Test 1: Emergencies in Eyecare Flashcards
Dr. Kal’s definition of emergency
conditions that could result in loss of life or function, loss of vision, permanent structural damage to the eye or visual system
office triage policies and protocols
providers are responsible for all info communicated to patients
create office policies and protocols regarding who has authority to triage patient complaints
train your staff
document, document, document
when in doubt - see the patient
levels of urgency
immediate - within 1 or 2 hours
urgent - within 24 hours
semi-urgent - within a week
routine - within 3-6 months
what should be documented
the patients name, date of birth
time and date of call
brief synopsis of patient’s complaint, recommendations made by doctor or staff and the action the patient took
real ocular emergencies
GCA aneurysm - third nerve palsy, pupil involved orbital cellulitis endophthalmitis acute angle closure hypertensive crisis painful horner's syndrome trauma microbial keratitis retinal detachment (mac on)
hypertension
normal below 120/80
prehypertension - 120-139/80-89
hypertension - 140+/90+
hypertensive urgency 180/110+ - call doctor while patient is in room
hypertensive emergency - 180/120+ - call 911
in office management of HTN crisis
have a written policy and follow it plan ahead call PCP? call 911? send to ER?
what is GCA
the most common vasculitis in adults over age 50
granulomatous multinucleate inflammation of medium and large blood vessels, particularly in temporal, ophthalmic and short posterior ciliary arteries
the inner vessel walls (intima and media) expands and occludes the vessel which leads to choroidal ischemia or ischemic optic neuropathy
GCA
incidence 1/150,000 over 60, increased to 44/100,000 over 90
mean age 70s
more common in caucasian, then black, hispanic, or asian
50% of patients with GCA will have some vision symptoms
a study estimates that one out of five patients diagnosed with GCA will develop monocular vision loss due to AAION with more than 1/3 experiencing one or more episodes of transient vision loss prior to event
if left untreated, ~50% will lose vision in the other eye within days to weeks
AAION symptoms
sudden painless loss of vision patient 55 years or older headache jaw claudication scalp tenderness tender, nonpulsatile temporal artery muscle/joint pain fever anorexia
signs of AAION
vision loss - usually 20/200 or worse
APD
pale, swollen optic nerve with flame shaped disc hemorrhage
late stage - optic atrophy and cupping
age of onset AAION vs NAION
8th decade vs 6th-7th decade
gender AAION vs NAION
females > males
females = males
associated symptoms AAION vs NAION
jaw claudication, headache, scalp tenderness, myalgia, constitutional symptoms
<10% mild pain
associated systemic conditions AAION vs NAION
polymyalgia rheumatica
diabets, hypertension, hypercholesterolemia, obstructive sleep apnea
visual acuity AAION vs NAION
often worse than 20/200
often better than 20/100
ophthalmic exam findings AAION vs NAION
- pallid, diffuse optic nerve edema, 2. retinal ischemia, 3. cotton wool spots
- hyperemic, segmental optic nerve edema, 2. small cup less disc in fellow eye
lab evlauation AAION vs NAION
abnormal ESR, CRP
no associated lab abnormalities
GCA - associated ophthalmic conditions
AAION 81% CRAO 14% amaurosis fugax 30% choroidal ischemia (CWS) <5% posterior ischemic optic neuroapthy 7% isolated EOM (usually CN 6) <5% if left untreated 90% will suffer vision loss in other eye in 1 day to 4 months
GCA diagnosis
lab tests and clinical findings
treatment should be started urgently based on clinical findings
lab testing - STAT ESR, CRP
temporal artery biopsies - skip lesions
age 50 or over, ESR over 50 mm first hour, superficial temporal artery tenderness, temporal HA, positive histology of temporal artery biopsy
no perfect tests for GCA
15-30% of patients with positive temporal artery biopsies have a normal ESR
biopsy of temporal artery carries a significant false negative rate 5-9% due to skip lesions
patients that present with an AAION and have other risk factors included in ACR 5 point test should be treated promptly
GCA treatment
patient will be hospitalized
usually under care of rheumatologist or internist
started on IV steroids
temporal artery biopsy performed while hospitalized (within 1 week of starting steroids)
oral steroids continued until symptoms improve and ESR normalizes (6-12 mos +)
incidence of aneurysm
9/100,00
aneurysm
majority of intracranial aneurysms develop on the carotid artery trunk including posterior communicating artery, ophthalmic artery, cavernous sinus
rupture of intracranial aneurysm peaks in 6th and 7th decade
rupture of PCOM aneurysm 85%
if pupil is involved it means the aneurysm is very large and ready to rupture
manifestations of aneurysm
the position of the aneurysm determines the ophthalmic manifestations
PCOM aneurysm is the most likely to cause CN 3 palsy with pupil involvement
three hallmark signs - complete ptosis, the eye is down and out, dilated non reactive pupil
symptoms of third nerve palsy with pupil involvement
diplopia
HA
near blur effected eye ?
