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
