My TMOD Flashcards

1
Q

RCE

A

Treatment

Acute episode: Cycloplegic drop (e.g., cyclopentolate 1%) three times daily and ophthalmic antibiotic ointment (e.g., erythromycin, bacitracin) four to six times daily. Can use 5% sodium chloride ointment q.i.d. in addition to antibiotic ointment. If the epithelial defect is large, a pressure patch or bandage contact lens and topical antibiotic drops q.i.d. may be placed (NEVER patch contact lens wearers). Oral analgesics as needed.
Never prescribe topical anesthetic drops.
After epithelial healing is complete, artificial tears four to eight times per day and artificial tear ointment q.h.s. for at least 3 to 6 months, or 5% sodium chloride drops four times per day and 5% sodium chloride ointment q.h.s. for at least 3 to 6 months.
If the corneal epithelium is loose or heaped and is not healing, consider epithelial debridement. Apply a topical anesthetic (e.g., proparacaine) and use a sterile cotton-tipped applicator or cellulose sponge (e.g., Weck-Cel surgical spear) to gently remove all the loose epithelium.
For erosions not responsive to the preceding treatment, consider the following:
Prophylactic medical treatment with 5% sodium chloride ointment q.h.s.
Oral doxycycline (matrix metalloproteinase inhibitor) 50 mg b.i.d. with or without a short course of topical corticosteroid drops (e.g., fluorometholone 0.1% b.i.d. to q.i.d. for 2 to 4 weeks).
Extended-wear bandage soft contact lens for several months with a topical antibiotic and routine changing of the lens.
Anterior stromal puncture can be applied to localized erosions, such as in traumatic cases, outside the visual axis in cooperative patients. It can be performed with or without an intact epithelium. Stromal puncture may be applied manually at the slit lamp or with Nd:YAG laser. This treatment may cause small permanent corneal scars that are usually of no visual significance if outside the visual axis.
Epithelial debridement with diamond burr polishing of Bowman membrane or phototherapeutic keratectomy (PTK). Both are highly effective (up to 90%) for large areas of epithelial irregularity and lesions in the visual axis. Excimer laser ablation of the superficial stroma can be particularly helpful if repeated erosions have created anterior stromal haze or scarring.
Follow-Up

Every 1 to 2 days until the epithelium has healed, and then every 1 to 3 months, depending on the severity and frequency of the episodes. It is important to educate patients that persistent use of lubricating ointment (5% sodium chloride or tear ointment) for 3 to 6 months following the initial healing process reduces the chance of recurrence.

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2
Q

Filamentary keratitis

A

Treatment

Treat the underlying condition.
Consider debridement of the filaments. After applying topical anesthetic (e.g., proparacaine), gently remove filaments at their base with fine forceps or a cotton-tipped applicator. This gives temporary relief, but the filaments will recur if the underlying etiology is not treated.
Lubrication with one of the following regimens:
Preservative-free artificial tears six to eight times per day and lubricating ointment q.h.s.
Punctal occlusion.
Acetylcysteine 10% q.i.d.
NOTE
Acetylcysteine is not commercially available as a drop but can be made by a compounding pharmacy.

If the symptoms are severe or treatment fails, then consider a bandage soft contact lens (unless the patient has severe dry eyes as underlying etiology). Extended-wear bandage soft contact lenses may need to be worn for weeks to months. Concomitant prophylactic or therapeutic topical antibiotics such as a fluoroquinolone drops are typically given, especially if associated with a corneal abrasion/epithelial defect.

Follow-Up

In 1 to 4 weeks. If the condition is not improved, consider repeating the filament removal or applying a bandage soft contact lens. Long-term lubrication must be maintained if the underlying condition cannot be eliminated.

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3
Q

Thygeson SPK

A

Treatment
Mild

Artificial tears four to eight times per day.
Artificial tear ointment q.h.s.

Note
Treatment is based more on patient symptoms than corneal appearance.

Moderate to Severe

Mild topical steroid (e.g., fluorometholone 0.1% or loteprednol 0.2% to 0.5% q.i.d.) for 1 to 4 weeks, followed by a very slow taper. May need prolonged low-dose topical steroid therapy.
If no improvement with topical steroids, a bandage soft contact lens can be tried.
Cyclosporine 0.05% drops daily to q.i.d. may be an alternative or adjunctive treatment, especially in patients with side effects from steroids.

Follow-Up

Weekly during an exacerbation, then every 3 to 6 months. Patients receiving topical steroids require intraocular pressure (IOP) checks every 4 to 12 weeks.

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4
Q

Band keratopathy

A

Treatment
Mild (e.g., Foreign Body Sensation)
Artificial tears four to six times per day and artificial tear ointment q.h.s. to q.i.d. as needed. Consider a bandage contact lens for comfort.
Severe (e.g., Obstruction of Vision, Irritation not Relieved by Lubricants, Cosmetic Problem)
Removal of the calcium may be performed at the slit lamp or under the operating microscope by chelation using disodium ethylenediamine tetraacetic acid (EDTA):

Disodium EDTA 3% to 4% is obtained from a compounding pharmacy.
Anesthetize the eye with a topical anesthetic (e.g., proparacaine) and place an eyelid speculum.
Debride the corneal epithelium overlying the calcium with a sterile scalpel or a sterile cotton-tipped applicator.
Wipe a cellulose sponge or cotton swab saturated with the EDTA solution over the band keratopathy until the calcium clears (which may take 10 to 60 minutes).
Irrigate with normal saline, place an antibiotic ointment (e.g., erythromycin), a cycloplegic drop (e.g., cyclopentolate 1% to 2%), and a pressure patch on the eye for 24 hours. Alternatively, a bandage soft contact lens or an amniotic membrane may be used to cover the epithelial defect with a topical antibiotic (e.g. moxifloxacin, gatifloxacin q.i.d.).
Consider giving the patient a systemic analgesic (e.g., acetaminophen with codeine).

Follow-Up

If surgical removal has been performed, the patient should be examined every few days until the epithelial defect has healed.
Residual anterior stromal scarring may be amenable to excimer laser PTK to improve vision. PTK may also be used to try to improve the ocular surface and prevent recurrent erosions.
The patient should be checked every 3 to 12 months, depending on the severity of symptoms. EDTA chelation can be repeated if the band keratopathy recurrs.

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5
Q

Bacterial keratitis

A

**corneal ulcer

Treatment summary
Small non-staining peripheral ulcers may be started on fluoroquinolone drops every 2 to 6 hours. For ulcers with epithelial defects and an anterior chamber reaction, a fluoroquinolone drop every hour around the clock is recommended. Large or vision threatening ulcers (with moderate to severe anterior chamber reaction and/or involving the visual axis) are usually treated with fortified tobramycin or gentamicin (15mg/ml) every hour around the clock alternating with fortified vancomycin (25mg/ml) every hour around the clock.

Treatment
Ulcers and infiltrates are initially treated as bacterial unless there is a high index of suspicion of another form of infection. Initial therapy should be broad spectrum. Remember that bacterial coinfection may occasionally complicate fungal and Acanthamoeba keratitis. Mixed bacterial infections can also occur.

Cycloplegic drops for comfort and to prevent synechiae formation (e.g., cyclopentolate 1% t.i.d.; atropine 1% b.i.d. to t.i.d. recommended if a hypopyon in present). The specific medication depends on severity of anterior chamber inflammation.

Topical antibiotics according to the following algorithm:

Low Risk of Visual Loss
Small, nonstaining peripheral infiltrate with at most minimal anterior chamber reaction and no discharge:

Noncontact lens wearer: Broad-spectrum topical antibiotics (e.g., fluoroquinolone [moxifloxacin, gatifloxacin, besifloxacin, levofloxacin] or polymyxin B/trimethoprim drops q1–2h while awake).

Contact lens wearer: Fluoroquinolone (e.g., moxifloxacin, gatifloxacin, ciprofloxacin, besifloxacin, levofloxacin) ± polymyxin B/trimethoprim drops q1–2h while awake; can add tobramycin or ciprofloxacin ointment one to four times a day.

Borderline Risk of Visual Loss
Medium size (1 to 1.5 mm diameter) peripheral infiltrate, or any smaller infiltrate with an associated epithelial defect, mild anterior chamber reaction, or moderate discharge:

Fluoroquinolone (e.g., moxifloxacin, gatifloxacin, ciprofloxacin, besifloxacin, levofloxacin) ± polymyxin B/trimethoprim q1h around the clock. Consider starting with a loading dose of q5min for five doses and then q30min until midnight then q1h.

