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Strabismus

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

• deviation (misalignment) of one eye from the other when the person is looking at an object
• neuromuscular disorder, thyroid disorder
• children may develop amblyopia

Pathophysiology

caused by weak or hypertonic muscle in one of the eyes

Risk Factors

Family hx, preterm birth

Symptoms

Diplopia
Eventual amblyopia (lack of a developed visual cortex for one or both eyes) for infants with strabismus.

Clinical Findings

Unsymmetrical light reflex (Hirshberg test), misalignment of the eyes (cover/uncover test, or sometimes visible without).

Dx/Labs

Cover/uncover test.

Treatment

Almost always surgical.

Treat amblyopia with patching (put a patch over the good eye)
Nystagmus

Etiology
Pathophysiology
Clinical Findings
Dx/Labs
Etiology

Congenital: horizontal, non-gaze dependent, asymptomatic. Spontaneous: If it resolves within a few days it was probably due to a lesion to the labyrinth or vestibular nerve; if it doesn''''t it''''s probably due to a lesion to the brainstem, cerebellum, or both. If the lesion is in the CNS the effects are significantly worse than if it''''s in the peripheral nerve/organ. Gaze-dependent nystagmus most often brought about by drug toxicity.

Pathophysiology

Impaired nerve or muscle function leads to “beating” eyes.

Clinical Findings

A “beating” of the eyes. Can be horizontal, vertical, torsional or a combination thereof. Can be gaze dependent or gaze independent. Can be position dependent or position independent.

Dx/Labs

EOMs
Diplopia

Etiology
Treatment
Etiology



  • Can come from strabismus, dysthyroid ophthalmopathy, CN III, IV or VI palsies


•Binocular diplopia - result of the misalignment of the two eyes
•monocular diplopia - w/one eye
•monocular polyopia - percieve >2 images


Pathophysiology

Disparate images cast on the retinas

Clinical Findings

Possible misalignment of eyes (sometimes only when testing EOMs), possible exopthalamos, possible dry, irritated eyes.

Dx/Labs

EOMs, Test thyroid function for Graves, slit lamp examination (i.e. referral)

Amblyopia

Etiology
Pathophysiology
Risk Factors
Symptoms
Treatment
Etiology

Is a reduction or dimness of vision for unknown reasons. It does not result from changes in refraction or from visible changes in the eye, however it is associated with diseases such as DM, renal failure, malaria and toxic substances such as tobacco and alcohol.

Pathophysiology

Causes are no transmission or poor transmission of visual image to the brain for a sustained period of dysfunction or childhood, it results are typically unilateral.

Risk Factors

Strabismus, cataracts, etc. Anything that decreases the ability of the eye to see clearly or produces disparate images on the retinas can lead to amblyopia (in one or both eyes depending on the origin).

Symptoms

This can range from mild to poor visual acuity, depth perception, spatial acuity, low sensitivity to contrast and higher deficits to vision as reduced sensitivity to motion.

Treatment

Eye patch over good eye to develop other eye''''s associated visual cortex (only work if child is very young)
Acute Angle Closure Glaucoma

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Differentials
Etiology

Congenital: people born with a narrow angle. People of Asian and Eskimo ancestry are at higher risk, age and family hx are factors; older women are affected more than men.

Pathophysiology

Occurs when increased pressure in the front chamber of the eye due to a acute blockage of vascular circulation of the fluid within the eye. The blockage takes place as a angle at the anterior chamber formed by its junction of the cornea with the iris, therefore where its name is derived form.

Risk Factors

Hereditary, women with advanced age.

Symptoms

Severe eye and facial pain, nausea and vomiting, decreased vision, blurred vision and seeing halos around light.

Clinical Findings

Early:Blurred vision, facial tenderness, photophobia.
Advance stage: the eye appears red, with a steamy clouded cornea and a fixed dilated pupil, this stage is a emergency the because the optic nerve damage and vision loss can occur within hours of the onset of the problem.

Dx/Labs

An eye exam, neuro exam and HEENT

Treatment

Administering medications to decrease pressure within the eye is done immediately.

Two Surgical procedures:

In the past, a piece of the iris was then surgically removed in a procedure called an iridectomy to make a hole in the iris and create a channel (other than the canal of Schlemm) to permit the free flow of fluid.

Today a comparable procedure can be done by laser to burn a small hole in the iris to keep the intraocular pressure within normal limits.

Differentials

Primary Open Angle Glaucoma
Primary Open Angle Glaucoma

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Differentials
AKA Chronic glaucoma

Etiology


Age over 40 and common in African Americans, elevated history of IOP, family hx and myopia.

