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OPTM 737 > Test 1: Emergencies in Eyecare > Flashcards

Test 1: Emergencies in Eyecare Flashcards

1
Q

Dr. Kal’s definition of emergency

A

conditions that could result in loss of life or function, loss of vision, permanent structural damage to the eye or visual system

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2
Q

office triage policies and protocols

A

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

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3
Q

levels of urgency

A

immediate - within 1 or 2 hours
urgent - within 24 hours
semi-urgent - within a week
routine - within 3-6 months

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4
Q

what should be documented

A

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

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5
Q

real ocular emergencies

A 
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)
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6
Q

hypertension

A

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

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7
Q

in office management of HTN crisis

A 
have a written policy and follow it 
plan ahead 
call PCP?
call 911?
send to ER?
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8
Q

what is GCA

A

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

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9
Q

GCA

A

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

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10
Q

AAION symptoms

A 
sudden painless loss of vision 
patient 55 years or older
headache 
jaw claudication 
scalp tenderness 
tender, nonpulsatile temporal artery 
muscle/joint pain 
fever
anorexia
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11
Q

signs of AAION

A

vision loss - usually 20/200 or worse
APD
pale, swollen optic nerve with flame shaped disc hemorrhage
late stage - optic atrophy and cupping

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12
Q

age of onset AAION vs NAION

A

8th decade vs 6th-7th decade

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13
Q

gender AAION vs NAION

A

females > males

females = males

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14
Q

associated symptoms AAION vs NAION

A

jaw claudication, headache, scalp tenderness, myalgia, constitutional symptoms
<10% mild pain

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15
Q

associated systemic conditions AAION vs NAION

A

polymyalgia rheumatica

diabets, hypertension, hypercholesterolemia, obstructive sleep apnea

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16
Q

visual acuity AAION vs NAION

A

often worse than 20/200

often better than 20/100

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17
Q

ophthalmic exam findings AAION vs NAION

A
  1. pallid, diffuse optic nerve edema, 2. retinal ischemia, 3. cotton wool spots
  2. hyperemic, segmental optic nerve edema, 2. small cup less disc in fellow eye
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18
Q

lab evlauation AAION vs NAION

A

abnormal ESR, CRP

no associated lab abnormalities

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19
Q

GCA - associated ophthalmic conditions

A 
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
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20
Q

GCA diagnosis

A

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

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21
Q

no perfect tests for GCA

A

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

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22
Q

GCA treatment

A

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 +)

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23
Q

incidence of aneurysm

A

9/100,00

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24
Q

aneurysm

A

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

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25
Q

manifestations of aneurysm

A

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

26
Q

symptoms of third nerve palsy with pupil involvement

A

diplopia
HA
near blur effected eye ?
glare complaint ? - from blown pupil

27
Q

signs of third nerve palsy with pupil involvement

A

ptosis
eye position down and out
dilated, non reactive pupil

28
Q

diagnosis and management of aneurysm

A

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

29
Q

treatment of aneurysm

A

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

30
Q

orbital cellulitis

A

inflammation of the periocular tissues posterior to the orbital septum

31
Q

etiology of orbital cellulitis

A

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

32
Q

incidence of orbital cellulitis

A

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

33
Q

pathway of orbital cellulitis infection

A 
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
34
Q

symptoms of orbital cellulitis

A 
red eye with swollen lids
blurred vision 
pain on eye movement 
diplopia 
recent URI, sinus or dental infection 
fever
headache
35
Q

signs of orbital cellulitis

A

eyelid edema and erythema
conj injection and chemosis
proptosis
severe cases - APD, retinal venous congestion, disc edema, elevated IOP, purulent discharge

36
Q

differential diagnosis of orbital cellulitis

A

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

37
Q

orbital complications of orbital cellulitis

A

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

38
Q

intracranial complications of orbital cellulitis

A

meningitis 2%
cavernous sinus thrombosis 1%
intracranial, epidural or subdural abscess

39
Q

cavernous sinus thrombosis

A

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

40
Q

diagnosis and management of orbital cellulitis

A

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

41
Q

additional testing of orbital cellulitis

A

confirmatory diagnosis will be made with CT/MRI of orbits and sinuses, blood cultures and CBC
ER will order consult neuro, ENT, infectious disease

42
Q

treatment of orbital cellulitis

A

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

43
Q

infectious endophthalmitis

A

infiltration of intraocular structures by an infectious agent with associated inflammatory reaction involving anterior and/or posterior segments of the eye

44
Q

exogenous endophthalmitis

A

penetrating ocular surgeries - cataract surgery, glaucoma surgery (blebs), vitreoretinal surgery (vitrectomy), corneal surgery (PKP)
intravitreal injections
microbial corneal infections

45
Q

endogenous endophthalmitis

A

blood born bacteria, fungus or parasite localizes in the eye
IV drug users, in dwelling catheters, endocarditis

46
Q

symptoms of endophthalmitis

A

decreased vision

pain ?

47
Q

signs of endophthalmitis

A

conjunctival hyperemia
intraocular inflammation including hypopon ?
eyelid edema
corneal edema

48
Q

differential diagnosis of endophthalmitis

A

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

49
Q

treatment of endophthalmitis post-op cataract patients

A

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

50
Q

treatment of other endophthalmitis

A

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)

51
Q

outcomes of endophthalmitis

A

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

52
Q

primary angle closure

A 
anatomical predisposition 
pupillary block 
plateau iris 
thick iris/peripheral roll 
lens induced 
aqueous misdirection
53
Q

secondary angle closure

A 
pathological conditions 
neovascularization 
peripheral synechia 
inflammation 
medications (topical or systemic)
54
Q

risk factors of angle closure

A 
hyperopia 
shallow anterior chamber 
short axial length 
thick lens
family history 
asian (chinese) or inuit 
increased age 
female
55
Q

mechanism of pupillary block angle closure

A

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

56
Q

symptoms of angle closure

A 
pain
blurred vision 
halos/rainbows around lights 
frontal/temporal headache 
nausea/vomiting
57
Q

signs of angle closure

A 
closed angle in painful eye 
very high IOP
corneal edema 
conjunctival injection 
fixed, mid-dilated pupil 
narrow angle in fellow eye
58
Q

treatment and management of angle closure

A

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

59
Q

other forms of acute angle closure

A

treatment for other forms of angle closure vary widely based on etiology
urgent consultation with surgeon (if post-op) or glaucoma specialist is recommended

60
Q

outcome of angle closure

A

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

OPTM 737 (6 decks)

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