Eye 1 Flashcards
eyelid
-blepharitis
-anterior
-posterior
-hordeolum
-chalazion
-entropion
-extropion
blepharitis
-common recurrent disorder of eye
-chronic inflammation of eye lid margin
-eye discomfort, redness and tearing
-dry eyes, burning, itching, light sensitivity, and irritating sandy gritty sensation
-anterior eye lid- eye lashes and sebaceous glands of Zeiss
-Posterior eye lid- has the opening of the meibomian glands
anterior blepharitis
-affects the outside front of eyelid, where the eyelashes are attached
-2 most common causes of anterior blepharitis:
-bacteria (staphylococcus)
-seborrheic dermatitis
staphylococcal infection: anterior blepharitis
-scaling, matted, hard crusts around eye lashes
-red rimmed
-mostly bilateral
-may have difficulty opening the eyes in the morning
-removing crust may leave small ulcers that bleed and ooze
-loss of eyelashes may occur
-sty may form (hordeolum)
-Treatment- warm compresses, lid hygiene
-baby shampoo*
-antibiotic ointment- erythromycin, bacitracin, sulfacetamide
-topical ophthalmic azithromycin 1% solution
-steroid use- for staph. marginal ulcer
anterior blepharitis: seborrheic
-greasy flakes/scales along eye lashes and lid margin
-pts have seborrheic dermatitis
-treatment:
-warm compress
-eye lid scrubs
-baby shampoo
posterior blepharitis
-meibomian gland dysfunction
-glands are plugged with oily secretions
-chronic red irritated eyes (from rubbing)
-lid margins- hyperemic with telangiectasis- blood spots
-commonly seen in pts with acne rosacea OR seborrheic dermatitis
-treatment:
-warm compresses
-lid scrubs
-bacitracin or erythromycin eye ointment
-oral tetracycline and/or short term topical corticosteroids
hordeolum
-acute purulent eyelid inflammation- localized
-staphylococcus aureus- usual pathogen
-acute onset
-painful
-red
-localized swellings with abscess formation
-may lead to generalized cellulitis of the lid
-external hordeola- due to blockage and infection of ciliary follicle and the adjacent sebaceous glands of Moll or Zeis (ciliary glands)
-internal hordeola- due to blockage and infection of meibomian sebaceous glands located in the tarsal plate
hordeolum treatment
-usually self limiting
-resolving within 5-7 days when they drain
-warm compresses/soaks are the mainstay of treatment
-may need incision if no resolution in 48 hours
ointment
-stays for longer period of time that solution
-sticky
-difficulty seeing
chalazion
-focal, chronic, inflammatory lesion of eyelid due to obstruction of a sebaceous gland, often following an internal hordeolum
-lipogranulomas- not infected
-slow growing, painless nodules in middle (usually) of eyelid
-redness and swelling of adjacent conjunctive
-can become quite large and last for many months
-warm compresses/soaks for 10 mins 4 times a day
-antibiotic therapy or surgical drainage may be required
-steroid injection- if no infection and/or no response to treatment
angioedema
-often but not always bilateral
-abrupt onset over minutes to hours- may follow an exposure
-abrupt onset BUT not rapid or immediate -> differentiates allergic rxn**
-scaling usually absent
-often self limited -> avoid inciting agents
-emergency medial attention required in pts with upper airway obstruction -> IM epinephrine
-mild cases may benefit from oral antihistamines and/or glucocorticoids
cellulitis
-often presents with severe edema, deep violaceous color, and pain
-onset over hours to days
-history of preceding upper respiratory tract infection, local skin trauma, abscess, insect bite, or impetigo; sinusitis* with 60-80% of orbital cellulitis
-get good hx
-orbital cellulitis (post septal)
steroid drops
-any suspicious of herpes simplex
-DO NOT USE STERIOD DROPS
proptosis
-protrusion of eye
-post septal infection gathers behind the eye and pushes it out
-decreased visual acuity, pain with eye movement, limitation of extraocular movements, and afferent pupillary defect
-seen with orbital cellulitis (post septal)
afferent pupillary defect
-an interference with the input of light to the pupillomotor system resulting in a symmetrical decrease in contraction of both pupils to light given to the damaged eye, compared with light given to the less damaged or normal eye
-oculomotor nerve constricts
-this is seen with proptosis which can be caused by post septal cellulitis
pre-septal cellulitis management
-out patient basis with broad spectrum oral antibiotics
-dicloxacillin OR amoxicillin/clavulanate (augmentin) and close follow up
-less than 4- hospitalize
orbital cellulitis work up/management
-post septal
-WBC, conjunctival cultures, and blood cultures
-orbital cellulitis- contrast computed tomography (CT)
-referral to ophthalmologist or otolaryngologist
-IV ampicillin/sulbactam (Unasyn), 2nd or 3rd generation
-cephalosporins
-MRSA: clindamycin, vancomycin
entropion
-inward turning of the eye lid
-usually the lower lid
-can cause ulcers
-degeneration of lid fascia
-may follow extensive scarring of conjunctiva and tarsus
-treatment- botulinum toxin injection
ectropion
-outward turning of the lower lid
-a lot of tearing
-can cause ulcers
-can get dry eye
-common with advanced age
-treatment- surgery
-if excessive tearing (epiphora), exposure keratitis or cosmetic problem
pinguecula
-yellow elevated nodule on either side of the cornea
-benign
-more common on nasal side -sunlight exposure
->35 years
-rarely grow
-inflammation occurs
-artificial tears beneficial
-short course of NSAIDS or weak steroid
pterygium
-fleshy triangular area of conjunctive
-nasal side of cornea
-associated with constant wind, sun, sand and dust exposure
-unilateral or bilteral
-sunglasses
-artificial tears beneficial
-short course of NSAIDs or weak steroid
-excision if growth interfering with vision
dacroadenitis
-infection of the lacrimal sac due to obstruction of nasolacrimal system
-may be related ot malformation of the tear duct, injury, eye infection, trauma
-affects infants and persons > 40 years
-usually unilateral
-epiphora and discharge
-tenderness, redness, swelling
-acute- staphylococcus aureus, B-hemolytic strep.