May also result from:
  • Uveitis
  • Ocular trauma
  • Corticosteroid therapy


Pathophysiology

Aqueous flow in the anterior chamber is blocked (though anatomically normal). Atrophy of the retinal ganglion cell layer in the presence of increased IOP (intraocular pressure)

Risk Factors

  • Age (15% of individuals over 80 get it)
  • Family history
  • Diabetes mellitus
  • Obesity
  • African american race
  • Ocular trama
  • Myopia

Symptoms

Vision loss (though it is so insidious that it might not be realized)

Clinical Findings

Clinical triad: increased IOP, optic nerve cupping and characteristic vision loss.

Dx/Labs

HEENT and Neuro( if warranted)

Treatment

Refer to Ophthalmologist; also, drugs such as: prostaglandin analogs, β-blockers such as timolol. Surgery if indicated, such as laser trabeculoplasty or guarded filtration procedure
Bacterial Conjunctivitis

Etiology
Pathophysiology
Symptoms
Clinical Findings
Treatment
Differentials
Etiology

• More common in children
• Pneumococcus, S. aureus, M. cattarhalis, H. influenzae
•highly contagious

Pathophysiology

Transferred by direct contact.

Symptoms

"Pink eye"
•redness, itching, and foreign body sensation
•eyelids and eyelashes are matted shut upon awakening

Clinical Findings

watery to hyperpurulent (grey-yellow) discharge. Chronic mild mucoid discharge and crusting. Mild edema in conjunctiva (chemosis) and lids.

Treatment

•Hand washing & use of separate towels
•Erythromycin or bacitracin.
•Topical sulfonamide.
•Resolves spontaneously 10-14 days

Differentials

dry eyes, corneal abrasion, blepharitis, acute uveitis, acute glaucoma, and corneal disorder
Viral Conjunctivitis

Etiology
Pathophysiology
Risk Factors
Symptoms (2)
Clinical Findings (5)
Treatment
Differentials
Etiology

•Most conjunctivits are viral, by adenovirus.
• Other viruses: herpes simplex, EBV, varicella zoster, molluscum contagiosum, coxsackie, and enterovirus

Transferred by direct contact.

Pathophysiology

Viral colonization of conjunctiva causes irritation

Risk Factors

Hx of URI.

Symptoms

•associated w/pharyngitis, fever, malaise
• copious watery discharge

Clinical Findings

•preauricular lymphadenopathy
•Red conjunctiva
•edematous eyelids
•pinpoint subconjunctival hemorrhages
•pseudomembrane formation

Treatment

•Should be isolated from other pts, examining rooms to be disinfected.
• Clear on its own in 2 weeks

Differentials

corneal abrasion, acute uveitis, acute glaucoma, and corneal disorder
Blepharitis

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Commonly staphylococcus aureus.

Pathophysiology

Anterior - involves eyelid skin, eyelashes, and associated glands Posterior - from inflammation of meibomian glands

Risk Factors

Poor hygeine

Symptoms

irritation, burning, and itching, foreign body sensation, excessive tearing and crusty debris around the eyelashes

Clinical Findings

lid erythema, collarettes (a fibrin crust encircling an eyelash), madarosis (missing lashes), trichiasis (an inturned lash), plugged meibomian glands, conjunctival injection

Treatment

•Clean eyelids using cotton tip.
1) bacitracin or erythromycin
2) azithromycin
3)tobramycin
Dacryocystitis

Etiology
Risk Factors
Symptoms
Clinical Findings
Treatment
Etiology

Infection of lacrimal sac due to nasolacrimal obstruction. Infection by Staphylococcus aureus and B-hemolytic streptococci.

Risk Factors

Poor hygeine

Symptoms

Pain, redness and swelling over the inner aspect of the lower eyelid, purulent discharge from lacrimal punta

Clinical Findings

suspect dacryocystitis if the problem recurs and is associated w/ fever and severe erythematous swelling around the nasal aspect of the lower lid

Treatment

•child - oral amoxicillin/ clavulanate (Augmentin) & acetaminophen
•adult - cephalexin (Keflex) or Augmentin & asprin
•warm compresses
Herpes Simplex Infection (eyes)

Etiology
Pathophysiology
Clinical Findings
Treatment
Differentials
Etiology

primarily in children 6months - 5 yrs old.