Note
Moxifloxacin and besifloxacin have slightly better gram-positive coverage. Gatifloxacin and ciprofloxacin have slightly better Pseudomonas and Serratia coverage.

Vision Threatening
Our current practice at Wills Eye is to start fortified antibiotics for most ulcers larger than 1.5 to 2 mm, in the visual axis, or unresponsive to initial treatment. If fortified antibiotics are not immediately available, start with a fluoroquinolone and polymyxin B/trimethoprim until fortified antibiotics can be obtained from a formulating pharmacy.

Fortified tobramycin or gentamicin (15 mg/mL) q1h, alternating with fortified cefazolin (50 mg/mL) or vancomycin (25 mg/mL) q1h. This means that the patient will be placing a drop in the eye every one-half hour around the clock. Vancomycin drops should be reserved for resistant organisms, patients at risk for resistant organisms (e.g., due to hospital or antibiotic exposure, unresponsive to initial treatment), and for patients who are allergic to penicillin or cephalosporins. An increasing number of methicillin-resistant Staphylococcus aureus (MRSA) infections are now community acquired. If the ulcer is severe and Pseudomonas is suspected, consider starting fortified tobramycin every 30 minutes and fortified cefazolin q1h; in addition, consider fortified ceftazidime q1h.

Note
All patients with borderline risk of visual loss or severe vision-threatening ulcers are initially treated with loading doses of antibiotics using the following regimen: One drop every 5 minutes for five doses, then every 30 to 60 minutes around the clock.

In some cases, topical corticosteroids are added after the bacterial organism and sensitivities are known, the infection is under control, and severe inflammation persists. Infectious keratitis may worsen significantly with topical corticosteroids, especially when caused by fungus, atypical mycobacteria, or Pseudomonas.

Eyes with corneal thinning should be protected by a shield without a pressure patch (a patch is never placed over an eye thought to have an infection). The use of a matrix metalloproteinase inhibitor (e.g., doxycycline 100 mg p.o. b.i.d.) and a collagen synthesis promoter such as systemic ascorbic acid (e.g., vitamin C 1 to 2 g daily) may help to suppress connective tissue breakdown and prevent the perforation of the cornea.

No contact lens wear.

Oral pain medication as needed.

Oral fluoroquinolones (e.g., ciprofloxacin 500 mg p.o. b.i.d.; moxifloxacin 400 mg p.o. daily) penetrate the eye well. These may have added benefit for patients with scleral extension or for those with frank or impending perforation. Ciprofloxacin is preferred for Pseudomonas and Serratia.

Systemic antibiotics are also necessary for Neisseria infections (e.g., ceftriaxone 1 g intravenously [i.v.] q12–24h if corneal involvement, or a single 1 g intramuscular [i.m.] dose if there is only conjunctival involvement) and for Haemophilus infections (e.g., oral amoxicillin/clavulanate [20 to 40 mg/kg/day in three divided doses]) because of occasional extraocular involvement such as otitis media, pneumonia, and meningitis.

Admission to the hospital may be necessary if:

  • Infection is sight threatening and/or impending perforation.
  • Patient has difficulty administering the antibiotics at the prescribed frequency.
  • High likelihood of noncompliance with drops or daily follow-up.
  • Suspected topical anesthetic abuse.
  • Intravenous antibiotics are needed (e.g., gonococcal conjunctivitis with corneal involvement). Often employed in the presence of corneal perforation and/or scleral extension of infection.
  • For atypical mycobacteria, consider prolonged treatment (q1h for 1 week, then gradually tapering) with one of the following topical agents: fluoroquinolone (e.g., moxifloxacin or gatifloxacin), amikacin (15 mg/mL), clarithromycin (1% to 4%), or tobramycin (15 mg/mL). Consider oral treatment with clarithromycin 500 mg b.i.d. Previous LASIK has been implicated as a risk factor for atypical mycobacteria infections.

Follow-Up

Daily evaluation at first, including repeat measurements of the size of the infiltrate and epithelial defect. The most important criteria in evaluating treatment response are the amount of pain, the epithelial defect size (which may initially increase because of scraping for cultures and smears), the size and depth of the infiltrate, and the anterior chamber reaction. The IOP must be checked and treated if elevated. Reduced pain is often the first sign of a positive response to treatment.

If improving, the antibiotic regimen is gradually tapered but is never tapered past the minimum dose to inhibit the emergence of resistance (usually t.i.d. to q.i.d. depending on the agent). Otherwise, the antibiotic regimen is adjusted according to the culture and sensitivity results.

Consider new or repeat cultures and stains (without stopping treatment) in the setting of non-responsive or worsening infiltrate/ulcer. Treat with fortified antibiotics and modify based on culture results and the clinical course. Hospitalization may be recommended.

A corneal biopsy may be required if the condition is worsening and infection is still suspected despite negative cultures.

For an impending or a complete corneal perforation, a corneal transplant or patch graft is considered. Cyanoacrylate tissue glue may also work in a treated corneal ulcer that has perforated despite infection control. Due to concern about drug penetration, antibiotics are often given for 1 to 2 days prior to glue application over an active area of infection.

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6
Q

Fungal keratitis

A

Treatment
Corneal infiltrates and ulcers of unknown etiology are treated as bacterial until proven otherwise. If the stains or cultures indicate a fungal keratitis, institute the following measures:

Admission to the hospital may be necessary, unless the patient is reliable. It may take weeks to achieve complete healing.

Natamycin 5% drops (especially for filamentous fungi), amphotericin B 0.15% drops (especially for Candida), or topical fortified voriconazole 1% initially q1–2h around the clock, then taper over 4 to 6 weeks.

Cycloplegic (e.g., cyclopentolate 1% t.i.d.; atropine 1% b.i.d. to t.i.d. is recommended if hypopyon is present).

No topical steroids. If the patient is currently taking steroids, they should be tapered rapidly and discontinued.

Consider adding oral antifungal agents (e.g., either fluconazole or itraconazole 200 to 400 mg p.o. loading dose, then 100 to 200 mg p.o. daily, or voriconazole 200 mg p.o. b.i.d.). Oral antifungal agents are often used for deep corneal ulcers or suspected fungal endophthalmitis.

Consider epithelial debridement to facilitate the penetration of antifungal medications. Topical antifungals do not penetrate the cornea well, especially through an intact epithelium. When culture results and sensitivities are known, intrastromal depot injections of amphotericin or voriconazole can also be considered.

Measure IOP (preferably with Tono-Pen). Treat elevated IOP if present

Eye shield, without patch, in the presence of corneal thinning.

Follow-Up
Patients are reexamined daily at first. However, the initial clinical response to treatment in fungal keratitis is much slower compared to bacterial keratitis. Stability of infection after initiation of treatment is often a favorable sign. Unlike bacterial ulcers, epithelial healing in fungal keratitis is not always a sign of positive response. Fungal infections in deep corneal stroma are frequently recalcitrant to therapy. These ulcers may require weeks to months of treatment, and therapeutic corneal transplantation may be necessary for infections that progress despite maximal medical therapy or corneal perforation. Intracameral antifungal medications (e.g., voriconazole 50 mcg/0.1 mL) at the time of therapeutic keratoplasty should be considered. Anterior lamellar keratoplasty is relatively contraindicated because there is a high risk of recurrence of infection

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7
Q

Acanthomoeba keratiitis

A

Treatment
One or more of the following are usually used in combination, sometimes in the hospital initially:

Polyhexamethylene biguanide 0.02% (PHMB) drops q1h or chlorhexidine 0.02% drops q1h.

Propamidine isethionate 0.1% drops q1h are typically added in addition to PHMB or chlorhexidine. Dibromopropamidine isethionate 0.15% ointment is also available.

Oral antifungal agent (e.g., itraconazole 400 mg p.o. for one loading dose, then 100 to 200 mg p.o. daily, ketoconazole 200 mg p.o. daily, or voriconazole 200 mg p.o. daily to b.i.d.).

        Note
        Alternative therapy includes hexamidine, clotrimazole 1% drops, miconazole 1% drops, or paromomycin drops q2h. Low-dose corticosteroid drops may be helpful in reducing inflammation after the infection is controlled, but steroid use is controversial.

    All patients:

Discontinue contact lens wear in both eyes.

