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other corneal and conjunctiva infections and inflammations


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what is the causitive organism for chlamydial infections
chlamydia trachomatis ; an obligate intracellular parasite that is a genus of its own
does chlamydia have viral or bacterial characteristics
it has both viral and bacterial characterisitics
what is the most common STD in the US
what are the two forms of chlamydia
adult inclusion conjunctivitis and trachoma
what is the most common form of chlamydial infections in the industrialized world
inclusion conjuctivitis
how does a person get adult inclusion conjunctivitis
from sexual exposure
s/s of adult inclusion conjunctivitis
acute follicular and papillary conjunctivitis with scant mucopurulent discharge; nonsymptomatic genitally; PAN
what is the incubation period of inclusion conjunctivitis
5-12 days
what may inclusion conjunctivitis mimic
EKC with SEI's
which conjunctiva is more infected
the lower palpebral conj more infected as oppose to trachoma
what does cytology studies reveal
monocytes and neutrophils
what prompts suspecion of chlamydia
red eyes non-responsive to standard therapy
treatment for chlamydia
azithromycin 1g QD(once a day) x 1 dose
alternate treatment for chlamydia
doxycycline 100mg BID 1st day , then 100 mg QD x 21 days
in patients who are allergic use what
tetracycline 250 mg QID x 21 days; erythromycin 500mg QID x 21 days; do not use doxycycline or tetracycline in children under 8 years old or in pregnant or lactating mothers
what is the most common form of chlamydia in underdeveloped countries and rarely in the US (in southwest among native americans)
how is trachoma transferred
from eye to eye via fly infestation
what is the most common cause of preventable blindness or decreased vision in the world
which conjunctiva is more infected in trachoma
upper and lower palpebral and limbal follicles and papillae
s/s of trachoma
photophobia, tearing, mild mucopurulent discharge (secondary bacterial infection)
what are ARLT's line
they represent superior tarsal conjunctiva scarring and leads to entropion, trichiasis, and mucin-deficient dry eye from goblet cell destruction
punctal stenosis and trachoma
this is possible secondary to scarring but is rarely enough to combat the induced dry eye symptoms
what are herbert's pitts
a sign of trachoma, scarred limbal follicles -- small depressions around limbus -- diagnostic of trachoma
main diagnostic signs of trachoma
ARLT's line, Herbert's pitts, superior SPK, pannu, edema, punctal stenosis, entropion, trichiasis, mucin deficient dry eye,
stage 1 of trachoma
immature follicles on superior tarsus with minimal papillary hypertrophy, may see SPK or pannus
stage 2 of trachoma
follicular hypertrophy, limbal follicles, pannus, and corneal SEI's, Papillary hypertrophy, intensification of inflammatory response with obliteration of follicles by papillae, necrosis of follicles
stage 3 of trachoma
cicatrizing trachoma; ARLT's line, Herbert's pits, entropion and trichiasis may form
stage 4 trachoma
healed trachoma; inflammation has resolved and is replaced by scar tissue; no follicles or papillae; no SEI's; corneal involvement in the form of secondary bacterial keratitis may lead to blindness and results from corneal insult from trichiasis and scarring
treatment of trachoma
zithromax 1g QD x 1 dose; doxycycline 100mg BID for 1st day then 100 mg QD for 21 days; tetracycline 250 mg QID x 21 days, erythromycin 500 mg QID x 21 days
Toxic and Irritative Follicular Conjunctivitis causes
caused by long term use of certain ocular medications, heavy makeup use, environmental irritants, radiation, soaps, etc.