Pathophysiology

trigger factors include fever, trauma, emotional stress, menstruation, exogenous immunosuppressive agents, & UV radiation

Clinical Findings

variable pain & tenderness upon palpation, as well as ↑ lacrimation in severe cases. swollen preauricular node . small vesicles or pustules along the lid margin

Treatment

no specific treatment, self-limiting within 2-3 weeks. Warm saline compresses w/ a topical drying agent (e.g., 70% alcohol)

Differentials

blepharitis or blepharoconjuncti vitis.
Bacterial Corneal Ulcers (keratitis)

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Treatment
Etiology

• contact lens wear overnight
• corneal trauma - including refractive surgery
• P. aeruginosa, Pneumoncoccus, Moraxella sp., & staphylococci

Pathophysiology

result of trauma to the surface of the eye

Risk Factors

Vit A deficiency

Symptoms

pain, photophobia, a foreign-body sensation, tearing, blurred vision

Clinical Findings

red eyes w/circumcorneal injection, purulent or watery discharge. Cornea hazy, central ulcer & adjacent stromal abscess

Treatment

Referral to ophthamologist. Fluoroquinolones 1st line . Gram (+) tx w/cephalosporin (cefazolin)
Fungal Corneal Ulcers

Etiology
Pathophysiology
Symptoms
Clinical Findings
Treatment
Etiology

Corneal injury involving plant material or in an agricultural setting.
• contact lens wear

Pathophysiology

result of trauma to the surface of the eye

Symptoms

pain, photophobia, a foreign-body sensation, tearing, blurred vision

Clinical Findings

red eyes w/circumcorneal injection, purulent or watery discharge. Cornea hazy, central ulcer & adjacent stromal abscess

Treatment

Referral to ophthamologist. Natamycin & amphotericin topical agents.
Subconjunctival Hematoma

Etiology
Pathophysiology
Symptoms
Clinical Findings
Treatment
Etiology

Can be from systemic disease, can be from eye trauma

Pathophysiology

blood vessel on the conjunctiva may break, causing a solid red patch of blood on the white of the eye.

Symptoms

No pain, vision is not affected.

Clinical Findings

Red area that fades over days to yellow and then disappears.

Treatment

Self healing
Chemical Burn (eye)

Etiology
Pathophysiology
Symptoms
Treatment
Etiology

can lead to scarring, perforation of the eye, and blindness.

Pathophysiology

Painful -> close eyes -> keep substance in eye for prolonged period may worsen damage

Symptoms

Burning sensation

Treatment

•proparacaine + Irrigate w/water or saline in rm temp x 30- 120 mins.
•May dilate eyes (homatropine) to relax iris.
•Antibiotic ointment (ciprofloxacin)
Foreign Body (eye)

Pathophysiology
Symptoms
Clinical Findings
Dx/Labs
Treatment
Pathophysiology

The foreign object sets off an inflammatory cascade, resulting in dilation of the surrounding vessels & edema of the lids, conjunctiva and cornea.

Symptoms

Excessive tearing, blurred vision and photophobia

Clinical Findings

lid edema, focal or circumlimbal conjunctival injection, & mild to moderate anterior chamber reaction

Dx/Labs

Ensure object did not perforate cornea. Instill fluorescein to inspect for aqueous leakage through the wound (Seidel’s sign). May need Xray

Treatment

•If no penetration, remove the object under topical anesthesia (proparacaine).
•sterile irrigating solution may dislodge object
•may need referral
Diabetic Retinopathy

Etiology
Pathophysiology
Risk Factors
Clinical Findings
Dx/Labs
Treatment
Etiology

Leading cause of blindness in adults 20-65 yrs old. Nonproliferative - dilation of veins, MA, hemorrhages, retinal edema, hard exudates
Proliferative: neovascularization

Pathophysiology

new blood vessels form at the back of the eye as a part of proliferative diabetic retinopathy (PDR), they can bleed (hemorrhage) and blur vision

Risk Factors

affects up to 80% of all patients who have had diabetes for 10 years or more

Clinical Findings

cotton-wool spots, flame hemorrhages, and dotblot hemorrhages.

Dx/Labs

Slit lamp exam/ophthalmoscope

Treatment

panretinal laser phtocoagulation @ ophthalmologist office
Hypertensive Retinopathy

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Treatment
Etiology

Hypertension leads to sclerosis and eventually weakened artery walls

Pathophysiology

small blood vessels that involve the eye are damaged, thickening, bulging and leaking

Risk Factors

Hypertension (leading to a whole new set of risk factors)

Symptoms

Some may report decreased vision or headaches.