Cycloplegic (e.g., cyclopentolate 1% t.i.d. or atropine 1% b.i.d.).

In presence of inflammation, pain, and/or scleritis, oral nonsteroidal anti-inflammatory agents (e.g., naproxen 250 to 500 mg p.o. b.i.d.) may be used. Additional narcotic oral analgesics are often needed.

    Follow-Up
    Every 1 to 4 days until the condition is consistently improving, and then every 1 to 3 weeks. Medication may then be tapered judiciously. Treatment is usually continued for 3 months after resolution of inflammation, which may take up to 6 to 12 months.
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8
Q

HSV keratitis / conjunctivitis

A

Treatment
Eyelid/Skin Involvement

Topical acyclovir ointment, five times per day, is an option, although it has not been proven effective. Any dermatologic and nonocular preparation of acyclovir ointment should be used on the skin only. Erythromycin or bacitracin ophthalmic ointment is often used b.i.d. for bacterial prophylaxis. Ganciclovir 0.15% ophthalmic gel five times per day may also be effective.
Warm or cool soaks to skin lesions t.i.d. or p.r.n.
Eyelid margin involvement: Add ganciclovir 0.15% ophthalmic gel or trifluridine 1% drops, five times per day, to the eye. Vidarabine 3% ointment five times per day is useful for small children. These medications are continued for 7 to 14 days until resolution of the symptoms.

Note
Many physicians give oral acyclovir 400 mg five times per day, valacyclovir 500 mg p.o. t.i.d., or famciclovir 250 mg p.o. t.i.d. for 7 to 14 days, to adults suspected of having primary herpetic disease.

Conjunctivitis
Ganciclovir 0.15% ophthalmic gel, trifluridine 1% drops, or vidarabine 3% ointment five times per day. Discontinue the antiviral agent after 7 to 14 days; if the conjunctivitis has failed to improve, reevaluation is recommended.
Corneal Epithelial Disease

Ganciclovir 0.15% ophthalmic gel five times per day, trifluridine 1% drops nine times per day, or vidarabine 3% ointment five times per day. (Topical ganciclovir gel appears to have a lower incidence of corneal toxicity than trifluridine.) Oral antiviral agents (e.g., acyclovir 400 mg p.o. five times per day, valacyclovir 500 mg p.o. t.i.d., or famciclovir 250 mg p.o. t.i.d. for 7 to 10 days) are effective alternatives to topical antiviral agents and can be used when topical medications cannot be given due to compliance problems, especially in children.
Consider cycloplegic agent (e.g., cyclopentolate 1% t.i.d.) if an anterior chamber reaction or photophobia is present.
Patients taking topical steroids should have them tapered rapidly.
Limited debridement of infected epithelium can be used as an adjunct to antiviral agents.

Technique: After topical anesthetic instillation, a sterile, moistened cotton-tipped applicator or semisharp instrument is used carefully to peel off the lesions at the slit lamp. After debridement, antiviral treatment should be instituted or continued as described earlier.

For epithelial defects that do not resolve after 1 to 2 weeks, bacterial coinfection or Acanthamoeba keratitis should be suspected. Noncompliance and topical antiviral toxicity should also be considered. At that point, the topical antiviral agent should be discontinued, and a nonpreserved artificial tear ointment or an antibiotic ointment (e.g., erythromycin) should be used four to eight times per day for several days with careful follow-up. Smears for Acanthamoeba should be performed whenever the diagnosis is suspected.

Disciform keratitis
Mild. Consider treatment with cycloplegic (e.g., cyclopentolate 1% t.i.d.) in conjunction with antiviral prophylaxis.

Moderate to severe or central (i.e., vision is reduced).
Cycloplegic, as above.
Topical steroid (e.g., prednisolone acetate 1% or loteprednol 0.5% q.i.d. to q2h). If an epithelial lesion is present, it should be treated before starting high frequency corticosteroids.
Antiviral prophylaxis: Ganciclovir 0.15% ophthalmic gel three to five times a day, trifluridine 1% t.i.d. to q.i.d., acyclovir 400 mg p.o. b.i.d., valacyclovir 500 mg p.o. one to two times a day.

Note
Chronic use of prophylactic oral antivirals may help prevent subsequent episodes of HSV keratouveitis.

Adjunctive medications which may be used include:

  • Topical antibiotic (e.g., erythromycin ointment q.h.s.) in the presence of epithelial defects.
  • Aqueous suppressants for increased IOP. Avoid prostaglandin analogues due to association with recurrent HSV infections and uveitis.

Necrotizing IK: Treated as severe disciform keratitis. The first priority is to diagnose and treat any associated overlying epithelial defect and bacterial superinfection with antibiotic drops or ointment. Tissue adhesive or corneal transplantation may be required if the cornea perforates (this is more common with neurotrophic keratitis). Oral antiviral treatment may be beneficial.

Note

Topical steroids are contraindicated in those with infectious epithelial disease.
Rarely, a systemic steroid (e.g., prednisone 40 to 60 mg p.o. daily tapered rapidly) is given to patients with severe stromal disease accompanied by an epithelial defect and hypopyon. Cultures should be done to rule out a superinfection.
While oral antivirals (e.g., acyclovir, famciclovir, and valacyclovir) have not been shown to be beneficial in the treatment of stromal disease, they are typically employed, and may be beneficial in the treatment of herpetic uveitis.
Valacyclovir has greater bioavailability than acyclovir. Little has been published on famciclovir for HSV, but it may be better tolerated in patients who have side effects to acyclovir such as headache, fatigue, or gastrointestinal upset.
Dosing of antivirals discussed above (e.g., acyclovir, famciclovir, and valacyclovir) need to be adjusted in patients with renal insufficiency. Checking BUN and creatinine is recommended in patients at risk for renal disease before starting high doses of these medications.
Valacyclovir should be used with caution in patients with human immunodeficiency virus due to reports of thrombocytopenic purpura and hemolytic uremic syndrome in this population.
The persistence of an ulcer with stromal keratitis is commonly due to the underlying inflammation (requiring cautious steroid therapy); however, it may be due to antiviral toxicity or active HSV epithelial infection. When an ulcer deepens, a new infiltrate develops, or the anterior chamber reaction increases, smears and cultures should be taken for bacteria and fungi.

Follow-Up

Patients are reexamined in 2 to 7 days to evaluate the response to treatment and then every 1 to 2 weeks, depending on the clinical findings. The following clinical parameters are evaluated: the size of the epithelial defect and ulcer, the corneal thickness and the depth of corneal involvement, the anterior chamber reaction, and the IOP. Patients with necrotizing keratitis need to be followed daily or admitted if there is threat of perforation.
Topical antiviral medications for corneal dendrites and geographic ulcers should be continued five times (for ganciclovir and vidarabine ophthalmic gel) to nine times (for trifluridine drops) per day for 7 to 14 days until healed, then two to four times per day respectively for 4 to 7 days, then stopped.
Topical steroids used for corneal stromal disease are tapered slowly (often over months to years). The initial concentration of the steroid (e.g., prednisolone acetate 1%) is eventually reduced (e.g., loteprednol 0.5% or prednisolone acetate 0.125%). Extended taper includes dosing q.o.d., twice weekly, once weekly, etc., especially with a history of flare-ups when steroids are stopped. Prophylactic systemic agents (e.g., acyclovir 400 mg b.i.d.) or less commonly, topical antiviral agents (e.g., ganciclovir 0.15% or trifluridine 1% t.i.d.), are used until steroids are used once daily or less.
Corneal transplantation may eventually be necessary if inactive postherpetic scars significantly affect vision, though an RGP lens and maximization of the ocular surface with aggressive lubrication should be tried first.
Recommend long-term oral antiviral prophylaxis (e.g., acyclovir 400 mg b.i.d.) if a patient has had multiple episodes of epithelial disease or stromal disease.

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9
Q

HZV

A

Treatment
Skin involvement:
In adults with a moderate-to-severe skin rash for <4 days in which active skin lesions are present and (consider) if the patient presents later in the first week with active lesions:

Oral antiviral agent (e.g., acyclovir 800 mg p.o. five times per day, famciclovir 500 mg p.o. t.i.d., or valacyclovir 1,000 mg p.o. t.i.d.) for 7 to 10 days. If the condition is severe, as manifested by orbital, optic nerve, or cranial nerve involvement, or the patient is systemically ill, hospitalize and prescribe acyclovir 5 to 10 mg/kg i.v. q8h for 5 to 10 days.
Ophthalmic antibiotic ointment (e.g., bacitracin or erythromycin) to skin lesions b.i.d.
Warm compresses to periocular skin t.i.d.