which type of medication mostly causes toxic and irritative follicular conjunctivitis
strong miotics
toxic and irritative follicular conjunctivitis etiology
may be due to toxic protein reaction or from hypersensitivity reaction
s/s of toxic and irritative follicular conjunctivitis
minimal mixed papillae and follicles; unilateral
treatment for toxic and irritative follicular conjunctivitis
switch ocular medications when possible, encourage better hygiene in heavy makeup users, remove irritants where possible, artificial tears for supportive therapy
s/s of superior limbic keratoconjunctivitis
chronic and recurrent inflammation of the superior palpebral and bulbar conjunctiva and cornea
course of superior limbic keratoconjunctivitis last for how long
several months to years
etiology of superior limbic keratoconjunctivitis
where is there marked hyperemia in superior limbic keratoconjunctivitis
in superior conjunctival and cornea with irritation
where does the number of goblet cells increase in superior limbic keratoconjunctivitis
palpebral conjunctiva
where does the number of goblet cells decrease in superior limbic keratoconjuctivitis
bulbar conjuctiva
what systemic disease is superior limbic keratoconjunctiva associated with
thyroid disease and dry eye
what is the diagnostic sign for superior limbic keratoconjunctivitis
rose bengal staining of entire area involved
what is the area involved for superior limbic keratoconjuctivitis when using diagnostic sign
bilateral but asymmetrical
symptoms of superior limbic keratoconjucntivits
FBS, photophobia, pain, may have filaments present
Treatment for superior limbic keratoconjunctivitis
Artificial tears, punctal occlusion, pulse of steroids, acetylcysteine (to break up mucus) drops, cromolyn sodium drops, 0.5% silver nitrate, bandage SCL, thermal cautery of conjuctiva, surgical conjunctiva resection (highly successful)
what are the two types of phlyctenulosis
conjunctival and corneal
sign of conjunctival phlyctenulosis
focal nodule of limbal tissue, inflammatory
etiology of conjunctival phlyctenulosis
in respones to staphylococcal exotoxins (staph bleph), less commonly TB (order chest x-ray)
treatment of phlyctenule and staph bleph
staph is almost always present so when treat this the phlyctenule also disappears
treatment of phlyctenule
vasoconstrictors or steroids/antibiotic combination drop if moderate to severe
corneal phlyctenule s/s
appears whitish plaque on the cornea itself; same associations as conjunctival variety
ophthalmia neonatorium
conjunctivitis in a neonate
when might ophthalmia neonatorium occur
3-5 days postpartum (any time within a few weeks after birth is still considered ophthalmia neonatorium
how many newborns are affected with ophthalmia neonatorium
what are the three routes of inoculation of ophthalmia neonatorium
ascending infection from cervix and vagina secondary to a premature membrane rupture; mom has an infection in birth canal; postpartum contact
what are the major organisms that cause ophthalmia neonatorium
s. aureus, s. pneumoniae, s. pyogenes, h. flu, gonococcus, pseudomonas aeruginosa, chlamydia, gonococcal infection
what is the leading agent for infectious neonatal conjunctivitis in the U.S.
sign of ophthalmia neonatorium from chlamydia
papillary response only, no follicular response bcs the lymph system is not fully developed until 4-5 months after birth; a mild to moderate mucopurulent exudate with lid edema, chemosis, and pseudomembrane formation, can cause pneumonitis
which are more common causes of ophthalmia neonatorium bacterial or virus
bacteria are more common causes; viral are less common but HSV can have severe ocular consequences, while CMV also has severe systemic complications
prophylaxis treatment is mandatory in all states what is the treatment
erythromycin 0.5% ung (effective against chlamydia and gonococcus), use to use crede's prophylaxis 1% silver nitrate (effective against gonococcus but causes toxic conjunctivitis)
treatment for ophthalmia neonatorium chlamydia
oral erythromycin 10-14 days
treatment for ophthalmia neonatorium gonococcal
IV cillin drugs x 7-14 days
treatment for ophthalmia neonatorium non-gonococcal
topical bacitracin ung with gentamicin solution 3-4 hours, tapered as response improves
treatment for ophthalmia neonatorium HSV
viroptic 1% drops every 2 hours up to 9 doses max daily taper dose as improvement occurs, continue treatment for a total of 3 weeks
what is neurotrophic keratopathy
loss of innervation to corneal tissue causing epithelial defect
causes of neurotrophic keratopathy
S/P infection by varicella zoster, HSV; stoke, complications of CN V surgery; complication of irradiation to eye or adjacent structure; tumor (acoustic neuroma)
signs of neurotrophic keratopathy
loss or reduction of corneal sensation; epithelial defects with fluorescein staining; perilimbal injection; possible corneal ulcer with associated iritis
how does the ulcer look in neurotrophic keratopathy
gray heaped up border, oval in shape, and is usually located in lower half of cornea
symptoms of neurotrophic keratopathy
red eye, FBS (inspite of reduced corneal sensitivity), swollwen eyelid
workup for neurotrophic keratopathy
careful history with attention on prior infections, injuries, surgeries, test corneal sensation (compare one eye to the other); look for signs of corneal exposure; CT/MRI if tumor is suspected
treatment of neurotrophic keratopathy
if mild lubricants; if corneal defect, treat as if corneal abrasion(antibiotic ung, cycloplege, pressure patch or bandage SCL); if this sterile ulcer becomes secondarily infected now you have a infectious corneal ulcer treat accordingly; tarsorrhaphy; bandage soft CL