-chronic- staphylococcus epidermidis
-anaerobic species- candida albicans
-treatment- acute, responds well to systemic antibiotics
-relief of obstruction- only cure especially in chronic form
-dacryocystorhinostomy
foreign bodies: ocular trauma
-c/o something in my eye
-hx consistent with symptoms
-FB usually in cornea or conjunctiva
-BASELINE visual acuity recorded**- do eyes separately using chart or hands if they cant see
-need to do this to see how treatment effects vision
-local anesthetic drops- never give this to pt at home
-fluorescien
-examine eye
-sterile wet cotton tipped applicator- used to flip the upper eye lid and examine
-polymyxin-bacitracin ophthalmic ointment
-FOLLOW UP IN 24 HOURS / REFERRAL
steel FB
-leaves rust ring
-tissue excised under local anesthesia using slit lamp
-look for abrasion when you put fluroescien drops in
FB under upper eye lid
-local anesthetic inserted
-lid everted
-FB removed with applicator
-sterile wet cotton tipped applicator flips the upper lid
ocular trauma
-corneal abrasions
-h/o trauma to eye
-fingernail, paper, contact lens
-c/o pain, photophobia, tearing, blepharospasm, FB sensation
-visual acuity recorded**
-cornea and conjunctive examined- rule out FB
-instill fluorescien-> examine with light
-abrasion seen as darker green area
-treatment- polymyxin-bacitracin ophthalmic ointment
-mydriatic, analgesics
-follow up in q24 hours till healing and referral
corneal abrasions
-surface epithelium sloughed off
-stains with fluroescein
-usually due to trauma
-pain, FB sensation, tearing, red eye
corneal laceration
-significant ocular trauma
-typically form metallic object- hand tool
-fingernail scratches- do not usually have enough force to lacerate cornea
-c/o intense pain initially
-may diminish slightly due to corneal desensitization
-photophobia and profuse lacrimation
-significant uveitis
-anterior chamber shallow or even flat in full thickness laceration
-intraocular pressure- ranges from 2-6 mmHg (normal- 10-21 mm Hg)
-bubbles within the anterior chamber- key finding**
-visual acuity significantly reduced
-lens dislocation, iridodialysis, and hyphema
hyphema
-collection of blood in anterior chamber
-treatment of lacerations
-referral to ophthalmologist ASAP
-manipulation kept to a minimum- dont want to move them around
-cover with shield lightly so nothing worse happens
-pain mediations
-keep NPO- in case of surgery
-x-ray/CT done
corneal ulcer
-infection:
-bacterial- adnexal infections, lid malposition, dry eye, CL
-viral- HSV (dendritic ulcer), H. zoster Oticus
-fungal-
-protozoan- acanthamoeba in contact lens wearer
-mechanical or trauma
-chemical- alkali injuries are worse than acid -> irrigation!!
