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ICM Unit 3 HEENT > Eye Manifestation of Systemic Diseases > Flashcards

Eye Manifestation of Systemic Diseases Flashcards

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1
Q

Uveal tract and sclera

A

Episcleritis, Scleritis, Uveitis

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2
Q

Vascular Disorders

A

Retinal vein occlusion
Retinal artery occlusion - ischemic optic neuropathy
Temporal arteritis

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3
Q

Retinopathy

A

Diabetic retinopathy
Hypertensive retinochoroidopathy (incl optic disc swelling)
HIV: HIV retinopathy and CMV Retinitis
Blood dyscrasias

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4
Q

Neuropathy/Neuritis

A

Optic Neuritis and ischemic optic neuropathy

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5
Q

simple anatomy

A

medial canthus
lateral canthus
eyelids
conjunctiva (bulbar and palpebral)
cornea (corneal limbus)
Iris
Pupil
Sclera
Meibomian gland

Be able to ID

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6
Q

What is the ciliary body, choroid and iris together called?

A

Uveal tract/ middle of the eye

(vascular layer according to anatomy)

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7
Q

Retina receives a dual blood supply, with the inner retina supplied by the

A

central retinal artery

from ophthalmic artery from internal carotid a.

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8
Q

the outer reti­na supplied by the choroidal circulation

A

via branches of the posterior ciliary arteries

ophthalmic artery branch as well

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9
Q

History questions of importance

A

Photophobia (have lights been bothering your eyes before or after this in the past?)

Diplopia (double vision)

Have you ever had visual loss of both or one eye(s) at the same time?

Haziness of vision

Flashing or flickering of lights/floaters

Decreased vision

Medical Illnesses

Headache? (did you have a HA associated with this before or after these events? Do you have a HA now?)

Pulsating artery near the temple?

Arthralgias?

Nausea/Vomiting

Tearing

Eye irritation (dryness, foreign body sensation, drainage, pruritis)

Any recent medication changes

Do you wear contacts or glasses?

Recent trauma to the eye?

Last 2 should be primary questions

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10
Q

Episcleritis

A

Inflammation localized to the episclera
Typical young – 30’s-40’s
Benign, recurrent and usually self-limiting

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11
Q

Episcleritis increased risk individuals

A

Anyone

Gout, allergic rhinitis, autoimmune (RA, IBD, SLE) (30% will have other autoimmune d/o

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12
Q

Episcleritis - Clin Findings

A

Often sudden onset with red eye, and minor discomfort (not usually painful)

Irritation
Redness (Dilatation of the episcleral vessels)
Watering of eye
Pain is unusual unless associated nodule or is chronic in nature

No affect to vision

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13
Q

Episcleritis - Tx (in order)

A

IN ORDER

Artificial tears
Topical NSAID’s/Oral NSAID’s
Ophthalmology

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14
Q

Scleritis

A

Much more severe of a condition if found

Worse symptoms – especially pain

Can result in structural damage to eye and more association with an underlying condition

Average age of onset ~ 48 but range is high

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15
Q

2 types scleritis

A

Anterior and Posterior

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16
Q

Scleritis causes - autoimmune

A

RA (Rheumatoid arthritis)
SLE (Systemic Lupus Erythematosus)
UC (Ulcerative Colitis)
PsA (Psoriatic arthritis)
Vasculitis

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17
Q

Scleritis causes - infections

A

TB
Syphilis
HSV
HZV
Pseudomonas
Staph/Strep

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18
Q

other causes Scleritis

A

Sarcoidosis
Chemical/Physical agents (burns, acid/alkali)
Trauma
Lymphoma
Gout

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19
Q

Scleritis - Clin Findings (anterior)

A

Boring or piercing pain, even at night

Scleral inflammation with painful EOM’s

Deep violaceous discoloration of the globe often with edema

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20
Q

Scleritis - Clin Findings (Posterior)

A

Involves nonvisible portion of sclera (so sclera is usually white) and can potentially cause blindness

Pain (most but not all)

Visual disturbances such as blurring, diplopia

Visual loss

Proptosis

Optic disk swelling

VERY DIFFICULT TO DIAGNOSE CLINICALLY

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21
Q

Scleritis Dx and Tx

A

Refer to ophtho

Ask questions that may indicate systemic disease (fevers, arthralgias, rashes, etc.)

