Cataracts/retinopathy/detachment

Question 1

Question 3

Cataracts facts & Exam

Answer 3

• Gradually progressive blurred vision
• No pain or redness
• Lens opacities (may be grossly visible)

Usually bilateral (blurred vision)
Unilateral: may be diplopia/double vision. Essentially, each eye is seeing something different.

Cataracts are opacities of the lens & usually bilateral
They are the leading cause of blindness worldwide.
Age-related cataract is by far the most common cause
Can be caused by SEVERAL other things/ diseases
Cigarette smoking increases the risk of cataract formation

DM, steroid use, statins, trauma, radiation of the eye, congenital (rubella and CMV)

Question 4

Answer 4

Cataracts

Question 5

cataracts

What do we see on exam?

Answer 5

Red reflex is red appearance of retina…if something alters clarity of lens (cataract), or if retina is not normal reddish color, then red reflex is altered or absent

Small cataracts - dark defects in red reflex

Large cataract may obliterate red reflex

Question 6

Cataracts

Sx

Answer 6

The predominant symptom is progressive blurring of vision
Glare/halo, worse in bright light or when driving at night
change of focusing
development of nearsightedness
monocular double vision may also occur

Question 7

cataracts

Tx

Answer 7

The only treatment for cataract is surgical extraction of the opacified lens.
Patients with cataracts should be referred to an ophthalmologist when their visual impairment adversely affects their everyday activities

Question 8

Cataract surgical treatment

Answer 8

Functional visual impairment is the reason for surgery
Surgery improves visual acuity in 95% of cases
Complications include
intraocular hemorrhage
damage to posterior capsule
displacement of lens fragments into the vitreous
infection (endophthalmitis)
corneal edema
incorrect refractive outcome

Question 9

Hypertensive Retinopathy

general

Answer 9

1. Hypertensive retinopathy can be a red flag for current and future nonocular end-organ damage.
2. Its detection is aided by fundal photography.
3. Acute elevations of blood pressure result in loss of autoregulation in the retinal circulation, leading to breakdown of endothelial integrity and occlusion of precapillary arterioles and capillaries that manifest as cotton-wool spots, retinal hemorrhages, retinal edema, and retinal exudates, often in a stellate appearance at the macula
4. Chronic hypertension accelerates the development of atherosclerosis. The retinal arterioles become more tortuous and narrower and develop abnormal light reflexes (“silver-wiring” and “copper-wiring”). There is increased venous compression at the retinal arteriovenous crossings (“arteriovenous nicking”), predisposing to branch retinal vein occlusions. Flame-shaped hemorrhages occur in the nerve fiber layer of the retina.
5. Can happen in young patients with abrupt elevations of blood pressure, such as may occur in pheochromocytoma, malignant hypertension, or preeclampsia-eclampsia.

Question 10

HTN retinopathy

Exam Findings

Answer 10

AV Crossing Changes
Arterial Changes
Decrease in arteriovenous ratio to 1:3 (normal ratio is 2:3).
Change in the arteriolar light reflex (light reflex appears as copper and/or silver wiring)
Retinal Changes
Retinal hemorrhages:Dot-blot hemorrhages: Bleeding in inner retinal layer
Flame shaped hemorrhage:Bleeding in superficial retinal layer
Retinal exudates:Hard exudates: Lipid deposits in retina
Soft exudates: cotton wool spots due to ischemia of nerve fibers
Macular Changes
Macular star formation due to deposition of hard exudates around the macula.
Optic Nerve Changes
Optic disk swelling (also known as hypertensive optic neuropathy)

Question 11

Question 12

HTN retinopathy

Tx

Answer 12

Management depends on severity:
Mild:control BP.
Moderate:exclude associated factors like DM, check for cardiovascular disease. BP control.
Severe:urgent treatment and referral, strong association with mortality. Look for damage in renal, cardiovascular, and brain. Lower BP carefully to prevent ischemic damage to vital organs such as optic nerve and brain.

Question 13

Diabetic Retinopathy

general

Answer 13

Diabetic macular edema: central retinal swelling; can occur with any severity level of diabetic retinopathy; can reduce visual acuity.

Question 14

Diabetic Retinopathy

categories

Answer 14

Two main categories: nonproliferative and proliferative.

Nonproliferative retinopathyis subclassified as mild, moderate, or severe

Proliferative retinopathy less common but causes more severe visual loss

Question 15

Diabetic retinopathy

screening

Answer 15

Adult and adolescent patients with diabetes mellitus should undergo regular screening by fundal photography or slit-lamp examination.

Question 16

Diabetic Retinopathy - nonproliferative

patho

Answer 16

Retinal capillaries leak proteins, lipids, RBCs into the retina.
Microaneurysms, retinal hemorrhages, retinal edema, cotton wool spots (preproliferative), hard exudates.
Retinal edema and hard exudates caused by breakdown of blood-retina barrier, allowing leakage of serum proteins, lipids.
In mild cases, mild retinal abnormalities without visual loss.
Reduction of vision is most commonly due to macular edema.

Question 17

Diabetic retinopathy- proliferative

general

Answer 17

Proliferative retinopathy is characterized by neovascularization, arising from either the optic disk or the major vascular arcades
May end up with tractional retinal detachment

Vision is usually normal until vitreous hemorrhage or retinal detachment occurs.

Proliferative retinopathy can occur in both types of diabetes but is more common in type 1, developing about 7–10 years after onset of symptoms

Question 18

diabetic Proliferative retinopathy

Tx

Answer 18

Proliferative retinopathy is usually treated by panretinal laser photocoagulation, preferably before vitreous hemorrhage or tractional detachment has occurred. Regression of neovascularization can also be achieved by intravitreal injection of a VEGF inhibitor.

