCE where the lens is fragmented with ultrasound before removal. Allows for a much smaller incision that rarely requires sutures, as the aqueous will push against the corneal flap to close it
◦ Typical utilizes a clean cornal incision for lens removal
Femtosecond laser for cataract surgery
◦ A fairly new addition to the traditional cataract surgery performed by some surgeons. It is used for corneal incisions, anterior capsulorhexis, and lens fragmentation
Types of IOLs
Toric (4D), aspheric, multifocal/bifocal, accommodating, monovision
Design of IOLS
Foldable, rigid, injectable
Placement of IOLS
AC, iris fixed, ciliary sulcus fixed, scleral fixed, or in the capsular bag (most common
Post op complications (cat surgery)
Striate keratopathy Acute post op endophthlmitis Delayed post op endophthalmitis Toxic anterior seg syndrome Lens subluxation PCO CME RD Wound leak Suprachoroidal hemorrhage Elevated IOP Corneal edema Diplopia Ptosis UGH syndrome Induced cornea astigmatism Iritis
Striate keratopathy after cataract surgery
post op corneal edema and folds in descemets membrane; typically resolves without treatment within days
Acute post op endophthalmitis: cataract surgery
rare complication that occurs in 1/1000 cases; however, even with early treatemnt, 50% of eyes become blind
‣ Stmptoms occur within days (2-4) of the procedure and include progressively decreased vision, redness, and increasing eye pain
‣ 70% of cases are gram + bacteria, including staph epi and staph aureus. The normal bacterial flora from the eyelids and conjunctiva are the most likely sources of infection
‣ Signs include a significant AC reaction that can be accompanied by hypopyon, vitritis, chemosis, eyelid edema, fibrous exudate, mucous discharge, corneal edema, and reduced red reflex
Delayed post op endophthalmitis: catract
symptoms occur within a week to one month after the procedure. Vision loss is insidious and pain gradually worsens. Fungal post op endophthalmitis is also commonly a delayed complication
Toxic anterior segment syndrome (TASS)
sterile inflammtory reaction that leads to toxic damage to the AC structures. Typically a result of chemical exposure during surgery
‣ Typically presents 12-48 hours pos op with decreased vision, no to mild pain, diffuse limbus corneal edema, hypopyon, fibrous membrane, no vitritis, and increased IOP
‣ MUST rule out infectious endophthalmitis
Lens subluxation after cataract surgery
rare in cataract surgery. Caused by pupillary capture and poor capsular support, findings are common common in PXF or Marfans syndrome
‣ Trauma is the number one cause of lens subluxation
‣ Systemic conditions that cause lens subluxation include: Marfans, Ehlers-Danlos, Weill-Marchesani syndrome, and homocystinuria
Difference between OI and ehlers danlos
• Ehlers Danlos and OI cause similar effects including keratoconus, blue sclera, megalocornea; ehlers danols differs in that it can also cause lens subluxation. In marfans, RDs are common and are the most serious ocular complication
PCO after cataract
the most common post op complication following cataract surgery. Also referred to as a secondary cataract
‣ Equatorial epithelial cells migrate to and proliferate over the posterior capsule, resulting in opacification most commonly within 2-6 months after surgery
‣ Elschnig Pearls are a type of PCA that is most common in children who undergo cataract extraction
Most common post op complication from cataract surgery
PCO
CME after catract surgery
one of the most common reasons for decreases acuity after cataract surgery. The surgical trauma results in inflammation; with the disruption of the lens/vitreous interface, inflammatory cells have an easier time getting to the posterior pole to cause inflammation
‣ The most common cause of CME is post cataract surgery (Irvine Gas’s syndrome). Remember that CME develops within the OPL (Henles)
‣ Peak incidence is within 6-10 weeks following cataract surgery. CME is common on FA but only about 1.5% of patients have significant and symptomatic CME with modern surgical procedures. FA will show hyperfluroescent leakage within the macula (petaloid pattern) and around the ON
‣ Most cases resolve with treatemtn around 6 months
When can CME occur
after intraocular surgery or in DR, retinal vein occlusion, uveitits, RP, ARMD, ERM, retinal vasculitis, and Coat’s
Wound leak after cataract surger
occurs early in the post op period and may be initiated by valsalva maneuver, trauma, or suture failure
‣ Signs include a positive Seidel signs, hypotony, iris prolapse (will point towards the wound), choroidal detachement (fluid accumualtes in the suprachorodial space) and a shallow AC
‣ Patients with an open wound are at risk for endophthalmitis and should be promptly treated
Suprachoroidal hemorrhage after cataract surgery
Super chorodial hemorrhage: rare complication characterized by the accumulation of blood between the choroid and sclera during surgery. This is a devastating complication that is mroe common in the elderly and has an unknown etiolgoy
Elevated IOP after cataract surgery
make be caused by retained viscoelastic, steroid response, inflammtory debris or RBC clogging the TM, pupillary block, or retinae lens material
Corneal edema after cataract surgery
typically an early complication characterized by folds in Descemets membrane, bullae, and/or Microcysts that slowly resolve. Potential causes
‣ High IOP-can cause microsystic edema
‣ Low IOP- can cause descemets folds
‣ Surgical trauma-causes edema due to the shock waves from phacoemulsification. This is less common with the intraoperative use of viscoelastic material
‣ Pre-existing corneal Disease predisposes patients to corneal edema
‣ Bullous keratopathy (occurs later in life in the post op period) is more common in aphakia and with AC IOLs
‣ Haptic rubbing on the endothelium can cause damage and edema
Ptosis after cataract
permanent ptosis can be due to levator dishiscence by the lid speculum. A temporary ptosis may be due to spot op swelling or use of local anesthetic
UGH syndrome
Uveitits, glaucoma, hyphema Syndrome (UGH): most likely due to an ill fitting AC IOL that rubs the Iris, causing hyphema and uveitis. The accumulation of RBC in the TM causes an elevated IOP. Very uncommon complication now that AC-IOLs are less commonly used
Iritis after catraact surgery
secondary to surgical trauma, retained lens material (will appear as fluffy, white material behind the iris), endophthalmitis, or occurs in an eye that is predisposed to uveitis and is then aggravated again by surgery