Clinical Findings

1. arterioles tortuous, "copper wiring"
2. Ischemic changes ("cotton wool spots")
3. Hemorrhages, often flame shaped.
4. Edema (macular star)
5. Papilledema

Dx/Labs

Slit lamp exam/ophthalmoscope

Treatment

Treat the hypertension
Chalazion

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment (2)
Etiology

Localized swelling of eyelid resulting from chronically obstructed meibomian gland (lump of the lid that is caused by obstruction of an oil gland within the upper or lower eyelid).

Pathophysiology

Chronically inspissated meibomian gland. Gladular secretions become fossilized within the tarsal plate, producing a firm, nonmobile subQ nodule.

Clinical Findings

Hard, immoveable, lump on upper or lower eyelid

Treatment

Warm soaks with or without antibiotic ointment. Incision and urettage are reserved for lg lesion or those lasting longer than 1 mo.

Differentials

Hordeolum
Hordeolum

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Differentials
Etiology

Commonly referred to as a stye

Pathophysiology

Acute focal infection of a Meibomian or Zeiss gland

Symptoms

Painful, may produce bleparoptosis if on upper lid. A sty, or hordeolum, represents an acute infection of the gland

Clinical Findings

Bump on eyelid, may be edematous and warm.

Treatment

Warm compresses over a period of days, if turns into cellulitis, abx are needed.
Entropion

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Treatment
Etiology

Congenital, age and travel to South Asia and North Africa (Trachoma)

Pathophysiology

Congenital, spasm and weakening of muscles surrounding theupper/lower part of eye causing the lid to turn inward.

Risk Factors

Aging, chemical burn, trachoma infection (causes scarring of the inner lower lid)

Symptoms

Decreased vision if cornea damaged, excess tearing, eye discomfort/pain, eye irritation and redness, sensitivity to light and wind, sagging skin around the eye

Clinical Findings

Have the patient squeeze the lids together and then open them to reveal a less obvious entropion.

Treatment

1. Seek medical care if you’ve traveled to N. Africa or S. Asia and your eyes are red.
2. Artificial tears to prevent dryness and lubricate cornea. Surgery to correct eyelid position
3. Surgery in severe cases to protect the eye
Ectropion

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Treatment
Etiology

Common in elderly, or defect before birth, facial palsy, scar tissue from burns

Pathophysiology

Margin of lower lid turns outward exposing palpebral conjunctiva. If punctae exposed – eye will not drain and excess tearing occurs. Weakening of the connective tissue of the eyelid.

Risk Factors

Congenital, prior surgeries, seen after infections or secondary to scarring.

Symptoms

Dry, painful eyes, excess tearing, eyelid turned out, chronic conjunctivitis, keratitis, redness of lid and cornea of eye.

Clinical Findings

Sagging skin around the eye exposing the palpebral conjunctiva, red, irritated conjunctiva.

Treatment

1. No prevention
2. Use artificial tears to prevent corneal complications (dryness-> abrasions, ulcers and infections). Ulcers can threaten vision. Surgery for chronic or symptomatic cases.
3.Constituted symptomatic emergenices: decreased vision, pain, light sensitivity and rapidly increasing redness.
Pterygium

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Found in people w/outdoor occupations.

Pathophysiology

Triangular fibrovascular mass of bulbar conjunctiva extending from the limbus onto cornea- usually on the nasal side. usually associated with constant exposure to wind, sun, sand, and dust.

Risk Factors

UV light

Symptoms

ocular cosmoesis, ocular irritation, reduced vision

Clinical Findings

fleshy, triangular encroachment of the conjunctiva onto the nasal side of the cornea

Dx/Labs

Slit lamp and fluorescein staining

Treatment

•No tx, but artifical tears may be beneficial
• UV sunglass protection
•Indications for surgery is when growth threatens vision.
Pinguecula

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Unknown. Chronic sunlight exposure and eye irritation may contribute to the condition.

Pathophysiology

Yellow-white slightly raised mass on the bulbar conjunctiva near the cornea usually on the nasal side caused by a degeneration of collagen fibers in the conjunctiva.

Risk Factors

UV exposure, welding is a significant occupational risk, outdoor workers.

Symptoms

Small painless yellow-white nodule on the conjunctiva that increases in size over many years.

Clinical Findings

Yellow-white nodule on the nasal conjunctiva.

