Posterior Chamber and Retinal Disorders Flashcards
1
Q
What are 8 posterior chamber/retinal disorders?
A
Central Retinal Artery Occlusion Central Retinal Vein Occlusion Amaurosis Fugax Optic Neuritis Retinal Detachment Giant Cell Arteritis Papilledema Macular Degeneration
2
Q
What is the primary event that leads to retinal detachment?
A
a retinal tear
3
Q
What is the pathology behind detachment?
2
A
- Fluid vitreous passes though the tear and lodges behind the sensory retina (between neural retina layer and outer pigmented layer)
- Combined traction and pull of gravity results in progressive detachment (pull sensory layer away from pigmented layer)
4
Q
Predisposing factors are?
6
A
Age – 50-75 Myosis Cataract extraction Trauma Family history Advanced diabetes
5
Q
Retinal detachment is also called?
A
posterior vitreous detachment
6
Q
Signs and symptoms of retinal detachment?
4
A
Blurred Vision
Floaters
Flashing lights(photopsias)
NO PAIN OR REDNESS
7
Q
What are the flashing lights in retinal detachment caused by?
A
the tugging on the retinal surface by the separating vitreous
(last less than a second)
8
Q
What will cause the retina to die quickly?
A
Lack of oxygen, retina is one of the most highly metabolically active tissues in the body. High oxygen uptake
9
Q
Treatment for retinal detachment?
4
A
Cryotherapy (freezing)
Scleral buckle
Intravitral gas
Vitrectomy
10
Q
What happens in a central retinal artery occlusion (CRAO)?
A
Emboli enter and occlude the retinal artery
11
Q
Prediposing factors for central retinal artery occulsion (CRAO)?
6
A
Age – mean is 60-80, can happen earlier Carotid artery disease Atrial fibrillation Hypertension Diabetes Temporal Arteritis
12
Q
In CRAO what will the area that the blocked vessel is supplying look like?
A
Whiteish yellow region/area
13
Q
Signs and symtpoms of a central retinal artery occlusion?
3
A
- Sudden profound monocular visual loss (seconds, minutes, perm) aka amarousis fugax
- Painless
- What happens to visual acuity
- Can detect hand movements but can’t count fingers
14
Q
What does the fundoscopic exam reveal about CRAO?
6
A
- Pallor of the optic disc
- Ischemic retinal whitening
- Cherry red spot on macula or fovea
- Arteriole narrowing
- “boxcar” segmentation of the retinal veins
- Marked afferent pupillary defect
15
Q
What can happen if we don’t catch CRAO right away?
A
Very poor prognosis for vision (particularly if not resolved within 90 minutes)!
REFER, REFER, REFER immediately
16
Q
Treatment of CRAO?
3
A
Ocular massage
Anterior chamber paracentesis
Revasularization techniques
–Thrombolysis (clot busting)
17
Q
What color will the retina appear in diabetes or hypertensive retinopathy?
A
yellow or pink
18
Q
Why are you at risk for retinal detachment if you have myosis?
A
Retina is thinner and easier to tear apart
19
Q
Where does vision loss is a retinal detachment start?
A
superior temporal area and expands fairly rapidly.
20
Q
When do you have no hope for recovery of vision is a retinal detachment?
A
When the macula has peeled off
21
Q
What will you see in a fundoscope exam for a retinal detachment?
A
wrinkled area. like bubbled wallpaper
Grey cloud with fluid shifting maybe
22
Q
What is another way to describe CRAO?
A
Stroke of the eye
23
Q
What is the cherry red spot in CRAO pathology?
A
The macula. the retina itself is a light color so it makes the macula look darker
24
Q
Where does the emboli start in CRAO?
How could we prevent this early?
A
probably starts in the carotid and moves to the central retinal artery
Listen for bruit in the carotid before it goes to the brain
25
Temporal arteritis can cause CRAO. How do we treat it?
IV steriods
26
What do retinal vein occlusions cause?
| 3
dilated veins and leaky hemorrhages
cotton wool spots- little microinfarcts (dead areas of the retina)
optic disc swelling
27
Systemic etiologies of central retinal vein occlusion?
| 4
Increasing age
HTN
Coagulation disorders
Diabetes
28
Ocular etiologies of central retinal vein occlusion?
| 2
```
Raised intraocular pressure (> 25 mmHg)
vein inflammation (vasculitis)
```
29
Signs and symptoms of central retinal vein occlusion?
3
How can the diagnosis be made?