Adults with a skin rash of more than 1-week duration or without active skin lesions:

Ophthalmic antibiotic ointment (e.g., bacitracin or erythromycin) to skin lesions b.i.d.
Warm compresses to periocular skin t.i.d.

Children: Discuss with a pediatrician and consider weight-based acyclovir dosing (20 mg/kg q8h) for children <12 years of age or under 40 kg, otherwise use adult dosage above. Treat as in (2) unless evidence of systemic spread. For systemic spread, hospitalize and prescribe intravenous acyclovir in conjunction with pediatric and infectious disease comanagement.

Ocular Involvement

Note
It is common clinical practice at Wills Eye for all patients with VZV ocular findings to receive 7 to 10 days of systemic oral antivirals (e.g., acyclovir 800 mg p.o. five times per day, famciclovir 500 mg p.o. t.i.d., or valacyclovir 1,000 mg p.o. t.i.d.) usually in conjunction with the following therapies.

Conjunctival involvement: Cool compresses and ophthalmic ointment (e.g., bacitracin or erythromycin) to the eye b.i.d.
SPK: Lubrication with preservative-free artificial tears q1–2h and ointment q.h.s.
Corneal or conjunctival pseudodendrites: Lubrication with preservative-free artificial tears q1–2h and ointment q.h.s. Topical antivirals (e.g., ganciclovir 0.15% gel or vidarabine 3% ointment) t.i.d. to q.i.d. may also be helpful. Consider antibiotic ointment to prevent bacterial superinfection.
Immune stromal keratitis: Topical steroid (e.g., prednisolone acetate 1%) started at a frequency of four to eight times per day and adjusted according to clinical response. Topical steroids are tapered over months to years using weaker steroids with a goal of less than daily dosing (e.g., q.o.d., twice weekly, once weekly, etc.).
Uveitis (with or without immune stromal keratitis): Topical steroid (e.g., prednisolone acetate 1%) four to eight times per day and cycloplegic (e.g., cyclopentolate 1% t.i.d.). Treat increased IOP with aggressive aqueous suppression; avoid prostaglandin analogues.
Neurotrophic keratitis: Treat mild epithelial defects with ophthalmic antibiotic ointment (e.g., erythromycin) four to eight times per day. If a corneal infiltrate occurs, obtain appropriate smears and cultures to rule out infection. If the infiltrate is sterile, and there is no response to ointment, consider a bandage contact lens, tarsorrhaphy, amniotic membrane graft, or conjunctival flap along with prophylactic topical antibiotics.
Scleritis
Retinitis, choroiditis, optic neuritis, or cranial nerve palsy: Acyclovir 10 mg/kg i.v. q8h for 1 week and prednisone 60 mg p.o. for 3 days, then taper over 1 week. Management of ARN or PORN may require intraocular antivirals. Consult infectious disease. Recommend neurologic consultation to rule out central nervous system involvement. Patients with severe disease can develop a large vessel cranial arteritis resulting in a massive CVA.
Increased IOP: May be steroid response or secondary to inflammation. If uveitis is present, increase the frequency of the steroid administration for a few days and use topical aqueous suppressants (e.g., timolol 0.5% daily or b.i.d., brimonidine 0.2% t.i.d., or dorzolamide 2% t.i.d. Oral carbonic anhydrase inhibitors may be necessary if the IOP is >30 mm Hg. If IOP remains increased and the inflammation is controlled, substitute fluorometholone 0.25%, rimexolone 1%, or loteprednol 0.5% drops for prednisolone acetate and attempt to taper the dose.

Note
Pain may be severe during the first 2 weeks, and narcotic analgesics may be required. An antidepressant (e.g., amitriptyline 25 mg p.o. t.i.d.) may be beneficial for both postherpetic neuralgia and depression that can develop in VZV. Capsaicin 0.025% or doxepin ointment may be applied to the skin t.i.d. to q.i.d. after the rash heals (not around the eyes) for postherpetic neuralgia. Oral gabapentin or pregabalin can be helpful for acute pain and for postherpetic neuralgia. Management of postherpetic neuralgia should involve the patient’s primary medical doctor or a pain management specialist.

Follow-Up
If ocular involvement is present, examine the patient every 1 to 7 days, depending on the severity. Patients without ocular involvement can be followed every 1 to 4 weeks. After the acute episode resolves, check the patient every 3 to 6 months (3 if on steroids) because relapses may occur months to years later, particularly as steroids are tapered. Systemic steroid use is controversial and requires collaboration with the patient’s internist.

Note
VZV is contagious for children and adults who have not had chickenpox or the chickenpox vaccine and is spread by inhalation. Varicella-naïve pregnant women must be especially careful to avoid contact with a VZV-infected patient. A vaccine for VZV is recommended for people aged 50 to 60 years or older; it was demonstrated to decrease the frequency and severity of HZO versus placebo.

Varicella Zoster Virus (Chickenpox)
Symptoms
Facial rash, red eye, foreign body sensation.
Signs

Early: Acute conjunctivitis with vesicles or papules at the limbus, on the eyelid, or on the conjunctiva. Pseudodendritic corneal epithelial lesions, stromal keratitis, anterior uveitis, optic neuritis, retinitis, and ophthalmoplegia occur rarely.
Late: Immune stromal or neurotrophic keratitis.

Treatment

Conjunctival involvement and/or corneal epithelial lesions: Cool compresses and ophthalmic antibiotic ointment (e.g., erythromycin t.i.d.) to the eye and periorbital lesions.
Stromal keratitis with uveitis: Topical steroid (e.g., prednisolone acetate 1% q.i.d.), cycloplegic (e.g., cyclopentolate 1% t.i.d.), and erythromycin ointment q.h.s.
Neurotrophic keratitis: Uncommon
Canalicular obstruction: Uncommon. Managed by intubation of puncta.

Note

Aspirin is contraindicated because of the risk of Reye syndrome in children.
Immunocompromised children with chickenpox may require i.v. acyclovir.
VZV vaccination is available and will likely prevent ophthalmic complications of chickenpox in immunocompetent patients if given at least 8 to 12 weeks before exposure.

Follow-Up

Follow-up in 1 to 7 days, depending on the severity of ocular disease. Taper the topical steroids slowly.
Watch for stromal or neurotrophic keratitis approximately 4 to 6 weeks after the chicken pox infection resolves. Stromal keratitis can have a chronic course requiring long-term topical steroids with a very gradual taper.

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10
Q

Interstitial Keratitis

A

Treatment

Acute disease:

Topical cycloplegic (e.g. cyclopentolate 1% t.i.d. or atropine 1% b.i.d.).
Topical steroid (e.g., prednisolone acetate 1% q2–6h depending on the degree of inflammation).
Treat any underlying disease.

Old inactive disease with central scarring:

Corneal transplantation may improve vision if minimal amblyopia is present.
Late decrease in vision often due to cataracts.

Recently inactive or old inactive disease:

If the treponemal-specific assay or FTA-ABS is positive and the patient has active or untreated syphilis, or if the VDRL or RPR titer is positive and has not declined the expected amount after treatment, then treatment for syphilis is indicated.
If PPD or IGRA is positive and the patient is <35 years and has not been treated for TB in the past, or there is evidence of active systemic TB (e.g., positive finding on chest radiograph), then refer the patient to an internist and infectious disease specialist for TB treatment.
If Cogan syndrome is present, refer the patient to an otolaryngologist and rheumatologist.
If Lyme antibody and titers are positive, treat

Follow-Up

Acute disease: Every 3 to 7 days initially, and then every 2 to 4 weeks. The frequency of steroid administration is slowly reduced as the inflammation subsides over the course of months (may take years). IOP is monitored closely and reduced with medications based on the degree of IOP elevation and overall health of the optic nerve.
Old inactive disease: Yearly follow-up, unless treatment is required for underlying

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11
Q

Staph Marginal Keratitis

A

Treatment
Mild
Warm compresses, eyelid hygiene, and an antibiotic drop q.i.d. (e.g., fluoroquinolone or trimethoprim/polymyxin B) and antibiotic ophthalmic ointment q.h.s. (e.g. bacitracin, erythromycin, bacitracin/polymyxin B).