They will perform specialized testing and slit lamp exam
B-Scan US (looks for edema)
Possible CT/MRI scan

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22
Q

Uveitis (uvea=?)

A

iris, ciliary body, choroid

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23
Q

Uveitis

A

Inflammation of the “middle layer” of the eye (intraocular)

Usually immunologic but possibly infective or neoplastic

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24
Q

4 catergories of Uveitis

A

Anterior, Intermediate, Posterior, Pan uveitis

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25
Iritis
Leukocytes/inflammation in the anterior chamber of eye
26
Cyclitis
Leukocytes/inflammation in the middle chamber of eye (intermediate)
27
Retinitis, choroiditis
Leukocytes/inflammation in posterior chamber
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Diffuse uveitis
Leukocytes/inflammation in all areas of uvea
29
Uveitis associated more commonly with
Systemic inflammatory conditions = (RA, Spondyloarthropathies - AS, Reiter’s syndrome) Psoriatic arthritis, IBD, Sarcoidosis, LE, Sjogren’s) Other causes – Infections – HSV, CMV, Zika, Cat-Scratch, TB, etc.
30
Uveitis- Clin Findings
generally most often anterior Pain Photophobia Blurred vision (note posterior may be painless and only have floaters and/or visual loss)
31
Uveitis - exam
Small and/or irregular pupil Circumcorneal redness Inflammatory cells or debris may be noted in anterior chamber
32
Uveitis - Tx
Refer to ophthalmology!! Needs detailed medical history May need testing according to potential associations (i.e. autoimmune, infectious) Topical steroids (prednisolone acetate); Cycloplegics/mydriatics (homatropine) – for anterior Intraocular injections (variable, often steroids) for the remainder If infectious – treat infectious cause – anti-virals/anti-biotics/anti-parasitics
33
Transient monocular blindness (ocular TIA)
Monocular vision loss (amaurosis fugax), lasting a few minutes (5-10) with complete recovery Characteristically: curtain passing vertically across the visual field with complete monocular visual loss lasting a few minutes and a similar curtain effect as the episode passes (which is called “amaurosis fugax” or fleeting blindness
34
Transient monocular blindness (ocular TIA) Potential causes
Retinal emboli from ipsilateral carotid disease Central Retinal Artery Occlusion Giant Cell Arteritis (Temporal arteritis) Also: Cardiogenic emboli (often with associated atrial fibrillation); Retinal Migraine; Anti-coagulant deficiency states (Protein C, S or others)
35
Transient monocular blindness (ocular TIA) - Risk factors
HTN HLD DM Atrial fibrillation
36
Transient monocular blindness (ocular TIA) - Tx
Needs to be treated as a TIA (transient ischemic attack) ASA 81 mg Refer immediately to ophthalmology - ED first Must consider ipsilateral carotid artery stenosis - Carotid US and possible stenting or endarterectomy if needed ECHO to determine any other abnormalities of heart Inflammatory markers (CRP/ESR)
37
Central Retinal Artery Occlusion - Clin Findings
Sudden monocular loss of vision (Amaurosis fugax) Profound….reduced to counting digits or worse, No pain or redness
38
Central Retinal Artery Occlusion - Ophthalmic exam
Widespread or sectoral retinal PALLID SWELLING and a CHERRY RED SPOT at the fovea (perifoveal atrophy) Retinal ARTERIES ATTENUATED (thin), “BOX-CAR” segmentation of blood in the arteries or venules (separation of arterial flow) Always consider Giant Cell Arteritis (Temporal Arteritis) in patients > 50 yo. Commonly associated with PMR – Polymyalgia Rheumatica (autoimmune)
39
Central Retinal Artery Occlusion - Tx and referral