describe thermal / UV keratopathy
damage to cornea from thermal burn or UV exposure; symptoms usually appear 8-12 hours following exposure
etiology of thermal/uv keratopathy
UV burns (sun, tanning bed, seen often in skiers, welders)
symptomos of thermal/uv keratopathy
moderate to severe ocular pain, FBS, Red Eyes, Tearing, Photophobia, Blurred vision
signs of thermal/uv keratopathy
confluent SPK in interpalpebral area (from squinting), conjunctival injection, eyelid edema, absence or minimal corneal edema, typically miotic pupils, may present as a droplet keratopathy
what is a droplet keratopathy
yellowish oily deposit in subepithelial cornea and conjuctiva
treatment of thermal / uv keratopathy
treat as if corneal abrasion: bandage SCL for mild cases, bilateral patching in severe cases, NSAIDs topical drops, 800 mg motrin over the counter
Thygeson's Superficial Punctate Keratopathy describe
coarse punctate epithelial keratitis of unknown etiology
s/s of thygeson's disease
photophobia, FBS, Tearing, Faint gray coarse PEK defects, usually round to oval and made up of miniscule opacities, bilateral, quiet white eye, strictly epithelial, no stromal involvement, usually chronic with recurrences for up to 30 years
what does thygeson's disease stain with
PEK stain with rose bengal slightly elevated, if microerosions occur with opacities NaFl stining occurs
treatment of thygeson's disease
weak topical steroids (pred Mild, alrex, FML QID for 3-4 days then quickly tapered); bandage CL and pressure patch ; if pt is contact lens wearer then discontinue CL wear
what is non-herpetic interstitial keratitis
vascularization and infiltration affecting all or part of the corneal stroma
what is non-herpetic interstitial keratitis associated with
systemic disease
major sign seen with non herpetic interstitial keratitis
ghost vessels from previous processes of active inflammatory vascularization are common. They appear as grayish lines or small tubes
most cases of non-herpetic interstitial keratitis is secondary to what
90% of all cases are secondary to congenital or acquired syphillis -- an immunologic reaction to spirochete
is non-herpetic interstitial keratitis associated with congenital syphilis unilateral or bilateral
what age does congenital non-herpetic interstitial keratitis affect
age 5 to late teens
is acquired non-herpetic IK bilateral or unilaterla
which is usually a mild case of non-herpetic IK
aquired syphilis usually casues a mild and easier to treat conditionof non herpetic interstial keratitis
what is the other cause of non-herpetic IK other than syphillis
Tuberculosis makes up the majority of non-syphilitic cases -- it is an autoimmune reaction to tuberculin protein
s/s of non herpetic IK in syphillitic cases
during acute phase show infiltration, edema of endothelium, KP's, miosis, and small stromal opacities; most cases will be residual effects --diffuse stromal scarring, opacification, ghost vessels
s/s of non herpetic IK in TB
cornea is typically involved in peripheral inferior sector only and is ring-shaped
Treatmento f non-herpetic interstitial keratitis
keratoplasty if vision is impaired, in active IK steroids suppress inflammation and may be necessary for 1 to 2 years ; also cycloplege; id and treat systemic infection
what is ocular cicatricial pemphigoid
a chronic autoimmune disease characterized by scarring of the mucous membranes (conjuctiva, soft palate, nasal mucosa, genito-urinary system esophagus,etc.) and skin
what is the average age of onset for ocular cicatricial pemphigoid
65 years old and females get it more than males
what is the initial sign of ocular cicatricial pemphigoid
chronic recurrent unilateral conjunctivitis
stage 1 of ocular cicatricial pemphigoid
subepithelial fibrosis
stage 2 of ocular cicatricial pemphigoid
fornix foreshortening
stage 3 of ocular cicatricial pemphigoid
symblepharon: adhesion of palpebral and bulbar conunctivia
stage 4 of ocular cicatricial pemphigoid
ankyloblepharon and surface keratinization: eyelid skin attaches to conjunctiva
what is a late finding in the disease process of ocular cicatricial pemphigoid
dry eye syndrome
why is vision lost in ocular cicatricial pemphigoid
vision is lost due to keratopathy, corneal neovascularization, and corneal ulceration and scarring
what is the histopathology of ocular cicatricial pemphigoid
submucosal scarring, chronic inflammation, perivasculitis, ans squamous metaplasia of the epithelium, with loss of goblet cells
what does natural history of ocular cicatricial pemphigoid show
periods of exacerbationand remission, sometimes quite profound
what does a firm diagnosis require for ocular cicatricial pemphigoid
immunohistochemical confirmation prior to initiating treatment
CP dry eye is treated with what?
non-preserved artificial tear dorps and ungs
what is used for CP blepharitis and meibomianitis
this is treated aggressively with lid hygiene, oral doxycline, topical antibiotics as necessary
CP treatment
topical retinoid ung (vitamin A) if benefit after monocular trial
CP treatment for cases that are active and rapidly progressive
prednisone 1 mg/kg/day, eventually tapered over a period of 8-16 weeks; cyclophosphamide 2 mg/kg/day, adjusted based on response
CP treatment for cases that are not rapidly progressive and less active
prednisone 1mg/kg/day, tapering as responds; dapsone 1mg/kg/day, not exceeding 200 mg/day
CP treatment if all esle fails
methotrexate; azathioprine
why should the patient with CP be managed by someone who is experienced in this area
to check for drug toxicity and tolerance
another name for Steven Johnson Syndrome is what?