1. Visual impairment is commonly first noticed upon waking
2. Usually a sudden monocular loss of vision
3. PAINLESS
Diagnosis can be made with ophthalmoscopic exam
Refer ALL to ophthalmologist
30
What do we find in a fundoscopic exam with someone who has central retinal vein occlusion?
6
1. Minimal APD (afferent pupillary defect)
2. venous tortuosity / dilatation
3. Retinal hemorrhages
4. variable cotton-wool spots
5. mild to moderate disc edema
6. macular edema
SWOLLEN EVERYTHING
31
What should patients with central retinal vein occlusion be screened for?
4
diabetes
systemic hypertension
hyperlipidemia
glaucoma
32
What are patients with central retinal vein occlusion at high risk for?
develop neovascular glaucoma
| proliferative retinopathy
33
What is neovascularization?
| and what surgery is good for it?
new little tiny vessels bleeding into the space will raise intraocullar pressure and lead to gluacoma
lazer surgery good for that
34
Whats amaurosis fugax?
Monocular loss of vision lasting a few minutes with complete recovery
35
What is amaurosis fugax caused by?
caused by retinal emboli from ipsilateral carotid disease
36
How is vision loss described as in amaurosis fugax?
a curtain passing VERTICALLY across the field of vision leading to complete loss of vision and then a similar curtain effect as the vision returns”
37
How would we diagnose amaurosis fugax?
| 2
1. MUST have evaluation of carotids by doppler ultrasound or CT/MRI angiography
2. ALL MUST also have EKG to ensure A. Fib is not cause of emboli
38
In all cases how would we treat amaurosis fugax?
In ALL CASES, place them on low dose ASA
39
Whats the differential diagnosis for amaurosis fugax?
| 5
1. Impending central retinal artery/vein occlusion
2. Impending OPHTHALMIC artery occlusion (total retinal blanching)
3. Carotid stenosis (bruit)- thinking strokes
4. Temporal arteritis (GCA)
5. Ocular migraine (slower onset, “scintillating scotoma”)
- migraine with aura
40
Labs to order to diagnose and treat amaurosis fugax?
CBC
Fasting blood sugar
ESR and CRP
Lipid profile
41
In amaurosis fugax patients, how do we evaluate for embolus source?
2
1. Carotid dopplers
| 2. cardiac evaluation including echocardiogram
42
How should we treat amaurosis fugax patients?
| 3
1. Ocular massage is
43
What does ESR and CRP tell us in the diagnosis of amaurosis fugax?
They are both fairly nonspecific tests. If these tests are normal then its not amaurosis fugax. But if they are irregular it could be a number of different things
44
When we see a young patient with vision loss and no immediate obvious exam findings what should we think?
optic neuritis
45
Signs and symtpoms of optic neuritis?
| 3
1. Unilateral decreased vision over 1-3 days
2. Occasional pain with eye movement
3. Age 18-45 female
46
Etiology of optic neuritis?
| 3
1. Multiple sclerosis (MS)
-optic neuritis is often the initial
manifestation of MS
-30% risk at 5 years
-Check MRI - consider IV steroids
2. Idiopathic
3. Viral infections,
-TB,
-sarcoidosis
47
What kind of vision is often lost in patients with optic neuritis?
What other sign is often seen?
color vision
affernet pupillary defect
48
What should we see in a fundoscopic exam in a patient with optic neuritis?
5
1. Optic nerve usually has a normal appearance acutely
2. Can have swollen disc, but less common
3. Relative afferent pupillary defect (RAPD)
4. Decreased color vision
5. May get worse with exercise or temperature increase (Uhtoff’s sign)
49
Differential diagnosis for optic neuritis?
| 5
1. Ischemic optic neuropathy (sudden Vision loss, no pain, pale nerve, older patient, hemifield defect)
2. Papilledema (bilateral, no decreased Visual acuity)
3. Severe HTN
4. Intraorbital or intracranial mass
5. Toxic (ETOH, malnutrition, heavy metals)
50
Work up and treatment for optic neuritis?
1. complete ophthalamic exam
2. complete neurologic exam/MRI and possibly IV steroids (never oral)
3. Do NOT use oral steroids!!!!!!!!!!!
4. Check BP
5. ESR/CRP/ temporal artery biopsy if you suspect giant cell arteritis (55+)
51
What specifically do we want to pay special attention to when we do a complete ophthalamic exam for optic neuritis?
4
1. pupils!!