Moderate to Severe
Treat as described for mild, but add a low-dose topical steroid (e.g., loteprednol 0.2% to 0.5% or prednisolone 0.125% q.i.d.) with an antibiotic (e.g., fluoroquinolone or trimethoprim/polymyxin B q.i.d.). A combination antibiotic/steroid can also be used q.i.d. (e.g., loteprednol 0.5%/tobramycin 0.3% or dexamethasone 0.1%/tobramycin 0.3%). Never use steroids without antibiotic coverage. Maintain until the symptoms improve and then slowly taper.
If episodes recur despite eyelid hygiene, add systemic doxycycline (100 mg p.o. b.i.d., for 2 weeks, and then daily for 1 month, and then 50 to 100 mg daily titrated as necessary) until the ocular disease is controlled for several months. This medication has an anti-inflammatory effect on the sebaceous glands in addition to its antimicrobial action. Topical azithromycin q.h.s. or cyclosporine b.i.d. may be helpful in controlling eyelid inflammation.
Low-dose antibiotics (e.g., bacitracin or erythromycin ointment q.h.s.) may have to be maintained indefinitely.

Note
Tetracyclines such as doxycycline are contraindicated in children <8 years, pregnant women, and breast-feeding mothers. Erythromycin 200 mg p.o. one to two times per day can be used in children to decrease recurrent disease.

Follow-Up
In 2 to 7 days, depending on the clinical picture. IOP is monitored while patients are taking topical steroids

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12
Q

Phlyctenulosis

A

Treatment
Indicated for symptomatic patients.

Topical steroid (e.g., loteprednol 0.5% or prednisolone acetate 1% q.i.d., depending on the severity of symptoms). A combination antibiotic/steroid can also be used q.i.d. (e.g., loteprednol 0.5%/tobramycin 0.3% or dexamethasone 0.1%/tobramycin 0.3%). If there is significant tearing, a steroid/antibiotic ointment (e.g., dexamethasone/tobramycin) may be more effective.
Topical ophthalmic antibiotic regimen in the presence of corneal ulcer. Otherwise antibiotic ointment (e.g., erythromycin, bacitracin) q.h.s.
Eyelid hygiene b.i.d. to t.i.d. for blepharitis. .
Preservative-free artificial tears four to six times per day.
In severe cases of blepharitis or acne rosacea, use doxycycline 100 mg p.o. daily. to b.i.d., or erythromycin 200 mg p.o. daily to b.i.d. See 5.8, Blepharitis/Meibomitis.
If the PPD, IGRA, or chest radiograph is positive for TB, refer the patient to an internist or infectious disease specialist for management.

Follow-Up
Recheck in several days. Healing usually occurs over a 10- to 14-day period, with a residual stromal scar. When the symptoms have significantly improved, slowly taper the steroid. Maintain the antibiotic ointment and eyelid hygiene indefinitely. Continue oral antibiotics for 3 to 6 months. Topical azithromycin or cyclosporine may be beneficial steroid-sparing agents in patients with recurrent inflammation

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13
Q

Acute Corneal Hydrops

A

Treatment

Cycloplegic agent (e.g., cyclopentolate 1% t.i.d.), ophthalmic antibiotic ointment (e.g., erythromycin or bacitracin) q.i.d.
Consider an aqueous suppressant such as brimonidine 0.1% b.i.d. to t.i.d.
Start sodium chloride 5% ointment b.i.d. until resolved (usually several weeks to months).
Glasses or a shield should be worn by patients at risk for trauma or by those who rub their eyes.
Intracameral air, SF6, or C3F8 may help edema resolve more quickly, but may be equivalent to conservative management in final BCVA.

Follow up

After an episode of hydrops, examine the patient every 1 to 4 weeks until resolved (which can take several months).

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14
Q

Fuch’s Endothelial Dystrophy

A

Treatment

Topical sodium chloride 5% drops q.i.d. and ointment q.h.s.
May gently blow warm air from a hair dryer at arm’s length toward the eyes for a few minutes every morning to dehydrate the cornea.
IOP reduction if indicated; also may help with corneal edema.
Ruptured corneal bullae are painful and should be treated as recurrent erosions (see 4.2, Recurrent Corneal Erosion).
Surgery: Endothelial keratoplasty is usually indicated when visual acuity decreases due to corneal edema; PK is indicated if significant anterior stromal scarring is present.

Follow-Up
Every 3 to 12 months to check IOP and assess corneal edema. The condition progresses very slowly, and visual acuity typically remains good until stromal edema, epithelial edema, or corneal scarring develop.

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15
Q

Corneal Graft Rejection

A
Treatment
Endothelial Rejection (Endothelial Rejection Line, Corneal Edema, and/or Keratic Precipitates)

Topical steroids (e.g., prednisolone acetate 1% q1h or difluprednate 0.05% q2h while awake; can add dexamethasone 0.1% ointment q.h.s.).
If rejection is severe, recurrent, or recalcitrant, consider systemic steroids (e.g., prednisone 40 to 80 mg p.o. daily) or, rarely, subconjunctival steroids (e.g., betamethasone 3 mg per 0.5 mL). In high-risk patients with severe rejection, consider hospitalization and methylprednisolone 500 mg i.v for a total of one to three doses.
In select cases, other systemic immunosuppressives may be considered including cyclosporine and tacrolimus.
Cycloplegic agent (e.g., cyclopentolate 1% t.i.d.).
Control IOP if increased. See 9.7, Inflammatory Open Angle Glaucoma.
Topical cyclosporine 0.05% to 2% b.i.d. to q.i.d. may be helpful in the treatment and prevention of graft rejection.

Epithelial and Stromal Rejection (Subepithelial Infiltrates or Epithelial Rejection Line)

Double the current level of topical steroids or use prednisolone acetate 1% q.i.d. (whichever is more).
Cycloplegic agent, topical cyclosporine, and IOP control as above.

Follow-Up
Institute treatment immediately to maximize the likelihood of graft survival. Examine the patient every 3 to 7 days. Once improvement is noted, the steroids are tapered very slowly and may need to be maintained at low doses for months to years. IOP must be checked regularly in patients taking topical steroids.

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16
Q

Viral Conjunctivitis/ EKC

A

Treatment

            Counsel the patient that viral conjunctivitis is a self-limited condition that typically gets worse for the first 4 to 7 days after onset and may not resolve for 2 to 3 weeks (potentially longer with corneal involvement).

            Viral conjunctivitis is highly contagious (usually for 10 to 12 days from onset) as long as the eyes are red (when not on steroids) or have active discharge/tearing. Patients should avoid touching their eyes, shaking hands, sharing towels or pillows, etc. Restrict work and school for patients with significant exposure to others while the eyes are red and weeping.

            Frequent handwashing.

            Preservative-free artificial tears or tear ointment four to eight times per day for 1 to 3 weeks. Advise single-use vials to limit tip contamination and spread of the condition.

            Cool compresses several times per day.

            Antihistamine drops (e.g., epinastine 0.05% b.i.d.) if itching is severe.

            If a membrane/pseudomembrane is present, it should be gently peeled with a cotton-tip applicator or smooth forceps to enhance comfort, minimize corneal defects, and help prevent symblepharon formation.

            If a membrane/pseudomembrane is present or if SEIs reduce vision and/or cause significant photophobia, topical steroids should be initiated. For membranes/pseudomembranes, use a more frequent steroid dose or stronger steroid (e.g., loteprednol 0.5% or prednisolone acetate 1% q.i.d.). Consider a steroid ointment (e.g., fluorometholone 0.1% ointment q.i.d. or dexamethasone/tobramycin 0.1%/0.3% ointment q.i.d.) in the presence of significant tearing to maintain longer medication exposure. For SEIs alone, a weaker steroid with less frequent dosing is usually sufficient (e.g., loteprednol 0.2% or 0.5% b.i.d.). Given the possible side effects, prescription of topical steroids is cautionary in the emergency room setting or in patients with questionable follow-up. Steroids may hasten the resolution of the symptoms but prolong the infectious period. Additionally, steroids often necessitate a long-term taper and delayed SEIs can recur during or after such a taper.

Note
Routine use of topical antibiotics for viral conjunctivitis is discouraged unless corneal erosions are present or there is mucopurulent discharge suggestive of bacterial conjunctivitis (see Bacterial Conjunctivitis).