Question 19

Diabetic retinopathy

Screening

Answer 19

Visual symptoms and visual acuity are poor indicators.
Adult/adolescent patients with DM should undergo regular screening by fundus photography (can use telemedicine) or dilated slit-lamp examination of retina.
Type 1 DM: begin screening 5 years after DM is diagnosed.
Type 2 DM: begin screening at diagnosis of DM.

Yearly if pre-existing retinopathy, otherwise every 2 years
More frequent screening required in women during pregnancy, planning for pregnancy.

Question 20

diabetic retinopathy

Prevention

Answer 20

Optimize blood glucose, blood pressure, kidney function, and serum lipids, although such measures are probably more important in preventing the development of retinopathy than in influencing its subsequent course.
Refer to ophthalmologist

Question 21

Diabetic nonproliferative Retinopathy

Tx
Severe nonproliferative retinopathy

Answer 21

if extensive retinal ischemia, may require prophylactic panretinal laser photocoagulation.

VEGF inhibitor therapy improves diabetic retinopathy severity in eyes at all levels of nonproliferative diabetic retinopathy and is the mainstay of treatment for diabetic macular edema.

Vitrectomy to remove persistent vitreous hemorrhage, to improve vision and allow panretinal laser photocoagulation, for treatment of tractional retinal detachment involving the macula.

Question 22

diabetic Proliferative retinopathy

Tx

Answer 22

Intravitreal injection of VEGF inhibitor or panretinal laser photocoagulation, preferably before vitreous hemorrhage or tractional detachment

Question 23

Papilledema

general
s/sx

Answer 23

Bilateral optic disc swelling from raised intracranial pressure.
Headache common.

Visual field testing: enlarged blind spots and peripheral constriction.

Peripheral visual field loss can progress in insidious fashion while optic nerve develops atrophy. In this case, reduction of optic disc swelling is an ominous sign of dying nerve rather than encouraging indication of resolving papilledema.

The term ‘papilledema’ is often used interchangeably with the term ‘optic disc edema’ which has many causes.
Evaluation of the finding of papilledema includes neuroimaging to R/O intracranial lesion.

pressure from the back goeing toward the globe

Question 24

Optic neuritis

essentials of Dx (3)

Answer 24

Subacute usually unilateral visual loss.
Pain exacerbated by eye movements.
Optic disk usually normal in acute stage but subsequently develops pallor.

lasts weeks to months
usually unilateral

Question 25

Optic Neuropathy/Optic Neuritis

RF

Answer 25

Strongly associated with:
Demyelinating disease, esp MS
Also occurs in:
VZV infection
Autoimmune disorders
Spread of inflammation from meninges, orbital tissues, paranasal sinuses

Question 26

Optic Neuritis

Clinical Presentation
Uni/bi? Loss of vision? Pain?

Answer 26

Unilateral loss of vision developing over a few days.
Field loss is usually central.
Pain behind the eye, exacerbated by eye movements.
Loss of color vision and afferent pupillary defect.
Optic disk may be swollen (papillitis) with or without peripapillary hemorrhages.
Visual acuity usually improves within 2–3 weeks and returns to 20/40 or better in 95% of previously unaffected eyes.
Optic atrophy subsequently develops if there has been damage to sufficient optic nerve fibers

Question 27

Optic neuritis

Question 28

Optic neuritis

Tx

Answer 28

Acute demyelinating optic neuritis: IVsteroids accelerate visual recovery
Phenytoinmay be neuroprotective
Atypical optic neuritis due to sarcoidosis, herpes zoster, or SLE has poorer prognosis, requires prolonged corticosteroid therapy, may require plasma exchange, may require long-term immunosuppression.

All patients should be referred urgently for ophthalmologic/neurologic assessment

Question 29

retinal detachment

general

Answer 29

Nearsightedness and cataract extraction are most common risk factors – penetrating/blunt trauma and prior ocular surgery are also risk factors.
Most cases due to development of ≥ 1 peripheral retinal tears/holes.
Most with retinal detachment are > 50. As patients age, vitreous liquefies and contracts, and traction tears develop, detaching retina from posterior wall of the eye.
Once there is a defect, vitreous is able to pass under the retina and progressive detachment results.

Tractional retinal detachment also occurs when there is preretinal fibrosis, such as in proliferative diabetic retinopathy or retinal vein occlusion.
Exudative retinal detachment results from accumulation of subretinal fluid, such as in neovascular age-related macular degeneration

Question 30

Retinal Detachment

Shafer’s Sign

Answer 30

Shafer’s Sign: “tobacco dust”
Collection of brown pigmented cells in anterior vitreous following a break in retina.
Pigment granules thought to come from shearing force of the break in retinal pigment epithelium

Red-pigmented cells in vitreous indicate vitreous hemorrhage - 70% correlation with retinal tears.

Question 31

retinal detachment

Answer 31

Question 32

retinal detachment

Tx

Answer 32

Close all retinal tears and holes using laser photocoagulation to form permanent adhesion between neurosensory retina/retinal pigment epithelium/choroid.

Uncomplicated retinal detachment may be treated by pneumatic retinopexy. Expansile gas injected into vitreous cavity followed by positioning of the patient’s head to put the gas against the hole to permit retina reattachment. Once retina is reattached, defects are surrounded by laser photocoagulation.
Protect the macula!

About 90% of uncomplicated rhegmatogenous retinal detachments can be cured with one operation.
Visual prognosis is worse if macula is detached or if detachment is of long duration.