transient monocular blindness” is a TIA – Treat as such! Evaluate for Giant Cell Arteritis (if no visible emboli) Emergent optho referral; Prognosis depends
40
Central Retinal Artery Occlusion - Tx other options
Anterior chamber paracentesis (reduces pressure) Place patient flat -ocular massage, and high concentration of oxygen administration IV acetazolamide (Diamox), and/or topical pressure lowering eye drops to reduce intra-ocular pressure (IOP) Possible thrombolytics
41
Central Retinal Artery Occlusion -others to order
Search for sources of carotid and cardiac emboli (this is essentially a stroke) Check for HTN, DM, HLD, other risk factors - Duplex US of carotid arteries, ECG, Echocardiography, +/- CT or MRI for carotid artery dissections
42
Temporal artheritis (Giant cell arteritis)
Inflammation of the blood vessels around the scalp (often large vessels) Occurs most often in elderly (>75) 50% found in patients with rheumatic condition – polymyalgia rheumatica
43
Temporal artheritis (Giant cell arteritis) Clinical findings
Headache Amaurosis fugax Fever/fatigue Myalgias Scalp tenderness/nodularity of artery Jaw Claudication Often (not always), tender temporal artery Some patients can have aneurysms of the subclavian, carotid, basilar and other arteries
44
Temporal artheritis (Giant cell arteritis) Dx
Inflammatory markers (CRP and ESR) – very high WBC – often normal Liver function test (alkaline phosphatase) Ultrasound
45
Temporal artheritis (Giant cell arteritis) Tx
Urgent -> Go to ED Prednisone (~80mg) then continue for 1 mo Needs a temporal artery bx
46
Retinal Vein occlusion - 2 types
BRVO - Branch of retinal vein CRVO - central retinal vein "blood and thunder"
47
Retinal Vein occlusion
Blockage of small veins (BRVO) occurs where retinal arteries that have been thickened/hardened by atherosclerosis cross over and place pressure on a retinal vein; also caused by other types of ischemia/thrombosis Blockage of central vein (CRVO)
48
Retinal Vein occlusion Clinical findings
Sudden monocular loss of vision, commonly first noted upon awakening (CRVO) No pain or redness Poor visual acuity (20/200 or worse)
49
Retinal Vein occlusion - exam
Central: Widespread or sectoral RETINAL HEMORRHAGES Retinal venous dilation and tortuosity Retinal cotton wool spots and optic disk swelling (i.e. papilledema)*
50
Retinal Vein occlusion - tX
BRVO and CRVO) All patients with RVO should be assessed for DM, HTN, Hyperlipidemia and glaucoma Tx: REFER!!! (really….laser treatment to prevent growth of new, abnormal blood vessels) Intravitreal injections of anti-VGEF May regain useful vision, however vision rarely returns to normal
51
Treatment of vascular disorders- SUMMARY
Control disease processes Assess vascular risk factors (HTN, DM, A-fib, etc.). If found often need anti-coagulants Occlusions: prompt referral to ophthalmologist for revascularization procedures immediately
52
Diabetic Retinopathy
Present in about 33% of Type 2 diabetic patients at time of diagnosis Risk of development is highest in Type I DM (60-75%) Most common microvascular complication of diabetes Primary Risk factors - Duration of diabetes - Level of control
53
Diabetic Retinopathy - Types
Nonproliferative (Background) retinopathy: - Mild retinal abnormalities without neovascularization or visual loss - Small hemorrhages, microaneurysms, hard exudates Proliferative retinopathy (less common): - new retinal vessels; causes more severe visual loss
54
Diabetic Retinopathy - Proliferative Clin Pres
“neovascularization” from the optic disk or major vascular arcades Proliferation into the vitreous of blood vessels, -> tractional retinal detachment Untreated, the prognosis is much worse than non-proliferative disease