-fern like- dendritic
blow out fracture
-h/o blunt ocular trauma
-usually caused by a large, low velocity object
-intense pressure or swelling of the eye associated with nose blowing may also be reported
-sports- related injuries are common
-recent trauma- symptoms of pain, local tenderness and double vision
-some patients- initially ignore treatment
-may present long after the initial inflammatory manifestation have subsided
-only relative enophthalmos (sunken in) and motility restriction, usually in upgaze and possible infraorbital hypoesthesia
orbital blowout fracture
-edema, ecchymosis of the lid tissues
-restriction of ocular motility, espiecally with vertical movements
-orbital crepitus (subcutaneous emphysema)- air under skin
-hypoesthesia of the ipsilateral cheek- entrapment of the infraorbital nerve in foramen in undereye
-orbital edema initially surrounds and displaces the globe
-eye appears proptotic
-as the swelling subsides- eye is likely to drop down and back, becoming enophthalmic -> sometime wait for this before surgery
-associated traumatic uveitis and/or hyphema
step off
-gloved finger along the under orbital bone
-fingers drops down
management of orbital blowout fracture
-cover eye and restriction movement
-all cases of blunt ocular trauma with resultant crepitus or motility restriction warrant orbital imaging studies
-CT scan- procedure of choice
-better at imaging the bony structures of the orbit than either plain skull films (x-ray) or MRI
-obtain both axial and coronal scans
-if floor fracture with associated herniation of the orbital contents
-surgical intervention considered- wait 1014 days
-recent trauma with significant diplopia in primary gaze or down gaze or unacceptable enophthalmos
orbital globe rupture
-ophthalmic emergency
-history of trauma
-cover eye
-NPO
-closed global rupture- globe doesnt come out but it is under
-open globe rupture- part of globe comes out
cataract
-any opacity of the lens
-localize or diffuse
-potentially causing problem with vision
-usually develop slowly over years, but can rarely develop quickly over months
-pathology of the lens (elasticity) - blurry vision or loss
-may be unilateral or bilateral
-most forms of cataracts do not affect both eyes symmetrically
-90% of cataracts are age related
-others- congenital, traumatic, metabolic, toxic, secondary, smoking, to another disorder
no MRI
-with metal FB
ophthalmic exam red reflex
-back of the eye vessels
-not seen with cataracts
-retina blastoma
cataracts etiology
-occur with aging
-painless
-other risk factors
-trauma
-smoking
-alcohol
-exposure to x-rays
-heat from infrared exposure
-systemic disease (diabetes)
-uveitis
-corticosteroids
-chronic ultraviolet (UV) exposure possibly
-congenital- associated with numerous syndromes and diseases
early symptoms of cataracts
-loss of contrast
-glare
-needing more light to see well
-problems distinguishing dark blue from black
later symptoms of cataracts
-progressive
-painlessty
-blurring of vision
-cataract can swell occluding drainage- secondary closed-angle glaucoma and pain (rare)
types of cataracts
-degree of blurring depends on location and extent of opacity
-nuclear cataract:*
-central lens nucleus
-myopia may develop in early stages, changing the refractive index of the lens so that presbyopic pt may be temporarily able to read without glasses (Second sight)
-posterior subcapsular cataract:*
-cataract beneath the posterior lens capsule
-reduces visual acuity more when the pupil constricts (in bright light or during reading)
-most likely to produce glare
-loss of contrast
cataracts diagnosis
-Best with the pupil dilated
-Well-developed cataracts
-Gray or yellow-brown opacities in the lens
-Examination of the red reflex through the dilated pupil discloses subtle opacities
-Small cataracts
-Stand out as dark defects in the red reflex
-A large cataract may obliterate the red reflex
-Slit-lamp examination provides more details about the character, location, and extent of the opacity
cataracts prevention and treatment
-UV coated eyeglasses or sunglasses
-reducing risk factors
-frequent refractions and corrective lens prescription changes- helps maintain useful vision
-indirect lighting- optimizes vision
-polarized lenses- decrease glare
-indications for surgery:
-maximally corrected vision < 20/40 (<6/12)
-vision that is subjectively limiting, preventing needed or desired activities (driving, reading, other occupational activities)
retinal detachement
-Posterior vitreous detachment -With age, the vitreous gel collapses and detaches from the retina
-when the vitreous membrane pulls on and creates a tear in the retina
-Vitreous fluid seeps into or underneath the retina
-Detachment occurs from the pigmented epithelium underneath
-Shower of floaters - These are thousands of blood cells being liberated from a tiny blood vessel which has been broken due to the tear (“shower of pepper”)
-Descent of a “web” or “veil” in front of the eye or in the periphery
-Permanent vision loss can result
-Detachment needs to be repaired as soon as possible- Argon laser or “cryotherapy”
age-related macular disease (ARMD)
-Macular degeneration
-Leading cause of irreversible blindness in the western world (>65)
-Debris from light-absorbent molecules accumulates in cells in the back of the eye
-Central part of the retina damaged; jeopardizing vision
-Eventually unable to: Read, drive a car and even recognize familiar faces
-AMD most common in later life
-Now an increasing number of younger people are developing it
wet and dry macular degeneration
-“Dry” macular degeneration - caused by a thinning of the macula’s layers, and vision loss typically is gradual
-“Wet” macular degeneration:
-Tiny, fragile blood vessels develop underneath the macula
-Results when these blood vessels hemorrhage, and destroy macular tissue
-Vision loss can be rapid—over months or even weeks
macular degeneration
-Earliest symptom - persistent blurred vision
-Objects become distorted (straight lines become crooked)
-Eventually, a small blind spot in the central visual field can develop and grow in size
-This can progress to the point of “doughnut” vision, where people’s faces are unrecognizable when looking directly at them, yet peripheral vision remains unaffected
******
emergently refer
-pts with visual loss not due to refractive error** should be referred to an ophthalmologist if the vision loss is associated with:
-pain
-marked redness
-due to central retinal artery occlusion**
-retinal detachment with good central vision
-giant cell arteritis
urgently refer
-pts should be referred if vision loss* associated with:
-redness
-due to vitreous hemorrhage
-retinal detachment
-retinal vein occlusion
-branch retinal artery occlusion
-diabetic maculopathy
-ischemic optic neuropathy
-optic neuritis
-sudden onset due to macular degeneration
-occurs in association with thyroid eye disease
