Posterior segment of eye (Vitreous and Retina

Vitreous hemorrhage presentation

sudden vision loss, abrupt onset of floaters (may progress in severity), complaint of "bleeding in eye", NO redness or inflammation

Vitreous hemorrhage etiology/pathophys

retinal tear +/- detachment, diabetic retinopathy, sickle cell retinopathy, retinal vein occlusion, retinal vasculitis, retinal arterial macroaneurysm, blood dyscrasia, therapeutic anticoag, trauma, subarachnoid hemorrhage, valvsalva

Vitreous hemorrhage dx

reduced acuity in affected eye, pupils and EOM unaffected, white and quiet eye, unable to see optic nerve head on DO or see focal area of blood, can only see light

Vitreous hemorrhage tx

referred urgently to ophthalmologist (retinal specialist is best)

retinal detachment must be repaired ASAP to prevent blindnesss

Retinal detachment presentation

rapid loss of vision in one eye +/- "curtain" spreading across vision

possible peripheral loss of vision and extends to central

can only see light

complaint of floaters/webs and flashing lights

Retinal detachment etiology/pathophys

due to 1 or more peripheral retinal tears or holes --> PVD (degenerative vitreous changes >50 yo), myopia or cataracts, trauma

retinal break allows for invasion of vitreous fluid and separates retina

Tractional RD

pre-retinal fibrosis secondary to proliferative retinal disease

-VEGF mediated

-assoc with proliferative diabetic retinopathy, central retinal vein occlusion, complications from rhegmatogenous RD

Exudative RD

Cause by accumulation of subretinal fluid

-choroidal neovascular membrane, choroidal tumor

Retinal detachment dx

retinal may be elevated and have an irregular surface on exam

ocular ultrasonography assists in the detection and characterization of RD

Rhegmatogenous RD dx

retinal tears/holes on scleral depression

Tractional RD dx

irregular retinal tissue adherent to scare tissue on the retinal surface sometimes extending into the vitreous

Exudative RD dx

Dome shaped and subretinal fluid shifts position with changes to posture

Retinal detachment tx: Rhegmatogenous

closing tears/holes by forming permanent adhesion with laser photocoagulation to retina or cryo to sclera

Retinal detachment tx: Tractional

reattachment via vitrectomy, direct manipulation of retina and internal tamponade of retina with air, expansible gas or silicone oil

Retinal detachment tx: Exudative

dependent on etiology

retinal detachment management

Good central vision: emergent

All RD: urgent to retinal specialist

Central retinal artery occlusion presentation

sudden monocular vision loss, no pain or redness in eye

Central retinal artery occlusion etiology/pathophys

Pt > 50 yo: consider giant cell arteritis

cardiac or carotid emboli --> lodges --> cannot profuse retina

Diabetes HTN, hyperlipidemia

Younger pt: migraines, oral birth control, systemic vasculitis, thrombopilia, hyperhomocysteinemia

Branch retinal artery occlusion presentation

sudden monocular vision loss in one sector of the visual field

no pain or redness in eye

Branch retinal artery occlusion etiology/pathophys

cardiac or carotid thrombi --> lodge --> cannot profuse retina

Diabetes HTN, hyperlipidemia

Younger pt: migraines, oral birth control, systemic vasculitis, thrombopilia, hyperhomocysteinemia

Central retinal artery occlusion dx

reduced acuity to counting fingers

+APD in affected eye

white and quiet eye

diffuse retinal whitening (ischemia) with a cherry red spot at macula

+/- emboli in artery, varying perfusion

Branch retinal artery occlusion dx

sudden loss of vision on acuity if macula is involved or loss of discrete field

white and quiet eye

sectoral retinal whitening (ischemic)

+/- emboli

Retinal arterial occlusion systemic evaluation

Identify cardiac sources of emboli (a fib? cardiac valvular dx?)