2. color vision
3. decreased light brightness sensitivity with penlight
4. visual field test
52
Visual signs for optic neuritis?
| 2
color vision loss
| central scotoma
53
Etiology of papilledema?
| 6
1. Intracranial tumors
2. Hydrocephalus (too much CSF)
3. Pseudotumor (young, obese females)
4. Subdural hematoma (trauma)-not intraocular pressure but brain pressure!!!
5. Brain abscess / Meningitis
6. bilateral usually thats how you know its intracranial and not inrtaocular
54
Signs and symptoms of papilledema?
| 2
1. Slow vision loss from increased ICP / optic nerve swelling
2. Can have acute attacks of vision loss when lying flat
55
Is papilledema usually bilateral or unilateral?
bilateral.
| intracranial pressure not intraocular
56
What will the fundoscopic exam/patient experience look like in a papilledema patient?
3
1. disc margins blurred
2. Often peripapillary disc hemorrhages
3. may have double vision if CN VI plasy from increased intracranial pressure
57
How do we treat papilledema?
directed at underlying cause
58
Signs and symptoms of giant cell arteritis/temporal arteritis?
8
1. Patients >55 years old
2. Sudden, painless, non-progressive visual loss
3. Headache
4. Scalp tenderness
5. Jaw claudication (very much one sided)
6. Fever
7. Weight loss
8. Polymyalgia rheumatica association
- -Muscle and joint aches
59
What kind of vision problems with GCA will you see?
usually painless in the eye
| tenderness/headache
60
How will the pulse feel in temporal arteritis?
you wont be able to feel it
61
What lab tests will be high in temperal arteritis?
| 2
ESR
| CRP
62
What will you see on a fundoscopic exam for GCA/temporal arteritis?
2
positive afferent pupillary defect
| pale, swollen, optic disc
63
What lab is very specific to GCA?
ESR BUT go by symptoms!
| ESR and CRP can be normal in 20% of patients
64
HOw do we make a definitive diagnosis in temporal arteritis?
Temporal artery biopsy
| ---need at least 2-3 cm of vessel specimen on bx (i.e. skip lesions)
65
What will the histology show on a temporal artery biopsy?
shows granulomatous infiltrate of internal elastic lamina of artery
occlusion of vessel lumen
giant cells present (you see big cells)
66
How should we treat temoral arteritis?
TREAT WITH STERIODS EVEN BEFORE BIOPSY IS DONE! (dont want to wait and have progresstion)
67
What is our treatment goal with temporal arteritis?
preserve visual loss in the other eye
68
If their is no symtpoms or mild symptoms what should we use to treat temporal arteritis?
60-90mg of prednisone po qd
69
If severe symtpoms or visual loss from temporal arteritis what should we treat it with?
2
1. 1gm Solumedrol IV q 6 hrs x 3-5 days, then SLOW taper off oral steroids over 2 weeks
2. Refer to surgery for biopsy
70
What is the most common type of age related macular degeneration?
dry kind
71
What happens in age related macular degeneration?
| 2
1. “wearing out” of retina / photoreceptors
| 2. Degradation products form “drusen” in retina
72
Risk factors from macular degeneration?
| 5
1. Age
2. Smoking (2x higher)
3. Family history
4. Caucasian
5. sun exposure
73
What are the two types of ARMD?
Dry and wet or exudative
74
Characteristics of dry macular degeneration?
| 2
gradual vision loss
| Drusen
75
What do patients complain of when they have dry ARMD?
gradual loss of vision in one or both eyes
76
Characteristics of wet (exudative) ARMD?
| 3
1. sudden vision loss
2. subretinal neovascularization
3. Accumulation of fluid and blood
77
What do patients complain of when they have wet ARMD?
| 2
1. Acute distortion in vision, especially distortion of straight lines, or loss of central vision.
2. Symptoms usually appear in one eye, although the disease is generally in both eyes.
78
What is the worst kind of ARMD?
wet type
more rapid and more severe loss of central vision due to fluid between retinal pigmented layer and Bruch's layer
79
Mimizing effects of ARMD?
| 5
1. monitor with Amsler grid
2. Stop smoking
3. control cardiovascular disease
4. diet high in friuts and veggies lowers risk (folic acid and B12)
5. Antioxidants from foods might help
80
Treatment of ARMD?
| 6
supportive measures. Not much they can do
Vitamin C 500mg
Vitamin E 400 IU
Beta carotene 15 mg (non-smokers only)
Risk of lung CA associated with beta carotene
Zinc 80mg
Copper 2 mg