    Follow-Up
    In 2 to 3 weeks, but sooner if the condition worsens significantly or if topical steroids are prescribed.
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17
Q

Allergic Conjunctivitis

A

Treatment

Eliminate the inciting agent. Frequent washing of hair and clothes may be helpful.

Cool compresses several times per day.

Topical drops, depending on the severity.

Mild: Artificial tears four to eight times per day.

Moderate: Use antihistamine and/or mast-cell stabilizer drops. Convenient medications with daily dosing include olopatadine 0.2% or 0.7% and alcaftadine 0.25% drops. Common medications with b.i.d. dosing include olopatadine 0.1%, epinastine 0.05%, nedocromil 2%, bepotastine 1.5%, or ketotifen 0.025% (over-the-counter) drops. Pemirolast 0.1% and lodoxamide 0.1% drops can also reduce symptoms but are recommended at q.i.d. dosing.

        Note
        An ophthalmic nonsteroidal anti-inflammatory drug (NSAID) such as ketorolac 0.5% q.i.d. can also be effective in reducing ocular inflammation, but its use should be monitored given the known risk of corneal toxicity with chronic instillation.

Severe: Mild topical steroid (e.g., loteprednol 0.2% or fluorometholone 0.1% q.i.d. for 1 to 2 weeks) in addition to the preceding medications.

Oral antihistamine (e.g., diphenhydramine 25 mg p.o. t.i.d. to q.i.d. or loratadine 10 mg p.o. daily) in moderate-to-severe cases can be very helpful.

Note
Routine use of topical antibiotics or steroids for allergic conjunctivitis is discouraged.

    Follow-Up
    Two weeks. If topical steroids are used, tapering is required and patients should be monitored for side effects.
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18
Q

Vernal/ Atopic Conjunctivitis

A

**trantas dots, cobblestone papillae

Treatment

Treat as for allergic conjunctivitis except ensure prophylactic use of a mast-cell stabilizer or combination antihistamine/mast-cell stabilizer (e.g., olopatadine 0.2% or 0.7% daily, alcaftadine 0.25% daily, olopatadine 0.1% b.i.d., ketotifen 0.1% b.i.d., lodoxamide 0.1% q.i.d., pemirolast 0.1% q.i.d.) for 2 to 3 weeks before the allergy season starts.

If a shield ulcer is present, add:

Topical steroid (e.g., loteprednol 0.5% or prednisolone acetate 1% drops, dexamethasone 0.1% ointment) four to six times per day.

Topical antibiotic drop (trimethoprim/polymyxin B q.i.d) or ointment (e.g., erythromycin q.i.d., bacitracin/polymyxin B q.i.d.).

Cycloplegic agent (e.g., cyclopentolate 1% t.i.d.).

        Note
        Shield ulcers may need to be scraped to remove superficial plaque-like material before reepithelialization will occur.

Cool compresses q.i.d.

Consider cyclosporine 0.05% to 2% b.i.d. to q.i.d. if not responding to the preceding treatment. Inform the patient that maximal effect of this drop is not seen for several weeks.

If associated with atopic dermatitis of eyelids, consider tacrolimus 0.03% to 0.1% ointment q.h.s. or b.i.d. (preferred), pimecrolimus 1% cream b.i.d., or topical steroid ophthalmic ointment (e.g., fluorometholone 0.1% q.i.d.) to the affected skin for 1 to 2 weeks.

Follow-Up
Every 1 to 3 days in the presence of a shield ulcer; otherwise, every few weeks. Topical medications are tapered slowly as improvement is noted. Anti-allergy drops are maintained for the duration of the season and are often reinitiated a few weeks before the next spring. Patients on topical steroids should be monitored regularly with attention to IOP, even if used only on the skin.

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19
Q

Bacterial Conjununctivitis (non-gonnoccocal)

A

Treatment

Use topical antibiotic therapy (e.g., trimethoprim/polymyxin B or fluoroquinolone drops or ointment q.i.d.) for 5 to 7 days.

H. influenzae conjunctivitis should be treated with oral amoxicillin/clavulanate (20 to 40 mg/kg/day in three divided doses) because of occasional extraocular involvement (e.g., otitis media, pneumonia, and meningitis).

If associated with dacryocystitis, systemic antibiotics are necessary. See 6.9, Dacryocystitis/Inflammation of the Lacrimal Sac.

Follow-Up
Every 2 to 3 days initially, then every 5 to 7 days when stable until resolved. Antibiotic therapy is adjusted according to culture and sensitivity results.

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20
Q

Gonnorheal Conjunctivitis

A

Treatment
Initiated if the Gram stain shows gram-negative intracellular diplococci or there is a high clinical suspicion of gonococcal conjunctivitis.

A dual treatment regimen of ceftriaxone 1 g intramuscularly (i.m.) PLUS azithromycin 1 g p.o. both in a single dose is recommended. If corneal involvement exists, or cannot be excluded because of chemosis and eyelid swelling, hospitalize the patient and treat with ceftriaxone 1 g intravenously (i.v.) every 12 to 24 hours in place of i.m. ceftriaxone. The duration of treatment may depend on the clinical response. Consider an infectious disease consultation in all cases of gonococcal conjunctivitis.

If ceftriaxone is not available or unable to be tolerated (e.g., cephalosporin-allergic patients), consider the following treatment regimens:

Gemifloxacin 320 mg p.o. in a single dose PLUS azithromycin 2 g p.o. in a single dose

Gentamicin 240 mg i.m. in a single dose PLUS azithromycin 2 g p.o. in a single dose”

        Note
        Not only are fluoroquinolones contraindicated in pregnant women and children, but due to increased resistance, they are no longer recommended monotherapy for treatment of gonoccocal infections.

Topical fluoroquinolone ointment q.i.d. or fluoroquinolone drop q2h. If the cornea is involved, use a fluoroquinolone drop q1h (e.g., gatifloxacin, moxifloxacin, besifloxacin, levofloxacin, or ciprofloxacin).

Saline irrigation q.i.d. until the discharge resolves.

Treat for possible chlamydial coinfection (e.g., azithromycin 1 g p.o. single dose or doxycycline 100 mg p.o. b.i.d. for 7 days).

Treat sexual partners with oral antibiotics for both gonorrhea and chlamydia as described.

Follow-Up
Daily until consistent improvement is noted and then every 2 to 3 days until the condition resolves. The patient and sexual partners should be evaluated by their medical doctors for other sexually transmitted diseases.

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21
Q

Pediculosis Conjunctivitis

A

Treatment

Mechanical removal of lice and eggs with jeweler’s forceps.

Any bland ophthalmic ointment (e.g., erythromycin) to the eyelids t.i.d. for 10 days to smother the lice and nits.

Anti-lice lotion and shampoo as directed to nonocular areas for patient and close contacts.

Thoroughly wash and dry all clothes, towels, and linens.

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22
Q

Chlamydial Inclusion Conjunctivitis

A

Treatment

Azithromycin 1 g p.o. single dose, doxycycline 100 mg p.o. b.i.d., or erythromycin 500 mg p.o. q.i.d. for 7 days is given to the patient and his or her sexual partners.

Topical erythromycin or tetracycline ointment b.i.d. to t.i.d. for 2 to 3 weeks.

Follow-Up
In 2 to 3 weeks, depending on the severity. The patient and sexual partners should be evaluated by their medical doctors for other sexually transmitted diseases. Occasionally a 6-week course of doxycycline may be required.

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23
Q

Trachoma

A

Treatment

Azithromycin 20 mg/kg p.o. single dose, doxycycline 100 mg p.o. b.i.d., or erythromycin 500 mg p.o. q.i.d. for 2 weeks.

Tetracycline, erythromycin, or sulfacetamide ointment b.i.d. to q.i.d. for 3 to 4 weeks.

Note
Tetracycline derivatives are contraindicated in children younger than 8 years, pregnant women, and nursing mothers.

Follow-Up
Every 2 to 3 weeks initially, then as needed. Although treatment is usually curative, reinfection is common if hygienic conditions do not improve.

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24
Q

Tetracycline contraindications

A

Children <8yo, pregnant women or nursing

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25
Q

Molluscum contagiosum

A

Treatment
When associated with chronic conjunctivitis, lesions should be removed by simple excision, incision and curettage, or cryosurgery.

Follow-Up
Every 2 to 4 weeks until the conjunctivitis resolves, which often takes 4 to 6 weeks. If many lesions are present, consider human immunodeficiency virus (HIV) testing.