55
Diabetic Retinopathy -Tx
Focused on PREVENTION Control DM tightly Educate patient on risks of NOT controlling DM Treat HTN and HLD Annual eye exams with Optometrist +/- ophthalmologist (visual acuity PLUS fundoscopy/retinal scan) Proliferative retinopathy is usually treated by pan retinal laser photocoagulation Other options for some include vitrectomy Injections (specialized anti-VEGF – monoclonal antibody)
56
Diabetic retinopathy - summary
All diabetic patients with sudden loss of vision or retinal detachment should be referred emergently to an ophthalmologist Proliferative retinopathy or macular involvement requires urgent referral to an ophthalmologist Severe nonproliferative retinopathy or unexplained reduction of visual acuity requires early referral to an ophthalmologist
57
Hypertensive Retinopathy - General
Systemic HTN affects both retinal and choroid circulation Clinical symptoms vary with how fast the BP rises and the underlying state of HTN (how long the damage has been present)
58
Hypertensive Retinopathy - Chronic HTN changes in eye
Copper-wire changes = retinal arterioles more tortuous and narrow and develop abnormal light reflexes AV nicking = increased venous compression at the retinal A/V crossings Flame shaped hemorrhages = occur in the nerve fiber layer of retina Chronic HTN accelerates atherosclerosis (everywhere in the body)
59
Hypertensive Retinopathy - Pathogenesis
Acute elevations in BP (aka hypertensive crisis) +/- atherosclerosis** Loss of autoregulation in the retinal circulation causes breakdown of endothelial integrity and occlusion of precapillary arterioles and capillaries
60
Hypertensive Retinopathy - Clin findings
retinal manifestations = cotton wool spots; retinal hemorrhages, edema, exudates (flame) Choroid manifestations = retinal detachment and retinal pigment infarcts; may have optic disc swelling
61
Hypertensive Retinopathy - Tx
Need to get HTN under control Refer to ophthalmology – findings in eye can resolve over weeks/months with proper treatment
62
HIV Retinopathy
Most common ophthalmic abnormality in HIV
63
HIV Retinopathy Manifestations
Cotton-wool spots Retinal hemorrhages Microaneurysms
64
CMV retinitis
Less common w/use of ART Prevalent when CD4 <50
65
CMV retinitis - clinical findings
Progressively enlarging yellowish-white patches of retinal opacity w/retinal hemorrhages Asymptomatic until involvement of fovea or retinal detachment occurs The initial symptoms of CMV retinitis typically include one or more of the FOUR "F's": ((floaters, flashes, field deficits, or failing vision))
66
CMV retinitis - TX
Needs infections disease and ophthalmology consultation
67
Other HIV associated infxns of eye
Herpes simplex retinitis Toxoplasmosis Herpes zoster retinitis Kaposi’s sarcoma of conjunctiva Candida
68
Blood Dyscrasias Severe Anemia/Thrombocytopenia
(Retinal and Choroidal hemorrhages)
69
Blood Dyscrasias Leukemia and Endocarditis
“ROTH SPOTS” cotton wool spot surrounded by hemorrhage
70
Blood Dyscrasias Sickle Cell Retinopathy
“salmon patch”- "black sunbursts”
71
Optic Neuritis Most common etiology is...
Multiple Sclerosis (demyelinating disease) (also lupus, sarcoidosis, complications of varicella infection, encephalitis, and others) Up to 50% of patients who develop optic neuritis will develop MS within 15 years In 20-30% of patients who present with MS, optic neuritis is first manifestations
72
Optic Neuritis - Clinical Findings
Subacute/Acute unilateral visual loss (w/ signs of optic dysfunc) Pain: “behind” the eye, worse with EOM Optic disc usually normal in acute stage but subsequently develops pallor Later - Optic disc swelling if condition worsens w/flame-shaped peripapillary hemorrhages
