Opthomology

Question 1

Pterygium

• RF
• Defn
• Mgt

Answer 1

• increases with sun exposure and age
• A pterygium is a proliferation of fibrovascular tissue on the surface of the eye, which extends onto the cornea
  Pterygia are usually treated only when they interfere with vision. The standard therapy is surgical removal.

Question 2

Hordeolum

Answer 2

• Infection in the meibomian gland (internal hordeolum), often resolves into a chalazion
• Infection in the Zeiss or Moll’s glands (externdal hordeolum).
• Staphylococcus aureus is the causative agent in most cases

Question 3

Chalazion

Answer 3

Meibomian gland becomes blocked, often by blepharitis.
Blocked meibomian gland’s duct releases gland contents into the soft tissue of eyelid.
Gland contents cause a lipogranulomatous reaction.
Reaction can cause acute tenderness and erythema, which then resolves into a chronic nodule

Question 4

Management of Hordeolum?

Answer 4

Warm soaks, three to four times a day for 15 minutes, will elicit drainage in most cases.
Topical antibiotics (e.g., bacitracin ointment) may be beneficial for recurrent or spontaneously draining hordeolum.
Cases that do not respond to warm soaks or are extremely painful and swollen may be incised and drained with a stab incision. Make the incision on either the internal or external eyelid depending on where the hordeolum is pointing.
Antibiotics do not provide benefit after incision and drainage.
Systemic antibiotics are usually not needed unless patient has preseptal cellulitis.

Question 5

Management of chalazion?

Answer 5

Can be treated conservatively with lid hygiene and warm compresses. One study demonstrated a 58% response rate with conservative treatment along with 1% topical chloramphenicol.
Higher percentages of resolution can be achieved with either incision and curettage or injection with steroid (e.g., 0.3 mL triamcinolone acetonide) (80%–92%).
One study demonstrated a better response to incision and curettage in the following situations: Patients 35.1 years or older of age, with lesion duration 8.5 months and size 11.4 mm

Question 6

Scleral or conjunctival pigmentation?
DDx?
Worrisome features?
Mgt?

Answer 6

• DDx: benign or racial nevi, Primary acquired melanosis, secondary melanosis, melanoma, nevus of ota
  -Features seen higher in malignancy: Ulceration, hemorrhage, change in color, and formation of new vessels around the lesion.
  Refer any changing pigmented lesion in the eye to a specialist who can perform a biopsy.
  Two lesions can be monitored for changes without a biopsy: racial melanosis and nevi.

Question 7

Corneal abrasion/FB

- Dx

Answer 7

History of ocular trauma or eye rubbing (although corneal abrasions can occur with no trauma history).
Symptoms of pain, eye redness, photophobia, and a foreign body sensation.
Foreign body seen with direct visualization or a slit lamp
Fluorescein application demonstrates green area under cobalt-blue filtered light

Question 8

Corneal abrasion/FB

-Mgt?

Answer 8

Confirm diagnosis with fluorescein (for abrasion) if no foreign body is readily visible
Carefully inspect for a foreign body. Invert the upper eyelid for full visualization. Slit-lamp visualization may be needed to determine if the cornea has been penetrated
Remove (or refer for removal) nonpenetrating foreign bodies. Apply a topical anesthetic, such as proparacaine or tetracaine. Remove with irrigation, a wet-tipped cotton applicator, or a fine gauge needle.
Refer penetrating foreign bodies to an experienced eye surgeon.
Prescribe ophthalmic NSAIDs for pain if needed. SOR A
Consider topical antibiotics. SOR C Chloramphenicol ointment reduced the risk of recurrent ulcer in a prospective, nonplacebo controlled trial.3 While chloramphenicol is rarely used in the United States, other ophthalmic antibiotics such as erythromycin ointment are used for corneal abrasions.
Remove contact lenses until corneal is healed.4 SOR C
Avoid patching, it does not help.

Question 9

Etiology of conjunctivitis by age

Answer 9

Conjunctivitis is predominately infectious (bacterial or viral) or allergic, and the most common etiologies vary by age.