Check BP

Hematology: Diabetes, hyperlipidemia (Younger: lupus, antiphospholipid antibodies, inherited thrombophilia, elevated plasma homocysteine)

Giant cell arteritis questions to R/O

ipsilateral scalp tenderness, ipsilateral jaw claudication, general malaise, weight loss, sx of polymyalgia rheumatica

tenderness, thickening or loss of pulse in superficial temporal artery

Retinal arterial occlusion imaging

URGENT brain MRI with diffuse weighted imaging (DWI) to R/O cerebral infarction

Duplex sonography or CT or MRI of carotids

ECG and echo

Retinal arterial occlusion tx

Urgent referral to ED for stroke evaluation

ocular massage, high concentration inhaled O2, IV acetazolamide, anterior chamber paracentesis

Giant cell mediated Retinal arterial occlusion tx

IV methylprednisolone 1g/day x 3 days

When doe we see permanent vision loss with retinal arterial occlusion

after 90 minutes

Retinal arterial occlusion: ipsilateral carotid artery stenosis tx

refer to carotid artery endarterectomy or angioplasty with stenting

Retinal arterial occlusion: cardiac dx or hypercoagulable state tx

anticoag meds

Retinal arterial occlusion: cardiac valvular dx or patent foramen ovale tx

surgical intervention

Retinal arterial occlusion management

chronic management by ECP and low vision specialist

Central retinal vein occlusion clinical presentation

sudden monocular vision loss

no pain or redness in eye

widespread retinal hemorrhages, cotton wool spots, macular edema

Central retinal vein occlusion etiology/pathophys

predisposing factors of arteriosclerosis

glaucoma

Branch retinal vein occlusion presentation

sudden vision loss if involving macula or vitreous hemorrhage from neovascularization

Gradual vision loss if development of macular edema

Branch retinal vein occlusion etiology/pathophys

arteriosclerosis

glaucoma

Retinal vein occlusion dx

reduced acuity to counting fingers

+APD in affected eye

eye is white and quiet

Fundus- CRVO: diffuse retinal hemorrhages, cotton wool spots, optic disc swelling BRVO: sectoral retinal hemorrhages, cotton wool spots

Retinal vein occlusion systemic evaluation

Identify reversible risk factors (check BP, smoking?, glaucoma?)

Hematology: diabetes, hyperlipidemia, hyperviscosity (Younger: lupus, antiphospholipid antibodies, inherited thrombophilia, elevated plasma homocysteine)

Retinal vein occlusion tx: macular edema

intravitreal anti-vegf inj

intravitreal steroid inj

retinal vein occlusion tx: retinal neovascularization

pan retinal photocoagulation (PRP) to retinal

intravitreal anti-vegf

Diabetic retinopathy presentation

present in 1/3 of DM pts

MC for tx: diabetic macular edema --> reduced acuity

2 types of diabetic retinopathy

non-proliferative

proliferative (neovascularization) --> vitreous hemorrhage, tractional RD

Diabetic retinopathy etiology/pathophys

damaged vascular endothelial pericytes, retinal capillaries leak protein, lipid and RBC enter retina in macular region

Diabetic retinopathy dx

visual acuity dec

retinal imaging: OCT

Fluorescein angiography of retina: determines neovascularization and areas of the retinal non-perfusion

Diabetic retinopathy tx: diabetes

glycemic control

Diabetic retinopathy tx: diabetic macular edema

Intraveitreal anti-VEGF inj

Diabetic retinopathy tx: non-proliferative diabetic retinopathy

close monitoring with dilated fundus exam

Diabetic retinopathy tx: proliferative diabetic retinopathy

intravitreal anti-vegf inj

panretinal laser photocoagulation

Diabetic retinopathy management

Sudden vision loss: refer emergently

proliferative or macular edema: urgent refer

severe non-proliferative: normal referral

hypertensive retinochoroidopathy presentation

based on degree and rate of rise in BP and state of circulation of the eye

HTN retinopathy can mark current and future non-ocular end-organ damage

hypertensive retinochoroidopathy etiology/pathophys

chronic HTN accelerates development of atherosclerosis

-narrow and develop abnormal light reflexes

-AV nicking --> BRVO

-acute elevations of BP --> loss of autoregulation of circulation --> breakdown and occlusion of precapillary arterioles and capillaries