erythema multiform
etiology of steven johnson
S-J syndrome occurs idiosyndratically in some patients, and is seen as mucosal inflammation in response to the administration of various drugs or following systemic infectious disease
what can steven johnson syndrome appear similar to
a disease that can appear clinically similar to ocular cicatricial pemphingoid, but is not the relentless, progressive disease that OCP is.
s/s of acute phase of steven johnson
the patient may appear to have a severe pseudomembranous conjunctiva; following resolution fibrosis of the conjunctiva with associated entropion and trichiasis may be present
steven johnson is associatied with what other disease
patients who develop S-J syndrome may have a predisposition to autoimmune disease
treatment of S-J
treat aggressively with topical anti-inflammatory agents
common associationed diseases with S-J
ocular rosacea, psoriasis, connective tissue disease
ocular rosacea S-J s/s
general increase in lipid secretions; hyperemia of lid margins, FBS, BURNING, recurrent chalazia
treatment of ocular rosacea S-J
oral doxycycline 100 mg BID first day, then 50-100 mg QD thereafter for 21 days; Or Tetracycline 250 mg QID; or retinoic acid
psoriasis S-J affects which age group mostly
28 yrs old
psoriasis S-J s/s
hyperproliferation of keratinocytes in the epidermis. conjunctiva usually shows non-specific inflammation, chronic in nature and is associated with eyelid margin involvement; bleph can take the form of redness, edema, and skin plaques
why is psoriasis S-J confused with phlyctenules
the plaques seen in this disorder can extend onto the conjunctiva and cause scarring which can be confused with phylctenulosis
treatment of psoriasis S-J
supportive in conjunctiva with systemic treatment for psoriasis
connective tissue disease S-J etiology
usually thought to have and autoimmune etiology
what are the different connective tissue diseases
systemic lupus erythematosis, polyarteritis nodosa, relapsing polychondritis, reiter's syndrome and others(rheumatoid arthritis, scleroderma, dermatomyositis, rheumatic fever, thrombotic thrombocytopenic purpura (non specific conjunctival findings treat supportively)
systemic lupus erythematosis s/s
3rd -4th decade females more than males butterfly rash on face, non-specific conjunctiva (hyperemia, fine papillae)
systemic lupus erythematosis treatment
treat conjunctiva supportively, systemic treatment is with aspirin, chloroquine, steroids
polyarteritis nodosa s/s
arteritis of small and medium vessels from severe hypersensitivity; many systemic findingw with non-specific conjunctivitis (may see subconjunctival hemorrhages) males greater than females
polyarteritis nodosa treatment
treat supportively systemic condition with steroids
relapsing polychondritis s/s
recurrent inflammation of cartilage seen in 3rd-6th decades. Females equal to males. mild conjuctivitis, more often episcleritis.
relapsing polychondritis treatment
treat supportively, systemic with steroids
reiter's syndrome s/s
triad of nongonococcal conjunctivitis, urethritis, arthritis. May be associated with chlamydia infection 90% of patients are male. Mild nonspecific conjunctival findings
treatment of reiter's syndrome
oral tetracycline, steroids for systemic findings
treatment for non-specific conjunctival findings
treat supportively
which problem causes for a laboratory analysis to reach appropriate diagnosis and appropriate management plan
infectious conjunctivitis or keratitis
what does bacteriology use
gram stain
how can same day analysis be done
using gram stain of any discharge or purulent material present.
same day analysis is enough information for what
to select appropriate initial treatment based on whether the organism is gram positive or negative or possibly fungal
why is a culture done
if there is only scant discharge available at the time of examination and a gram stain would be non-productive or is inconclusive.
how is the culture done
This procedure is analogus to the throat culture in that the conjunctival lid margin or corneal tissues are swabbed or scraped and then the mateial is inoculated ont a petri dish or into a curture broth. 24-48 hrs later the bacteria grown are gram-stained
why do a sensitivity test
to see how effective a cetain antibiotic is for your specific patient's bug
how is the sensitivity test done
the organism isolated from your patient's culture is grown onto a petri dish surface then several antibiotic laden paper disc are placed onto the grown bacteria. After reincubation the antibiotic with the largest kill zone surrounding it is presumably the most effective antibiotic for your specific patient's bugs
why are cytology studies done
to analyze the patient's cellular response to the infection or inflammation.
what is cytology not a study of
it is not an analysis of the organism responsible for the condition
how is cytology done
cells are removed by various different means and then analyzed microscopically. Based on the patient's cellular response you can reasonably predict what category of disease you are dealing with
PMN's predicts what
bacterial infections
Lymphocytes predicts what
viral infections
Eosinophils and Basophils are predominant in what type of disorder
allergic disorders

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