Neonatal conjunctivitis is often caused by Chlamydia trachomatis and Neisseria gonorrhoeae.
Children younger than 6 years are more likely to have a bacterial than viral conjunctivitis.
Haemophilus influenzae was the most common infectious agent, cultured from 40% to 50% of children with conjunctivitis and 74% of children with concurrent otitis media prior to extensive use of HIB vaccination.
Adenovirus was cultured from 13% to 20% of children with conjunctivitis and 65% of children with concurrent pharyngitis.
Children older than 6 years are more likely to have viral or allergic causes for conjunctivitis.

Question 10

Clinical scoring for conjunctivitis (etiology)

Answer 10

A score of +5 to –3 is determined as follows:

Two glued eyes (+5); one glued eye (+2); history of conjunctivitis (–2); eye itching (–1).
A score of +5, +4, or +3 is useful in ruling in bacterial conjunctivitis with specificities of 100%, 94%, and 92%, respectively.
Scores of –1,–2, or –3 are useful in ruling out bacterial conjunctivitis with sensitivities of 98%, 98%, and 100%, respectively.

Question 11

Clinical hx of episcleritis

Answer 11

Segmental or diffuse inflammation of episclera (pink color), mild or no discomfort but can be tender to palpation, and no vision disturbance

Question 12

What is the uveal tract?

Answer 12

The uveal tract contains the iris (anterior), ciliary body (intermediate), and choroids (posterior).

Question 13

What is uveitis?

Answer 13

Uveitis refers to inflammation of any part of the uveal tract and is classified as anterior, intermediate, or posterior depending on the structures involved.

Question 14

Uveitis cause by location?

Answer 14

Uveitis can be caused by trauma, infections, inflammation, or rarely neoplasms. Most likely causes differ by location.
Anterior (iritis)—Trauma is common (Figure 17-2). In nontraumatic cases, causes include idiopathic (50%); seronegative spondyloarthropathies, i.e., ankylosing spondylitis, reactive arthritis, psoriatic arthritis, inflammatory bowel disease, (20%); and juvenile idiopathic arthritis (10%). Infections are less common and include herpes, syphilis, and tuberculosis.
Intermediate—Most are idiopathic3
Posterior—Toxoplasmosis is the most common, followed by idiopathic.
Panuveitis (affecting all layers)—Idiopathic (22%–45%) and sarcoidosis (14%–28%).

Question 15

Signs of anterior uveitis?

Answer 15

Anterior acute uveitis presents with:
Unilateral eye pain, redness, tearing, photophobia, and decreased vision.
360 degrees perilimbal injection, which is most intense at the limbus
History of eye trauma, an associated systemic disease, or risk factors for infection.
Severe anterior uveitis may cause a hypopyon from layering of leukocytes and fibrous debris in the anterior chamber

Question 16

Signs of intermediate and posterior uveitis?

Answer 16

Intermediate and posterior uveitis:
Presents with altered vision or floaters.
Often have no pain, redness, tearing, or photophobia.

Question 17

Signs of sarcoid uveitis?

Answer 17

Sarcoid uveitis presents with:
Panuveitis (anterior, intermediate, and posterior).
Gradual and usually a bilateral onset.
Few vision complaints unless cataracts or glaucoma develops.
Characteristic findings on slit lamp examination (i.e., mutton-fat keratic precipitates, posterior iris synechiae).

Question 18

Management of traumatic uveitis?

Answer 18

Traumatic uveitis—Dilated funduscopy for other ocular trauma, gonioscopy to evaluate intraocular pressure, and treatment may include cycloplegics for comfort.

Question 19

Management non traumatic uveitis?

Answer 19

Non-traumatic uveitis—Slit lamp examination and laboratory tests to assist with diagnosis of underlying cause; treatment is based on underlying cause but is usually topical steroid drops.
Therapeutic dilation is used to break up the synechiae that can occur,

Question 20

Pathophys of glaucoma?

Answer 20

Glaucoma is acquired optic nerve atrophy, after associated with increased intraocular pressure.

Increased intraocular pressure occurs from impaired outflow of aqueous humor as either:
Open-angle—Dysfunction of the aqueous humor drainage system with no visible pathology to the anterior chamber angle.
Angle-closure—Occlusion of the anterior chamber angle.

