Eye Manifestation of Systemic Diseases Flashcards
Uveal tract and sclera
Episcleritis, Scleritis, Uveitis
Vascular Disorders
Retinal vein occlusion
Retinal artery occlusion - ischemic optic neuropathy
Temporal arteritis
Retinopathy
Diabetic retinopathy
Hypertensive retinochoroidopathy (incl optic disc swelling)
HIV: HIV retinopathy and CMV Retinitis
Blood dyscrasias
Neuropathy/Neuritis
Optic Neuritis and ischemic optic neuropathy
simple anatomy
medial canthus
lateral canthus
eyelids
conjunctiva (bulbar and palpebral)
cornea (corneal limbus)
Iris
Pupil
Sclera
Meibomian gland
Be able to ID
What is the ciliary body, choroid and iris together called?
Uveal tract/ middle of the eye
(vascular layer according to anatomy)
Retina receives a dual blood supply, with the inner retina supplied by the
central retinal artery
from ophthalmic artery from internal carotid a.
the outer retina supplied by the choroidal circulation
via branches of the posterior ciliary arteries
ophthalmic artery branch as well
History questions of importance
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
Episcleritis
Inflammation localized to the episclera
Typical young – 30’s-40’s
Benign, recurrent and usually self-limiting
Episcleritis increased risk individuals
Anyone
Gout, allergic rhinitis, autoimmune (RA, IBD, SLE) (30% will have other autoimmune d/o
Episcleritis - Clin Findings
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
Episcleritis - Tx (in order)
IN ORDER
Artificial tears
Topical NSAID’s/Oral NSAID’s
Ophthalmology
Scleritis
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
2 types scleritis
Anterior and Posterior
Scleritis causes - autoimmune
RA (Rheumatoid arthritis)
SLE (Systemic Lupus Erythematosus)
UC (Ulcerative Colitis)
PsA (Psoriatic arthritis)
Vasculitis
Scleritis causes - infections
TB
Syphilis
HSV
HZV
Pseudomonas
Staph/Strep
other causes Scleritis
Sarcoidosis
Chemical/Physical agents (burns, acid/alkali)
Trauma
Lymphoma
Gout
Scleritis - Clin Findings (anterior)
Boring or piercing pain, even at night
Scleral inflammation with painful EOM’s
Deep violaceous discoloration of the globe often with edema
Scleritis - Clin Findings (Posterior)
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
Scleritis Dx and Tx
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
Uveitis (uvea=?)
iris, ciliary body, choroid
Uveitis
Inflammation of the “middle layer” of the eye (intraocular)
Usually immunologic but possibly infective or neoplastic
4 catergories of Uveitis
Anterior, Intermediate, Posterior, Pan uveitis
Iritis
Leukocytes/inflammation in the anterior chamber of eye
Cyclitis
Leukocytes/inflammation in the middle chamber of eye (intermediate)
Retinitis, choroiditis
Leukocytes/inflammation in posterior chamber
Diffuse uveitis
Leukocytes/inflammation in all areas of uvea
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.
Uveitis- Clin Findings
generally most often anterior
Pain
Photophobia
Blurred vision
(note posterior may be painless and only have floaters and/or visual loss)
Uveitis - exam
Small and/or irregular pupil
Circumcorneal redness
Inflammatory cells or debris may be noted in anterior chamber
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
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
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)
Transient monocular blindness (ocular TIA) -
Risk factors
HTN
HLD
DM
Atrial fibrillation
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)
Central Retinal Artery Occlusion - Clin Findings
Sudden monocular loss of vision (Amaurosis fugax)
Profound….reduced to counting digits or worse,
No pain or redness
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)
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
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
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
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
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
Temporal artheritis (Giant cell arteritis)
Dx
Inflammatory markers (CRP and ESR) – very high
WBC – often normal
Liver function test (alkaline phosphatase)
Ultrasound
Temporal artheritis (Giant cell arteritis)
Tx
Urgent -> Go to ED
Prednisone (~80mg) then continue for 1 mo
Needs a temporal artery bx
Retinal Vein occlusion - 2 types
BRVO - Branch of retinal vein
CRVO - central retinal vein
“blood and thunder”
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)
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)
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)*
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
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
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
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
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
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)
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
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)
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)
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
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
Hypertensive Retinopathy - Tx
Need to get HTN under control
Refer to ophthalmology – findings in eye can resolve over weeks/months with proper treatment
HIV Retinopathy
Most common ophthalmic abnormality in HIV
HIV Retinopathy Manifestations
Cotton-wool spots
Retinal hemorrhages
Microaneurysms
CMV retinitis
Less common w/use of ART
Prevalent when CD4 <50
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))
CMV retinitis - TX
Needs infections disease and ophthalmology consultation
Other HIV associated infxns of eye
Herpes simplex retinitis
Toxoplasmosis
Herpes zoster retinitis
Kaposi’s sarcoma of conjunctiva
Candida
Blood Dyscrasias
Severe Anemia/Thrombocytopenia
(Retinal and Choroidal hemorrhages)
Blood Dyscrasias
Leukemia and Endocarditis
“ROTH SPOTS”
cotton wool spot surrounded
by hemorrhage
Blood Dyscrasias
Sickle Cell Retinopathy
“salmon patch”-
“black sunbursts”
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
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
Optic Neuritis - Tx
Refer to ophthalmology
IV Prednisone and then oral prednisone
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
Graves Ophthalmopathy
Related to autoimmune HYPERthyroid disease (Graves)
Dysthyroid eye disease/Exophthalmos
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
Graves Ophthalmopathy - Clin findings
pt complaints = Surface irritation, dry eyes, diplopia
Graves Ophthalmopathy - Exam
Proptosis
Lid retraction
Lid lag
Conjunctival chemosis (swelling)
Episcleral inflammation
Extraocular muscle dysfunction (diplopia)
Graves Ophthalmopathy - Complications
Marked visual loss
Corneal exposure
Optic nerve compression
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
Papilledema - Clin Findings
Swelling of the optic disc that reflects increased intracranial pressure
Often bilateral
Papilledema
Must find and treat underlying cause of …
intracranial pressure (encephalitis, hemorrhage, tumor, abscess, glaucoma, etc.)
Think of uncontrolled hypertension
Nystagmus
Repetitive, uncontrollable movements of the eyes
Nystagmus types
Horizontal
Vertical
Rotary
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)
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)
other causes Nystagmus
Head injury
Stroke
BPPV
Retina or optic nerve disorders
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
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
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.
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)
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
Nystagmus Tx
depends on cause
