Test 1: Emergencies in Eyecare

Question 1

Dr. Kal’s definition of emergency

Answer 1

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

Question 2

office triage policies and protocols

Answer 2

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

Question 3

levels of urgency

Answer 3

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

Question 4

what should be documented

Answer 4

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

Question 5

real ocular emergencies

Answer 5

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)

Question 6

hypertension

Answer 6

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

Question 7

in office management of HTN crisis

Answer 7

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

Question 8

what is GCA

Answer 8

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

Question 9

GCA

Answer 9

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

Question 10

AAION symptoms

Answer 10

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

Question 11

signs of AAION

Answer 11

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

Question 12

age of onset AAION vs NAION

Answer 12

8th decade vs 6th-7th decade

Question 13

gender AAION vs NAION

Answer 13

females > males

females = males

Question 14

associated symptoms AAION vs NAION

Answer 14

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

Question 15

associated systemic conditions AAION vs NAION

Answer 15

polymyalgia rheumatica

diabets, hypertension, hypercholesterolemia, obstructive sleep apnea

Question 16

visual acuity AAION vs NAION

Answer 16

often worse than 20/200

often better than 20/100

Question 17

ophthalmic exam findings AAION vs NAION

Answer 17

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

Question 18

lab evlauation AAION vs NAION

Answer 18

abnormal ESR, CRP

no associated lab abnormalities

Question 19

GCA - associated ophthalmic conditions

Answer 19

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

Question 20

GCA diagnosis

Answer 20

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

Question 21

no perfect tests for GCA

Answer 21

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

Question 22

GCA treatment

Answer 22

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 +)

Question 23

incidence of aneurysm

Answer 23

9/100,00

Question 24

aneurysm

Answer 24

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

Question 25

manifestations of aneurysm

Answer 25

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

Question 26

symptoms of third nerve palsy with pupil involvement

Answer 26

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

Question 27

signs of third nerve palsy with pupil involvement

Answer 27

ptosis eye position down and out dilated, non reactive pupil

Question 28

diagnosis and management of aneurysm

Answer 28

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

Question 29

treatment of aneurysm

Answer 29

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

Question 30

orbital cellulitis

Answer 30

inflammation of the periocular tissues posterior to the orbital septum

Question 31

etiology of orbital cellulitis

Answer 31

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

Question 32

incidence of orbital cellulitis

Answer 32

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

Question 33

pathway of orbital cellulitis infection

Answer 33

``` 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 ```

Question 34

symptoms of orbital cellulitis

Answer 34

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

Question 35

signs of orbital cellulitis

Answer 35

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

Question 36

differential diagnosis of orbital cellulitis

Answer 36

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

Question 37

orbital complications of orbital cellulitis

Answer 37

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

Question 38

intracranial complications of orbital cellulitis

Answer 38

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

Question 39

cavernous sinus thrombosis

Answer 39

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

Question 40

diagnosis and management of orbital cellulitis

Answer 40

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

Question 41

additional testing of orbital cellulitis

Answer 41

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

Question 42

treatment of orbital cellulitis

Answer 42

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

Question 43

infectious endophthalmitis

Answer 43

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

Question 44

exogenous endophthalmitis

Answer 44

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

Question 45

endogenous endophthalmitis

Answer 45

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

Question 46

symptoms of endophthalmitis

Answer 46

decreased vision | pain ?

Question 47

signs of endophthalmitis

Answer 47

conjunctival hyperemia intraocular inflammation including hypopon ? eyelid edema corneal edema

Question 48

differential diagnosis of endophthalmitis

Answer 48

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

Question 49

treatment of endophthalmitis post-op cataract patients

Answer 49

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

Question 50

treatment of other endophthalmitis

Answer 50

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)

Question 51

outcomes of endophthalmitis

Answer 51

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

Question 52

primary angle closure

Answer 52

``` anatomical predisposition pupillary block plateau iris thick iris/peripheral roll lens induced aqueous misdirection ```

Question 53

secondary angle closure

Answer 53

``` pathological conditions neovascularization peripheral synechia inflammation medications (topical or systemic) ```

Question 54

risk factors of angle closure

Answer 54

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

Question 55

mechanism of pupillary block angle closure

Answer 55

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

Question 56

symptoms of angle closure

Answer 56

``` pain blurred vision halos/rainbows around lights frontal/temporal headache nausea/vomiting ```

Question 57

signs of angle closure

Answer 57

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

Question 58

treatment and management of angle closure

Answer 58

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

Question 59

other forms of acute angle closure

Answer 59

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

Question 60

outcome of angle closure

Answer 60

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