Treatment

1. Eye protection
2. Lubrication (artificial tears), temporary mild steroid eye drops or anti-inflammatory prescriptions. Surgery for discomfort or cosmetic reasons or if corneal overgrowth occurs
3. No emergencies
Retinoblastoma

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Differential
Etiology

Most common malignancy of childhood – autosomal dominant or sporadic

Pathophysiology

Defective allele passed on or mutations during embryogenesis produces a malignant tumor growth in the retina usually manifest by age 2. Can be singular tumor unilaterally or multiple tumors uni/bilaterally

Risk Factors

At risk for osteogenic sarcoma

Symptoms

Axial proptosis and decreased vision

Clinical Findings

Present with leukocoria or strabismus, orbital venous malformation, Fam Hx, decreased acuity, abnormal red reflex

Dx/Labs

CT Scan with contrast, Echography and/or MRI

Treatment

Early detection and use of external beam radiation, laser photocoagulation and episcleral plaque brachytherapy
Enucleation is recommended for late detection in unilateral cases. Radiation, laser ablation, cryotherapy and systemic chemo used in bilateral cases to treat the second eye.

Differentials

Leukocoria
Wilson's Disease (etiology and what happens to the eye)

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Etiology

Wilson disease is a rare autosomal recessive inherited disorder of copper metabolism.
Chromosome arm 13q present with in the first decade of life.

Pathophysiology

Excessive deposition of copper in the liver, brain, and corneal limbus (among other places)

Risk Factors

Genetic, family hx, more common in males than female 4:1

Clinical Findings

Kayser-Fleischer rings are formed by the deposition of copper in the Descemet membrane in the limbus of the cornea. The color may range from greenish gold to brown; when well developed, rings may be readily visible to the naked eye or with an ophthalmoscope set at +40
Dacryostenosis

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Treatment
Differentials
Etiology

A tube called the nasolacrimal duct normally drains tears from the surface of the eye into the nose. If this duct is blocked, the tears will build up and overflow onto the cheek, even when a person isn't crying.
In children, the duct may not be completely developed at birth. In adults, the duct can be damaged by infection, injury, or a tumor.

Pathophysiology

A blocked tear duct is a partial or complete blockage in the system that carries tears away from the surface of the eye into the nose.

Risk Factors

Untreated sinus infections.

Symptoms

Increased tearing that overflows onto cheeks and face

Clinical Findings

Examination of the nares, fluorescein stain to see how tears drain, ophthalmic exam

Treatment

1. Erythomycin
2. Pt with chronic problems may need sugery to reopen passage.

Differentials

Dacryocystitis, opthalmalogic allergies
Hyphema

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Differentials
Etiology

Blunt trauma to eye. Sickle Cell Disease (SCD) – may cause spontaneous anterior chamber bleeds.

Pathophysiology

Accumulation of blood in the anterior chamber of the eye due to blunt trauma, fluid in the eye increases the intraocular pressure (IOP) and may damage retinal vessels.
Sickled RBC’s may occlude retinal vasculature causing increased IOP and vessel damage.

Risk Factors

Activities where blunt trauma is imminent, African American in the U.S. (SCD), travel to equatorial countries (SCD)

Symptoms

Recent trauma, pain (maybe), vision blurred (maybe)

Clinical Findings

Blood in eye, no red reflex, hazy appearing iris, abnormal pupil reflex, acuity changes, impaired vision

Dx/Labs

IOP testing & Slit-lamp examination

Treatment

1. Wear protective eye wear when engaging in activities, restrict oral intake
2. Ice after trauma, if loss or blurred vision or blood accumulation noted in eye get it checked
3. Bed rest (head elevated), eye patch, dilate pupil with 1% atropine to prevent tearing a damaged vessel. Measure IOP – if >30 mmHg administer 1 drop .5% timolol, if IOP persists add 1 drop .5% apraclonidine. In refractory cases give 500mg Acetazolamide – unless the patient has SCD as acetazolamide will cause sickling in the anterior chamber. Mannitol 1-2g/Kg IV if IOP is still not controlled. Emergent eval by ophthalmologist.
Keratoconjunctivitis sicca

Etiology
Pathophysiology
Symptoms
Treatment
Etiology

aka Dry eye syndrome. May be caused by medications (ibuprofen, diphenhydramine, Tripolidine, Atenolol, Scopolamine, etc)

Pathophysiology

Defiency of tear film layers.

Symptoms

Gritty, foreign body sensation, burning, photophobia, and ↓VA.