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26
Q

Perinaud’s Oculoglandular Conjunctivitis

A

Treatment

Warm compresses for tender lymph nodes.
Antipyretics as needed.

Disease specific:

Cat-scratch disease: Generally resolves spontaneously in 6 weeks. Consider azithromycin 500 mg p.o. q.i.d., then 250 mg daily for four doses (for children, 10 mg/kg q.i.d., then 5 mg/kg daily for four doses); alternatives include trimethoprim/sulfamethoxazole (160/800 mg b.i.d.) or ciprofloxacin 500 mg p.o. b.i.d. Duration should be individualized. Use a topical antibiotic (e.g., bacitracin/polymyxin B ointment or gentamicin drops q.i.d.). The cat does not need to be removed.

Tularemia: Recommended therapy is gentamicin 5 mg/kg once daily i.m. or i.v. for 10 days. For mild illness, alternative therapies include ciprofloxacin 500 mg p.o. b.i.d. for 10 to14 days or doxycycline 100 mg p.o. b.i.d. for 14 to 21 days. Systemic medication should coincide with gentamicin 0.3% drops q2h for 1 week, and then five times per day until resolved. Often patients are systemically ill and under the care of a medical internist for tularemia; if not, refer to a medical internist for systemic management.

Tuberculosis: Refer to an internist for antituberculosis medication.

Syphilis: Systemic penicillin (dose depends on the stage of the syphilis) and topical tetracycline ointment

Follow-Up
Repeat the ocular examination in 1 to 2 weeks. Conjunctival granulomas and lymphadenopathy can take 4 to 6 weeks to resolve for cat-scratch disease

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27
Q

Wellbutrin side effect

A

anti-depressant

ADE: suicidal thoughts

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28
Q

TB Meds and ADEs

A

RIPE
Rifampin: pink/orange tears, hepatotoxic
Isoniazid: optic neuritis, hepatotoxic
Ethambutl: optic neuritis RETRObubar

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29
Q

Corneal thickness for surgeries

A

CXL: 400 microns (after epi removal to protect endo)
LASIK: 250 microns (remaining

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30
Q

Superior Limbic Keratoconjunctivitis

A

**asociated with thyroid

Treatment
Mild

Aggressive lubrication with preservative-free artificial tears four to eight times per day and artificial tear ointment q.h.s.
Consider punctal occlusion with plugs or cautery because of association with dry eyes.
Treat any concurrent blepharitis.
Consider treatment with cyclosporine 0.05% b.i.d. if not responding to lubrication.
In the absence of dry eyes, a therapeutic bandage disposable soft contact lens can be placed to help relieve symptoms and facilitate healing.

Moderate to Severe (in Addition to Preceding)

Autologous serum drops may be tried with intermittent dosing throughout the day.
Consider treatment with topical tacrolimus 0.03% ointment b.i.d. if no improvement with aggressive lubrication.
If significant amount of mucus or filaments are present, add acetylcysteine 10% drops three to six times per day. Low potency topical steroids like loteprednol, rimexolone, or fluorometholone can be used for short courses to treat exacerbations.
Application of silver nitrate 0.5% solution on a cotton-tipped applicator for 10 to 20 seconds to the superior tarsal and superior bulbar conjunctiva after topical anesthesia (e.g., proparacaine). This is followed by irrigation with saline and use of antibiotic ointment (e.g., erythromycin) q.h.s. for 1 week.

Note
Do not use silver nitrate (75% to 95%) cautery sticks, which cause severe ocular burns.

A low dose of doxycycline can be a helpful adjuvant to counteract matrix metalloproteinase upregulation caused by superior limbic keratoconjunctivitis.
Botulinum toxin can be injected into the muscle of Riolan for temporary relief of symptoms.
Surgical considerations include conjunctival cautery, cryotherapy, conjunctival resection (with or without amniotic membrane graft), recession of the superior bulbar conjunctiva, or high-frequency radiowave electrosurgery.

Follow-Up
Every 2 to 4 weeks during an exacerbation. If signs and symptoms persist despite multiple medical treatment strategies, surgical options should be considered.

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31
Q

Episcleritis

A

**Instill 2.5% phenyl and check in 10-15 for conj vessel blanching

Treatment

If mild, treat with artificial tears q.i.d.
If moderate to severe, a topical NSAID (e.g., diclofenac 0.1% q.i.d.) or a mild topical steroid (e.g., fluorometholone 0.1% or loteprednol 0.5% q.i.d.) often relieves the discomfort. Occasionally, more potent or frequent topical steroid application is necessary.
Oral NSAIDs may be used as an alternate steroid-sparing initial therapy and should be given with food or antacids (e.g., ibuprofen 200 to 600 mg p.o. t.i.d. to q.i.d., naproxen 250 to 500 mg p.o. b.i.d., or flurbiprofen 50 to 100 mg p.o. b.i.d. to t.i.d.) for at least 10 to 14 days.

Note
Many physicians prefer oral NSAIDs to topical NSAIDs or steroids as initial therapy.

Follow-Up
Patients treated with artificial tears need not be seen for several weeks unless discomfort worsens or persists. If topical steroids are used, recheck every 2 to 3 weeks until symptoms resolve. The frequency of steroid administration is then tapered. Episcleritis may recur in the same or contralateral eye.

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32
Q

Scleritis

A

** blue hue, boring pain wake sup at night
Classification
1. Diffuse anterior scleritis: Widespread inflammation of the anterior segment.
2. Nodular anterior scleritis: Immovable inflamed nodule(s)
3. Necrotizing scleritis with inflammation: thin, bluish sclera. Extreme pain. The sclera becomes transparent (choroidal pigment visible) because of necrosis. High association with systemic inflammatory diseases.
4. Necrotizing anterior scleritis without inflammation (scleromalacia perforans): Typically asymptomatic. Seen most often in older women with long-standing rheumatoid arthritis.
5. Posterior scleritis: May start posteriorly, or rarely be an extension of anterior scleritis, or simulate an amelanotic choroidal mass. Associated with exudative retinal detachment, disc swelling, retinal hemorrhage, choroidal folds, choroidal detachment, restricted motility, proptosis, pain, tenderness.

Treatment
Diffuse and nodular scleritis: One or more of the following may be required. Concurrent antiulcer medication (e.g., proton-pump inhibitor [e.g., omeprazole 20 mg p.o. daily] or histamine type 2 receptor blocker [e.g., ranitidine 150 mg p.o. b.i.d.]) may be helpful.

Oral NSAIDs (e.g., flurbiprofen 100 mg t.i.d., naproxen 250 to 500 mg p.o. b.i.d., or indomethacin 25 to 50 mg p.o. t.i.d.): Several different NSAIDs may be tried before therapy is considered a failure. If still no improvement, consider systemic steroids.

Oral steroids: Prednisone 60 to 80 mg p.o. daily for 1 week, followed by a taper to 20 mg daily over the next 2 to 6 weeks, followed by a slower taper. Once daily calcium with Vitamin D (e.g., 600 mg with 400 iU) supplements should be given to reduce risk of osteoporosis. An oral NSAID often facilitates the tapering of the steroid but significantly increases the risk of gastric ulceration. If unsuccessful or disease requires >7.5 to 10 mg prednisone/day for long-term control, immunosuppressive therapy is indicated.

Intravenous steroids: Methylprednisolone succinate 1,000 mg daily for 3 days (followed by oral steroids as above) is preferable to prednisone >80 mg/day because of reduced risk of ischemic necrosis of bone.

Immunosuppressive therapy (e.g., cyclophosphamide, methotrexate, cyclosporine, azathioprine, mycophenolate mofetil, anti-TNFα agents, other biologics): If one drug is ineffective or not tolerated, additional agents should be tried. Systemic steroids may be used in conjunction. Immunosuppressive therapy should be coordinated with an internist, rheumatologist, or uveitis specialist. Topical cyclosporine is rarely effective.

Conventional teaching is that topical therapy is of little benefit. However, difluprednate 0.05% drops are sometimes helpful (with or without a topical NSAID) and thus, in mild cases, may spare the need for systemic immunosuppressive agents.

Subconjunctival steroid injections (e.g., 0.1 to 0.3 mL of triamcinolone acetonide 40 mg/mL or dexamethasone sodium phosphate 4 mg/mL): May be very helpful in patients unable to tolerate systemic therapy. Side effects may include subconjunctival hemorrhage, cataract, glaucoma, and (rarely) catastrophic scleral melting. Do not use in cases of necrotizing scleritis.