-optic disc swelling = emergency

HIV retinopathy presentation

-cotton wool spots, retinal hemorrhages, microaneurysms --> decreased contrast sensitivity

-CMV retinitis (CD4 < 50 mcl): enlargening yellowish-white patches of retinal opacification and hemorrhages

HIV retinopathy opportunistic manifestations in AIDS pt

herpes simplex retinitis, acute retinal necrosis, toxoplasmic and candidal chorioretinitis, herpes zoster ophthalmicus, kaposi sarcoma of conjunctiva, orbital lymphoma

HIV retinopathy tx

systemic therapy = greater risk of non-ocular adverse effects but dec in incidence of retinitis in other eye

Age related macular degeneration (ARMD) presentation

retinal drusen --> yellow subretinal deposits

-soft: paler with less distinct margins

-hard: discrete deposits

Decreased or less of central vision with full peripheral field

2 forms of ARMD

Dry: drusen without neovascularization, +/- geographic atrophy in advanced cases

Wet/exudative: retinal neovascularization

ARMD etiology/pathophys

leading cause of permanent vision loss in older population

prevalence progressively inc over 50 yo

Drusen --> chronic outer retinal ischemia --> subretinal neovascularization or retinal atrophy

ARMD RF

females > males

HTN

Hypercholesterolemia

light iris color

smoking

ARMD dx

normal - severely reduced visual acuity

eye is white and quiet

full visual field

look for drusen or blood in macula

ARMD tx: Dry w/o geographic atropy

AREDS 2 Vitamins (preservision) --> reduce progression by 25%

smoking cessation

ARMD tx: Dry w/ geographic atropy

Infravitreal Synfovre (pegcetagoplan) inj

smoking cessation

low vision consultation

ARMD tx: wet/exudative

Anti-VEGF intravitreal inj (often require multiple rounds)

low vision consultation

Optic neuritis presentation

subacute, painful unilateral loss of vision

pain on EOM testing

Optic neuritis etiology/pathophys

inflammatory optic neuropathy is strongly associated with demyelinating disease (multiple sclerosis)

Optic neuritis dx acute presentation

-20/30 vision to no light perception

-central vision loss

-central color loss

-majority normal optic nerve

-minority edematous optic nerve with an occasional flame shaped peripapillary hemorrhage

Optic neuritis dx chronic presentation

-acuity returns to 20/40 within 2-3 weeks following attack

-optic atrophy if there is extensive damage (pale color)

-No known dx of MS and no recovery: MRI of head for periventricular white matter demyelination or compression of optic nerve

Optic neuritis tx

acute demyelinating: methylprednisolone IV followed by PO prednisolone to decrease acceleration

Optic neuritis management

referred emergently to an ECP

What is the prognosis for a dx of MS with first episode of optic neuritis?

MS will develop in 50% within 15 years

What is the likelihood of developing MS without demyelinating lesions on brain seen in MRI?

25%

What is the likelihood of developing MS with demyelinating lesions on brain seen in MRI?

72%

Major risk factors contributing to MS

female

multiple white matter lesions on brain MRI

Non-artheritic ischemic optic neuropathy (NAION) anterior presentation

sudden, painless loss of vision with signs of optic nerve head dysfunction

no other systemic sx

optic disc swelling

NAION anterior etiology/pathophys

inadequate perfusion of the posterior ciliary arteries that supply the anterior portion of the optic nerve

RF: congenitally crowned optic disk --> compromises circulation

NAION posterior presentation

sudden, painless loss of vision with signs of optic nerve head dysfunction

normal appearance of optic nerve

NAION posterior etiology/pathophys

PION involving retrobulbar optic nerve --> no swelling --> blood loss, non-ocular surgery, prolonged lumbar spine surgery in prone position (inc orbital pressure), severe burns, associated with dialysis --> consequence of hypotension and anemia