glare complaint ? - from blown pupil
signs of third nerve palsy with pupil involvement
ptosis
eye position down and out
dilated, non reactive pupil
diagnosis and management of aneurysm
if the clinical presentation is suggestive of aneurysm the patient should be transported to ER immediately by ambulance
at the ER: head CT, if CT inconclusive consider CT angiography (dye), if CT and angiography are negative LP should be performed
treatment of aneurysm
treatment for PCOM aneurysm includes surgical clipping or placement of a coil
if the aneurysm has ruptured the patients respiration and intracranial pressure are lowered
orbital cellulitis
inflammation of the periocular tissues posterior to the orbital septum
etiology of orbital cellulitis
spread of existing infection: ethmoid sinusitis most common (90% of all infections, all age groups), any periorbital infection (dacryocystitis, ocular adnexa), ear or dental infection
any trauma or surgery that perforates the septum increases risk
incidence of orbital cellulitis
more common in winter months
more common in children than adults
average age of onset in children is between 7-12
twice as common in males
pathway of orbital cellulitis infection
ethmoid bone is thin and has multiple perforations for nerves and blood vessels which allows infection to spread into the periorbital space supporting structures (muscle sheaths, septa, etc) allow for lateral and posterior spread venous drainage via the orbital veins (valveless) is a conduit for anterior and posterior spread
symptoms of orbital cellulitis
red eye with swollen lids blurred vision pain on eye movement diplopia recent URI, sinus or dental infection fever headache
signs of orbital cellulitis
eyelid edema and erythema
conj injection and chemosis
proptosis
severe cases - APD, retinal venous congestion, disc edema, elevated IOP, purulent discharge
differential diagnosis of orbital cellulitis
preseptal cellulitis - red swollen tender lid, no change in vision, no proptosis, no restriction of EOMs, no mild conj injection
orbital mass - slow growing, usually painless
not a complete list
orbital complications of orbital cellulitis
subperiorbital or orbital abscess formation may occur 7-9%
permanently reduced vision 11% of all cases - corneal damage secondary to exposure or neurotrophic keratitis, destruction of intraocular tissues, secondary glaucoma, optic neuritis, CRAO
blindness can occur with elevated IOP (extended) or direct infection of the ON
intracranial complications of orbital cellulitis
meningitis 2%
cavernous sinus thrombosis 1%
intracranial, epidural or subdural abscess
cavernous sinus thrombosis
a blood clot in the cavernous sinus
most common cause is spreading infection
up to 30% mortality rate
watch for rapid progression of clinical signs ie. increasing proptosis, mydriasis, decreasing VA, development of an APD
diagnosis and management of orbital cellulitis
careful clinical exam - critical signs of restricted EOM, blurred vision, proptosis
check vitals (fever?), mental status
neck flexibility
if orbital cellulitis is suspected send to the ER
additional testing of orbital cellulitis
confirmatory diagnosis will be made with CT/MRI of orbits and sinuses, blood cultures and CBC
ER will order consult neuro, ENT, infectious disease
treatment of orbital cellulitis
these are critically ill patients
broad spectrum IV antibiotics for up to 72 hours
orbital decompression surgery might be indicated
abscesses might need to be surgically drained
up to 14 days often needed to treat infections
infectious endophthalmitis
infiltration of intraocular structures by an infectious agent with associated inflammatory reaction involving anterior and/or posterior segments of the eye
exogenous endophthalmitis
penetrating ocular surgeries - cataract surgery, glaucoma surgery (blebs), vitreoretinal surgery (vitrectomy), corneal surgery (PKP)
intravitreal injections
microbial corneal infections
endogenous endophthalmitis
blood born bacteria, fungus or parasite localizes in the eye
IV drug users, in dwelling catheters, endocarditis
symptoms of endophthalmitis
decreased vision
pain ?