Treatment

Artificial tears
Iritis

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Differentials
Etiology

A form of anterior uveitis acute - heal independently within few weeks chronic - exists months or years

Pathophysiology

Inflammation of the iris

Risk Factors

autoimmune and infectious causes, HLA-B27 gene

Symptoms

pain, photophobia, and blurred vision

Clinical Findings

Perilimbal conjunctival injection may be present, and slit lamp examination demonstrates inflammatory cells and protein exudate (flare) in the anterior chamber

Dx/Labs

Slit-lamp exam.

Treatment

Initial episodes are usually treated symptomatically with prednisolone acetate 1% suspension four times a day and cycloplegic drugs (cyclopentolate 1 or 2% twice daily)-muscarinic antagonists that cause ciliary paralysis
Uveitis

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Anterior uveitis (iris & ciliary body)
Intermediate uveitis (posterior cillary body-pars plana)
Posterior uveitis (choroid) Panuveitis (all segments)

Pathophysiology

Inflammation of one or all parts of the urea.

Risk Factors

HLA-B27 gene, ankylosing spondylitis

Symptoms

redness of eye, blurred vision, photophobia, floaters, eye pain.

Clinical Findings

Inflammatory lesions may present in retina or choroid. May have retinal hemorrhages.

Treatment

Uveitis requires an urgent referral and thorough examination by an ophthalmologist. May need systemic or IV corticosteroids.
Graves Ophthalmopathy

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

• Autoimmune disorder that causes stimulation of the thyroid gland resulting in hyperthyroidism.
• 50% of children with Graves’ disease have exophthalmus

Pathophysiology

Thyroid eye disease -> inflammation & swelling of extraoccular eye muscles and orbital fat

Risk Factors

Genetic factors interacting with environmental triggers

Symptoms

change in eye appearance, ocular irritation, FBS, dryness, tearing, pain, ↓ vision, and diplopia

Clinical Findings

Staring gaze, proptosis, lid retraction & lid lag, conjunctival chemosis and episcleral inflammation & extraocular muscle dysfunction

Dx/Labs

TSH levels, circulating thyroid hormone levels, exophthalmometer, orbital imaging w/CT scanning or ultrasonography

Treatment

protecting the corneas from exposure, moisturizing drops, taping the eyelids closed at bedtime, High dose systemic steroids (not long term solution)
Ischemic Optic Neuropathy

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Differentials
Etiology

It can be nonarteritic (nonarteritic anterior ischemic optic neuopathy [NAION) or arteritic (AION) also known as giant cell arteritis or temporal arteritis.

Pathophysiology

inadequate perfusion of posterior iliary ateries that supply anterior portion of optic nerve

Risk Factors

• systemic HTN
• diabetes
• hyperlipidemia
• systemic vasculitis
• thrombophilia

Symptoms

sudden vision loss, loss of color vision

Clinical Findings

optic disk swelling & pale, afferent pupil defect

Dx/Labs

ESR & C-reactive protein (CRP) will be elevated, Angiography

Treatment

Emergency -> high dose systemic corticosteroid tx (Prednisone) to prevent vision loss in other eye

Differentials

Central retinal vein occulsion, ocular hypotony, papilledema.
Retinal Vein and Artery Occlusion

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Differentials
Etiology

RAO - Emboli are generally associated with carotid stenosis
RVO -HTN, athersclerosis, diabetes, glaucoma, elderly, high cholesterol, "blood and thunder presentation"

Pathophysiology

RAO - emboli -> ophthalmic artery or the central retinal artery RVO - thrombus formation ->pressure build up in the capillaries -> hemorrhage/edema

Risk Factors

Smoking, lack of exercise, atherosclerosis

Symptoms

RAO - sudden painless monocular vision loss, VA = CF or worse RVO - sudden painless vision loss, in single quadrant or whole visual field

Clinical Findings

RAO -> cherry red spot @ fovea, retinal arteries attenuated, retina whitened RVO -> retinal hemorrhage, retinal venous dilation & tortuosity, cotton wool spot, optic swelling

Dx/Labs

CBC, ESR, fibrinogen level, PT, aPTT, and serum protein. FA used by some clinicans.

Treatment

Referral

Differentials

•Hypertensive retinopathy
•ocular ischemic syndrome
•RAO
•retinal detachment
•giant cell arteritis
Amaurosis Fugax

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Can be of hemodynamic/embolic origin, Optic origin or neurologic origin

Pathophysiology



Risk Factors

Each has their own

Symptoms

Complete loss of vision in one eye

Clinical Findings

Depends on cause

Dx/Labs

Basic labs-checking for anemia, polycythemia, Wegener granulmatosis, coagulopathies sickle cell test, UA, BP, Neuroimaging, ECHO

Treatment

depends on cause

Differentials

RAO, RVO, dry eye syndrom, Giant cell arteritis, MS, Optic neuritis, Papilledema, partial epilepsies.
Herpes Keratitis

Etiology
Pathophysiology
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

•HSV-1, can be accompanied by conjunctivitis
•# 1 cause of infectious blindness in the US.