NAION dx

reduced acuity in affected eye

ipsilateral loss of upper or lower part of the visual field, but not across the horizontal midline (altitudinal)

ipsilateral APD

Assessment: anterior- ipsilateral disc swelling, posterior- optic nerve unaffected, cup-to-disc very small

NAION tx

no proven tx --> urgent referral to ECP

arteritic anterior ischemic optic neuropathy (AAION) presentation

5-10% of anterior ischemic optic neuropathies

>50 yo

rapid onset of unilateral vision loss accompanied by dec visual acuity

H/A, tenderness of temporal artery/scalp, jaw claudication, malaise, loss of appetite, fever

AAION etiology/pathophysiology

inflammation and thrombosis of the short posterior ciliary arteries from ophthalmic artery --> optic nerve head infarction

AAION dx

dec visual acuity (<20/200)

altitudinal defect MC visual field defect

ipsilateral APD

Chalky white pallor of the disc with edema

AAION systemic evaluation

hem: ESR, CRP

bx: superficial temporal artery (gold standard)

imaging: U/S of temporal artery

AAION tx

steroids: IV methylpred, PO pred for months-years

monoclonal abx: tucilzumab PO

Prognosis for AAION without tx

vision loss in 54-95% of patients

b/l involvement is dependent on aggressive steroid tx

AAION management

emergent ED/ECP to prevent b/l involvement

Angle Closure Glaucoma: primary presentation

pre-existing narrow anterior chamber

assoc with hyperopia, advanced cataract, short axial length, genetics, Inuit and Asian decent

precipitated by pupil dilation (dim conditions), anticholinergic drug

rarely pupil dilation

Angle Closure Glaucoma: secondary presentation

Does not require pre-existing narrow anterior chamber angle

Drug-induced, hemodialysis

Angle Closure Glaucoma presentation

extreme pain and blurred vision assoc with halos around lights

+/- nausea and vomiting

eye is red, cornea is cloudy, eye pressure is > 50 mmHg or hard

Pupil in mid-dilated state

Angle Closure Glaucoma dx

slit lamp/gross examination

-assess conjunctiva for redness

-assess cornea to determine if cornea is cloudy

-check IOP/palpate eye and determine is there is asymmetry in pressure

Angle Closure Glaucoma tx

Single dose of 500 mg IV acetazolamide followed by 250 mg QID PO

Topical meds: apraclonidine, timolol

+/- oral glycerin or IV mannitol

Angle Closure Glaucoma tx: primary

laser peripheral iridotomy (LPI): first line

cataract surgery

topical pilocarpine 4%

Angle Closure Glaucoma tx: secondary

D/C drug causing angle closure

Angle Closure Glaucoma management

emergent referral to ECP

Chronic glaucoma presentation

gradually progressive excavation (cupping) of optic disc with associated peripheral vision loss

can lead to complete blindness

intraocular pressure elevated --> reduced drainage through trabecular mesh work --> corneoscleral angle open

usually b/l

Chronic glaucoma RF/etiology

Afro-Caribbean, African American, Latino more frequent at an earlier age with severe damage

trauma

steroid use

pseudoexfoliative material, pigment dispersion

Chronic glaucoma dx

lacks sx and found on routine exam

Optic disc cupping: > 0.5 C/D ratio or difference btwn 0.2 is sus

Visual field abnormalities: initially develop in paracentral region --> peripheral visual field, central vision remains good until late in the disease

intraocular pressure: normal range is 10-21 mmHg

Chronic glaucoma tx

goal: lowering IOP

Topicals: PGAs (first line), beta-blockers, alpha adrenergic agonists, carbonic anhydrase inhibitors, rho-kinase inhibitors

Selective Laser Trabeculoplasty (first line surgery): inc outflow through meshwork

Surgical trabeculectomy: alternate flow of aqueous

MIGS procedure + cataracts in US

Chronic glaucoma management

urgent referral to ECP