Impaired outflow of aqueous humor elevates intraocular pressure in some patients, but many patients with open-angle glaucoma have normal intraocular pressures.

Optic nerve atrophy is seen as optic disc cupping and irreversible visual field loss. Investigate cup to disc ratio over 0.5.

Question 21

Clinical features of open angle glaucoma?

Answer 21

Risk factors—Older than 50 years, African descent, first-degree family history, high intraocular pressures.
History—Often asymptomatic, occasionally “tunnel vision.”
Physical examination—Optic cupping and/or elevated intraocular pressure (glaucomatous changes can occur with intraocular pressures in the normal range), loss of peripheral vision by automated perimetry (typically bilateral, but may be asymmetric).

Question 22

Clinical features of acute closed angle glaucoma?

Answer 22

Risk factors—Asian race, women.
History—Painful red eye (unilateral), vision loss, headache, nausea, and vomiting (Figure 18-3).
Physical examination—Shallow anterior chamber, optic cupping and elevated intraocular pressure, injection of the conjunctiva, and cloudy cornea

Question 23

Management of glaucoma?

Answer 23

Emergently refer patients with suspected angle-closure glaucoma to an ophthalmologist.

Evaluate (or refer for evaluation) patients with abnormal optic nerve cupping (cup-to-disc ratio of >0.5; difference in cup-to-disc ratio of 0.2 or greater between eyes; asymmetric cup) or increased intraocular pressure measured by tonometry or visual field deficits.

Refer patients with shallow anterior chambers, severe far-sightedness (hyperopia) or previous history of acute angle closure glaucoma to an ophthalmologist.

Document the location and extent of visual field deficits with automated perimetry.

Treat with topical agents to decrease intraocular pressure by 20% to 40%, which has been demonstrated to decrease glaucoma progression. SOR A Many medications are available including:
Nonspecific beta-blockers (e.g., levobunolol 0.5%, once or twice a day).
Prostaglandin analogs (e.g., latanoprost 0.005%, once a day).
Carbonic anhydrase inhibitors (e.g., dorzolamide 2%, three times a day).
Alpha agonists (e.g., apraclonidine 0.5–1.0%, three times a day).

Refer for surgical evaluation if you are unable to medically reduce the intraocular pressure.

Question 24

Epidemiology of diabetic retinopathy?

Answer 24

In developed nations, diabetic retinopathy is the leading cause of blindness among people younger than 40 years.

Twenty-one percent of patients diagnosed with type 2 diabetes mellitus already have retinopathy.

More than 60% of patients with type 2 diabetes mellitus have retinopathy within 20 years of diagnosis.

Most patients with type 1 diabetes mellitus as children develop retinopathy in their 20s or 30s.

Question 25

Pathophys of retinopathy?

Answer 25

Hyperglycemia results in microvascular complications including retinopathy.

Several biochemical pathways linking hyperglycemia and retinopathy have been proposed.

In nonproliferative retinopathy, microaneurysms weaken vessel walls. Vessels then leak fluid, lipids, and blood resulting in macular edema, exudates, and hemorrhages.

Cotton wool spots result when small vessel occlusion causes focal ischemia to the superficial nerve fiber layer of the retina.

In proliferative retinopathy, new blood vessels form in response to ischemia

Question 26

Diagnosis of retinopathy?

Answer 26

Definitive diagnosis is made by an eye specialist:

Gold standard is grading of stereoscopic color fundus photographs in seven standard fields.
In comparison to the gold standard, a single monochromatic digital photo through a nondilated eye holds promise for large population screening with a sensitivity and specificity of 78% and 86%, respectivey.

Dilated fundoscopic examination by an ophthalmologist has a sensitivity of only 34%.3

Clinical Features
Central vision loss as a result of macular edema.
Nonproliferative retinopathy—Microaneurysms are seen initially, followed by macular edema, cotton wool spots, superficial (flame) or deep (dot-blot) hemorrhages, and exudates.

Proliferative retinopathy—Neovascularization, i.e., growth of new blood vessels on the optic disc, the retina, or iris

Question 27

Besides diabetes, what else causes retinopathy?

Answer 27

Retinopathy is also seen with other systemic illnesses and infections including:

Hypertensive retinopathy—arterial narrowing or AV nicking in addition to cotton wool spots

HIV retinopathy—cotton wool spots and infections such as cytomegalovirus.