Pathophysiology

Herpes follows nerves into the eye and causes lesions.

Symptoms

Can cause blindness

Clinical Findings

Characteristic lesions -> dendritic ulcers

Dx/Labs

fluorescein staining, Clinical specimens or other bodily fluids can be sent to lab for analysis (60% sensitivity)

Treatment

Referral to an Opthalmalogist, even more so if the pt. is c/o blindness.
Toxoplasmosis

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Treatment
Etiology

Toxoplasma gondii (protozoan parasite)

Pathophysiology

After infection by oral route, can disseminate from GI tract and invate virtually any cell or tissue.

Risk Factors

AIDS

Symptoms

blurred vision, scotoma, pain, photophobia, epiphoria, macular involvement may impair central vision

Clinical Findings

“headlight in the fog” , typical retinal fundus lesion comprises an active yellow satellite adjacent to an old chorioretinal scar with a dense overlying vitritis.

Treatment

•pyrimethamine and sulfadiazine
•educate on handling raw meat & cat feces
Cytomegalovirus

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Sexually transmitted infection.

Pathophysiology

Immunocompent pts are at risk for this disease. May appear as a subacute unilateral visual loss or vitreous floaters, large areas of hemorrhagic infarction are seen with minimal vitritis.

Risk Factors

immunocompromised individuals (HIV+)

Symptoms

subacute unilateral visual loss, vitreous floaters

Clinical Findings

subacute unilateral visual loss, vitreous floaters in immunocompromised patients.

Dx/Labs

ophthalmoscopy. Fluorescein angiography may be needed to evaluate the circulatory system of the retina.

Treatment

IV ganciclovir (2.5-5.0 mg/kg every 8-12 hrs intravenously for 2-3 weeks of induction)
Foscarnet (e.g., 60 mg/kg intravenously every 8 hrs for 2 weeks, with maintenance dose of 60 mg/kg daily for 5-7 days/week, adjusted on basis of renal response)
Intravitreal ganciclovir (200 ug in .1 mL of water injected with a 30 gauge needle one to three times each week)
TB

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

M. tuberculosis, a acid fast bacillus that usually invades the lungs and affects the other organ systems

Pathophysiology

They can also migrate with the lymphatics and cause swollen nodes. Inflammatory responses are activated- wbc seal off the bacteria into what is known as a tubercle.

Risk Factors

Immunocponent pts. Such as those with HIV, can trigger a reactivation of this disease.

Symptoms

Wt loss, lethargy, low- grade fever.
Involves the uvea in approximately 1% of pulmonary cases. Iridocyclitis and diffuse choroiditis are the most common manifestations. Symptoms include painless progressive visual loss. Small yellow choroidal lesions may be seen, and retinal periphlebitis may occur secondarily. Intermediate- and second-strength purified protein derivative testing may be positive.

Dx/Labs

PPD

Treatment

Clinical response to a 3-week trial course of isoniazid strongly suggests tuberculosis
2ndry Syphilis

Etiology
Pathophysiology
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Spirochete Treponema pallidum; most contagious stage

Pathophysiology

After primary infection, bloodborne bacteria spread to all major organ systems

Symptoms

‘The Great Imitator’ General: Malaise, fever, HA, sore throat, body aches; Ocular: Photophobia, eye redness, blurry vision

Clinical Findings

•unequal reflexes
• irregular pupils
• anterior uveitis,
•neuroretinitis
•Argyll Robertson pupil

Dx/Labs

•Serologic testing for positive syphilis •genital exam

Treatment

•IV penicillin for 10-14 days, or • IM penicillin and oral penicillin together for 10-14 days. • sex education
Cataracts (in peds)

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Can be congenital (autosomal dominant) or result of an infection Associated w/ metabolic diseases (galactosemia, Lowe syndrome), radiation insult, and intrauterine infections

Pathophysiology

Lens opacity resulting from insult to nuclear fibers during development; location and pattern of opacification can determine timing of insult as well as etiology. Can affect vision depending on its density, size, and position

Risk Factors

Familial, 1/3 of cases are inherited, usually autosomal dominant Also in children with DM, Marfan Syndrome, and atopic dermatitis, or other ocular abnormalities such as pendular nystagmus or strabismus