signs of endophthalmitis
conjunctival hyperemia
intraocular inflammation including hypopon ?
eyelid edema
corneal edema
differential diagnosis of endophthalmitis
toxic anterior segment syndrome (TASS) - occurs 12-24 hours post-op, severe corneal edema, significant AC reaction (hypopyon possible)
post-op inflammation - vision is stable, mild to no pain, mild inflammation, responds well to topical steroid
retained lens material - severe, granulomatous inflammation with mutton fat KPs
treatment of endophthalmitis post-op cataract patients
the endophthalmitis vitrectomy study (mid 90s)
patients presenting with light perception only vision should have immediate vitrectomy
patients presenting with better than light perception vision don’t need immediate vitrectomy
systemic antibiotics considered, IV antibiotics not needed
treatment of other endophthalmitis
determine etiology through culture and gram staining - anterior chamber paracentesis, vitreous aspirate, pars plana vitrectomy
treatment depends on underlying cause but usually includes intravitreal injections, vitrectomy, systemic medication (oral or IV)
outcomes of endophthalmitis
outcome dependent on underlying cause, virulence of organism
visual outcome ranges from 20/100 to NLP
visual outcomes are usually worse when: endophthalmitis develops within 2 days of surgery, presents with vision of light perception or worse, with APD, concurrent with diabetes
enucleation needed rarely
primary angle closure
anatomical predisposition pupillary block plateau iris thick iris/peripheral roll lens induced aqueous misdirection
secondary angle closure
pathological conditions neovascularization peripheral synechia inflammation medications (topical or systemic)
risk factors of angle closure
hyperopia shallow anterior chamber short axial length thick lens family history asian (chinese) or inuit increased age female
mechanism of pupillary block angle closure
contact between the iris and lens at the pupil blocks the flow of aqueous from the PC to AC
pressure increases in the PC and pushes the iris anteriorly
the iris bows forward causing iridotrabecular apposition and angle closure
highest risk during mid-dilation
symptoms of angle closure
pain blurred vision halos/rainbows around lights frontal/temporal headache nausea/vomiting
signs of angle closure
closed angle in painful eye very high IOP corneal edema conjunctival injection fixed, mid-dilated pupil narrow angle in fellow eye
treatment and management of angle closure
start topical medications: three rounds separated by 15 min: beta blockers, alpha-2 agonists, prostaglandin analogs, CAI
perform indentation gonioscopy to attempt to break the attack
cautious use of acetazolamide 500 mg
recheck IOP and VA after one hour: repeat topical meds if IOP is not down
PI should be scheduled stat if cornea is clear enough
other forms of acute angle closure
treatment for other forms of angle closure vary widely based on etiology
urgent consultation with surgeon (if post-op) or glaucoma specialist is recommended
outcome of angle closure
dependent on duration from onset to treatment and underlying cause
IOP elevation has been shown to have less impact on future VA
as many as 2/3 of patients treated for AACG has no VF loss
chinese patients tend to have progressive disease