73
Optic Neuritis - Tx
Refer to ophthalmology IV Prednisone and then oral prednisone
74
Optic Neuritis - Prognosis
Visual acuity usually improves within 2-3 weeks and returns to 20/40 or better for 95%; if not CT/MRI of head and orbits to exclude lesion compressing optic nerve
75
Graves Ophthalmopathy
Related to autoimmune HYPERthyroid disease (Graves) Dysthyroid eye disease/Exophthalmos
76
Graves Ophthalmopathy - Pathogenesis
deposition of mucopolysaccharides and infiltration with chronic inflammatory cells of the orbital tissues, esp. extraocular muscles Worsened by: Radioactive iodine or smoking cigarettes
77
Graves Ophthalmopathy - Clin findings
pt complaints = Surface irritation, dry eyes, diplopia
78
Graves Ophthalmopathy - Exam
Proptosis Lid retraction Lid lag Conjunctival chemosis (swelling) Episcleral inflammation Extraocular muscle dysfunction (diplopia)
79
Graves Ophthalmopathy - Complications
Marked visual loss Corneal exposure Optic nerve compression
80
Graves Ophthalmopathy - Tx
Artificial tears, “prisms” (special eyeglass lens to stop diplopia) Selenium 100 mcq daily to reduce progression Control of thyroid hormone IV pulse prednisone, immunotherapy If Optic Nerve compression or severe corneal exposure: Surgical decompression Lid surgery if significant proptosis
81
Papilledema - Clin Findings
Swelling of the optic disc that reflects increased intracranial pressure Often bilateral
82
Papilledema Must find and treat underlying cause of ...
intracranial pressure (encephalitis, hemorrhage, tumor, abscess, glaucoma, etc.) Think of uncontrolled hypertension
83
Nystagmus
Repetitive, uncontrollable movements of the eyes
84
Nystagmus types
Horizontal Vertical Rotary
85
Nystagmus caused by
abnormal function in the areas of the brain that control eye mvmts Part of inner ear that senses mvmt and position helps control eye mvmts (labyrinth)
86
Nystagmus etiology
can be congenital and acquired MCC of Acquired is certain drugs or medication Dilantin (anti-seizure), MDMA ecstasy), Alcohol, SSRI’s (i.e.. Lexapro, Prozac, Zoloft) benzodiazepines (i.e. Xanax, Valium, Ativan)
87
other causes Nystagmus
Head injury Stroke BPPV Retina or optic nerve disorders
88
Nystagmus Classifications
Pendular = speed of mvmt of eyes is in same in both directions Jerk = eyes move slowly in one direction and then quickly “jerk” back in the other direction
89
Central nystagmus (Brain)
either normal or abnormal processes not related to the vestibular organ ex) lesions of the midbrain or cerebellum can result in up- and down-beat nystagmus
90
Peripheral nystagmus (Usually inner ear)
either normal or diseased functional states of the vestibular system may combine a rotational component with vertical or horizontal eye movements and may be spontaneous, positional, or evoked.
91
nystagmus - Clin FIndings Peripheral : otologic related
Otitis media, BPPV (benign paroxysmal positional vertigo, Meniere’s disease, labyrinthitis Comes on quickly Hearing loss Ear pain Ear drainage Tinnitus Vertigo (spinning sensation) Nystagmus stops with visual fixation and unidirectional (not vertical)
92
nystagmus - Clin FIndings Central : Brain related
Brainstem stroke, MS, ischemic changes to cerebellum, tumor Headache Visual changes Difficulty with swiping on phone Motion sensitivity TV (news ticker at the bottom) Gait issues (i.e.. Wide based gait) Nystagmus can be in multiple directions (including vertical) and does not stop with visual fixation
93
Nystagmus Tx
depends on cause

ICM Unit 3 HEENT (6 decks)

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