Symptoms

Loss of visual acuity and contrast sensitivity, poor fixation, leukocoria

Clinical Findings

Lamellar or zonular cataracts

Dx/Labs

Cultures or serologic tests for infectious causes

Treatment

•Early diagnosis and tx necessary to prevent deprivation amblyopia
•Glasses/contact lenses, occlusion of healthy eye (to treat amblyopia)
Cataracts related to aging

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Progressive yellowing of the lens nucleus and hydration of the lens cortex

Pathophysiology

Opacification of the crystalline lens, usually bilateral

Risk Factors

Prolonged exposure to UV radiation, cigarette smoking

Symptoms

Gradually progressive blurred vision, painless

Clinical Findings

As the cataract matures, retina becomes increasingly difficult to visualize until eventually fundus reflection is absent and pupil is white

Dx/Labs

Seen through dilated pupil with ophthalmoscope or slit lamp

Treatment

No known medical treatment, surgical extraction required for vision improvement; prosthetic intraocular lenses reduce the need for distance and reading glasses
Ophthalmia Neonatorum

Etiology (3)
Pathophysiology
Risk Factor
Symptoms (3)
Clinical Findings
Dx/Labs (3)
Treatment (3)
Etiology

•transmitted in utero or in postpartum period
•gram (-) Neisseria gonorrhoeae
•gram (-)Chlamydia trachomatis

Pathophysiology

Bilateral conjunctivitis causes blood vessel dilation, chemosis, excessive secretion

Risk Factors

Mother positive for Chlamydia or Gonorrhea at time of delivery

Symptoms

Eye pain, redness, purulent discharge

Clinical Findings

Gonococcus causes conjunctival inflammation, lid edema, erythema Chlamydia causes moderate eyelid swelling, palpebral or bulbar conjunctival injection

Dx/Labs

•conjunctival scraping for gram stain
•ELISA
•PCR

Treatment

•Irrigate to clear exudates
•Erythromycin ointment (Chlamydia),
•IM or IV ceftriaxone or cefotaxime 14 day course (gonococcal)
Age Related Macular Degeneration

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Precursor – age related maculopathy: characterized by retinal drusen
Exact cause unknown; prevalence increases with each decade over 50 yrs

Pathophysiology

Idiopathic atrophy of the photoreceptors and retinal pigmented epithelium – loss of central vision only; peripheral vision remains intact

Risk Factors

Smoking, HTN, hypercholesterolemia, Genetic variation in complement factor H, family hx, race (white), sex (female slightly predominant)

Symptoms

Dry – painless, progressive loss of central vision Wet – onset of visual loss more rapid and severe

Clinical Findings

Dry – pigmentary change in macula, drusen present
Wet – choroidal new vessels grow causing accumulation of serous fluid, hemorrhage, and fibrosis

Dx/Labs

Ophthalmoscopy, Amsler grid

Treatment

• Dry - Oral vitamins and antioxidants (Vit C, E, Beta carotene, zinc and copper)
• Wet –VEGF inhibitors
• Amsler grid home monitoring for metamorphopsia
Periorbital Cellulitis

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Most common in children under age 6.
Extension of sinus or tooh infection
• Staph aureus
• Strept pyrogenes
• H. influenzae

Pathophysiology

Inflammation and infection of superficial eyelid that does not penetrate the orbital septum.

Risk Factors

Sinusitis, children, male gender, lack of Hib vaccine in children, eyelid injury

Symptoms

fever may or may not be present, vision retained

Clinical Findings

swelling, redness of upper/lower eyelid, VA and pupillary reaction retained, full ocular motility

Dx/Labs

CBC, blood culture, Orbital/sinus CT

Treatment

Amoxicillin /clavulanate for children >5
Orbital Cellulitis

Etiology
Pathophysiology
Risk Factors
Symptoms
Clinical Findings
Dx/Labs
Treatment
Etiology

Extension of sinus or tooth infection
• Staph aureus
• Strept pyrogenes
• H. influenzae

Pathophysiology

Inflammatory process in eyelid structures penetrating the orbital septum.

Risk Factors

Sinusitis, children, male gender, lack of Hib vaccine in children, eyelid injury

Symptoms

fever, diplopia, vision loss

Clinical Findings

proptosis, restriction of extraocular movements, swelling w/redness of lids, pain w/eye movement

Dx/Labs

CBC, blood culture, Orbital/sinus CT

Treatment

Emergency referral to ophthalmologist. Nafcillin IV plus celftraxone IV plus metronidazole IV. May need surgery.
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