Question 28

Management of diabetic retinopathy?

Answer 28

Refer all patients with diabetes mellitus to an eye specialist for an yearly dilated eye examination. Control diabetes and vascular risk factors:

Glycemic control lowers the risk of retinopathy (35% risk reduction per 1 point HgbA1C reduction).
SOR A

Blood pressure control improves visual outcomes (34% risk reduction in retinopathy progression; 47% risk reduction risk for declines in visual acuity).2 SOR A

Patients with high lipids have more hard exudates and a higher risk of vision loss, but it is unclear if lipid control changes outcomes. SOR C

Work with an ophthalmologist to prevent vision loss:

Complications of diabetic retinopathy are vitreous hemorrhage, retinal detachment, and neovascular glaucoma. All these complications can result in devastating vision loss.

Ophthalmologists will determine when peripheral photocoagulation is indicated. Photocoagulation reduces the risk of severe visual loss by more than 50% with side effects of peripheral and night vision loss. SOR A Other surgical treatments, including vitrectomy have been less successful

Question 29

What are people with hypertensive retinopathy more at risk of?

Answer 29

Multiple studies show that patients with moderate hypertensive retinopathy are two to three times more likely to have a stroke than those without at the same level of blood pressure control independent of other risk factors

Question 30

What findings do you find with a person with hypertensive retinopathy on exam?

Answer 30

High blood pressure results in these retinal findings:

Retinal vessels become narrow and straighten at diastolic blood pressure (DBP) of 90 to 110 mmHg.

Arteriovenous “nicking” occurs when the arteriolar wall enlarges from arteriosclerosis, compressing the vein.

Microaneurysms result from the increased intravascular pressure.

DBP 110 to 115 mmHg causes leakage of plasma proteins and blood products resulting in cotton wool patches, retinal hemorrhages, or hard exudates.

Optic nerve swelling occurs at DBP of 130 to 140 mmHg

Question 31

How do you diagnose hypertensive retinopathy?

Answer 31

The diagnosis is made clinically from typical retinal findings in a patient with hypertension.

Clinical Features
Microaneurysms and retinal hemorrhages, arteriolar narrowing, and AV nicking.

Question 32

Differential for hypertensive retinopathy?

Answer 32

Retinal vessel narrowing, AV nicking, microaneurysms, retinal hemorrhages, hard exudates, and cotton wool spots are also seen in other conditions that impair blood flow, including:

Diabetic retinopathy
Radiation retinopathy.
Venous or carotid artery occlusive disease.
Systemic illnesses such as collagen vascular disease.

Optic nerve swelling and a macular star (blurring of the macula in a star-like pattern) also occur in:

Neuroretinitis.
Diabetic papillopathy.
Radiation optic retinopathy.
Optic neuritis.
Intracranial disease

Question 33

Management of hypertensive retinopathy?

Answer 33

Patients with funduscopic findings of hypertensive retinopathy should have their blood pressure measured and treated to reduce the risk of heart and cerebrovascular disease. SOR A

Assist patients in smoking cessation. This will result in the greatest benefit in morbidity and mortality.

Reduce weight or maintain normal BMI.
Eat a diet rich in fruits and vegetables and low in saturated fats.

Reduce sodium to less than 6 g of sodium chloride per day.

Engage in regular physical activity for 30 minutes most days of the week.

Limit alcohol to two drinks per day in men and one drink per day in women.

Start a thiazide diuretic to achieve blood pressure of less than 140/90 unless contraindicated; a blood pressure goal of 130/80 should be used for patients with diabetes. Consider an ACEI as an initial medication for patients with diabetes. Consider other medications only for patients with compelling indications.

Although the largest benefit in outcomes is seen with the first medication, additional medications should be considered to achieve blood pressure less than 140/90 after weighing the risks and benefits with the patient.

Evaluate and manage other risk factors for cardiovascular disease including high cholesterol and diabetes.

Patients with hypertension do not require routine funduscopic examination, unless they also have diabetes mellitus.5 SOR A Patients experiencing acute visual disturbances should be referred for evaluation of hemorrhage or optic nerve edema