            Necrotizing scleritis: Necrotizing scleritis associated with rheumatoid arthritis is associated with increased mortality due to coronary arteritis or cerebral angiitis and requires urgent, aggressive immunosuppressive therapy.

Systemic steroids and immunosuppressive therapies are used as above during the first month; the former is tapered slowly.

Scleral patch grafting may be necessary if there is significant risk of perforation, ideally once the inflammation is better controlled.

Posterior scleritis: Therapy may include systemic aspirin, NSAIDs, steroids, or immunosuppressive therapy as described previously. Consult a retina or uveitis specialist.

Infectious etiologies: Debridement and cultures/stains are essential. Treat with appropriate topical and systemic antimicrobials. Oral fluoroquinolones have good ocular tissue penetration. If a foreign body (e.g., scleral buckle [associated with Proteus or Pseudomonas]) is present, surgical removal is indicated.

Glasses or eye shield should be worn at all times if there is significant thinning and risk of perforation.

Note
Remember that periocular steroids are contraindicated in necrotizing scleritis where they can lead to further scleral thinning and possible perforation.

    Follow-Up
    Depends on the severity of the symptoms and the degree of scleral thinning. Decreased pain is the first sign of response to treatment, even if inflammation appears unchanged.
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33
Q

Blepharitis

A

Treatment

Scrub the eyelid margins twice a day with a commercial eyelid scrub or mild shampoo on a washcloth.

Warm compresses for 5 to 10 minutes b.i.d. to q.i.d.

If associated with dry eyes, use preservative-free artificial tears four to eight times per day.

If moderately severe, add erythromycin ointment or azithromycin gel-drop to the eyelids q.h.s.

Consider omega-3 fatty acid oral supplementation as well as cyclosporine 0.05% drops b.i.d.

Unresponsive meibomitis can be treated with topical ophthalmic antibiotic/steroid ointments (e.g., tobramycin 0.3%/dexamethasone 0.1% b.i.d. to t.i.d.). Also consider an oral agent such as doxycycline 100 mg p.o. daily for 1 to 2 weeks; slowly taper to one-fourth full dose and maintain for 3 to 6 months. Oral azithromycin 500 mg/day × 3 days for 3 cycles with 7-day intervals may also be used.

If demodex mite infestation is suspected, due to presence of collarettes, and patients have failed the above regimen, consider tea-tree oil eyelid scrubs or an eyelid cleansing agent with hypochlorous acid for a minimum of 6 weeks.

If little improvement has been made, consider LipiFlow, pulsed light laser therapy, microblepharoexfoliation, and probing of meibomian glands.

Note
Tetracycline derivatives such as doxycycline should not be used in pregnant women, nursing mothers, or children ≤ 8 years. Erythromycin 200 mg p.o. b.i.d. is an alternative in these cases.

Follow-Up
Two to 4 weeks depending on severity of presenting symptoms. Eyelid scrubs and warm compresses may be reduced to once daily as the condition improves but may need to be maintained indefinitely.

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34
Q

Ocular Rosacea

A

Treatment

Warm compresses and eyelid hygiene for blepharitis or meibomitis. Treat dry eyes if present .
Avoidance of exacerbating foods, beverages, and environmental factors.
Doxycycline 100 mg p.o. b.i.d. for 1 to 2 weeks then daily; taper the dose slowly once relief from symptoms is obtained. Some patients are maintained on low-dose doxycycline (e.g., 20 to 100 mg p.o. daily or less than daily) indefinitely if active disease recurs when the patient is off medication. Erythromycin 250 mg q.i.d. or oral azithromycin 500 mg/day × 3 days for 3 cycles with 7-day intervals is an alternative if doxycycline is contraindicated.

Note
Tetracycline derivatives such as doxycycline should not be given to pregnant women, nursing women, or children ≤8 years. Patients should be warned of increased sunburn susceptibility with use of this medication.

Note
Asymptomatic ocular rosacea without progressively worsening eye disease does not require oral antibiotics.

Consider oral omega-3 fatty acid supplements, cyclosporine 0.05% drops b.i.d., and topical steroids for chronic rosacea-related ocular and eyelid inflammation
Facial lesions can be treated with metronidazole gel (0.75%) application b.i.d.
Treat chalazia as needed
Corneal perforations may be treated with cyanoacrylate tissue adhesive if small (<3 mm), whereas larger perforations may require surgical correction. Doxycycline is indicated if there is concern for corneal thinning due to its anti-collagenase properties.
If infiltrates stain with fluorescein, an infectious corneal ulcer may be present. Smears, cultures, and antibiotic treatment may be necessary.

Follow-Up
Variable; depends on the severity of disease. Patients without corneal involvement are seen weeks to months later. Those with corneal involvement are examined more often. Patients with moderate-to-severe facial disease should also seek dermatologic consultation.

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35
Q

Tetracyclines

A

30s subunit - AT 30

  • Doxycycline
  • Minocycline
    • teeth discoloration so cant use in pregnant, nursing or children
    • need to take (not doxy) on empty stomach
    • CATS - pseudotumor cerebri
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36
Q

Aminoglycosides

A

30s subunit - AT 30
- tobramycin
- gentamycin
TobraGent30

**SPK

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37
Q

Macrolides

A

50s subunit - CEL 50

  • erythromycin
  • azithromycin
  • clarithromycin
  • *Azithro - taken on empty stomach - PAT
  • *Azithro - good for pregnant women - PAC
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38
Q

Conj condition w/ associated tumors

A

CIN –> SCC
- actinic keratosis —> SCC on lid
PAM –> melanoma 10-30%
Nevus –> melanoma
Nevus of Ota –> uveal melanoma (and glaucoma)
unilateral blepharoconunctivitis –> sebaceous carcinoma

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39
Q

Hordeolum/ Chalzion

A

Treatment

Warm compresses for 10 minutes q.i.d. with light massage over the lesion.
Consider a short course of topical antibiotic if lesion is draining or for associated blepharitis (e.g., bacitracin or erythromycin ointment b.i.d. for 1 to 2 weeks). Consider systemic therapy with doxycycline 100 mg p.o. daily to b.i.d. for its antibacterial and anti-inflammatory properties (e.g., multiple hordeola, ocular rosacea).
If a hordeolum worsens, consider incision and drainage and management as per preseptal cellulitis (see 6.10, Preseptal Cellulitis).
If the chalazion fails to resolve after 3 to 4 weeks of appropriate medical therapy and the patient wishes to have it removed, incision and curettage are performed. Occasionally, an injection of steroid (e.g., 0.2 to 1.0 mL of triamcinolone 40 mg/mL usually mixed 1:1 with 2% lidocaine with epinephrine) into the lesion is performed instead of minor surgery, especially if the chalazion is near the lacrimal apparatus. The total dosage depends on the size of the lesion. All recurrent or atypical chalazia must be sent for pathology.

Note
A steroid injection can lead to permanent depigmentation or atrophy of the skin at the injection site, especially in dark-skinned individuals. Similarly, vigorous injection can rarely result in retrograde intra-arterial infiltration with resultant central retinal artery occlusion. Because of these risks, some manufacturers of injectable steroids (e.g., triamcinolone, dexamethasone, and betamethasone) have historically recommended against their use intraocularly and in the periocular region. Off label use of the medications should include a detailed discussion between physician and patient.

Follow-Up
Patients are not routinely seen after instituting medical therapy unless the lesion persists beyond 3 to 4 weeks. Patients who have a procedure such as incision and curettage are usually reexamined in 1 week or PRN

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40
Q

Canaliculitis

A

Treatment

Remove obstructing concretions or retained plug. Concretions may be expressed through the punctum at the slit lamp. A canaliculotomy is usually required for complete removal or in the setting of a retained punctual plug. If necessary, marsupialize the horizontal canaliculus from a conjunctival approach and allow incision to heal by secondary intention.
If concretions are removed, consider irrigating the canaliculus with an antibiotic solution (e.g., trimethoprim sulfate/polymyxin B, moxifloxacin, penicillin G solution 100,000 units/mL, iodine 1% solution). The patient is irrigated while in the upright position, so the solution drains out of the nose and not into the nasopharynx.
Treat the patient with antibiotic drops (e.g., trimethoprim sulfate/polymyxin B or moxifloxacin) q.i.d. and oral antibiotics for 1 to 2 weeks (e.g., doxycycline 100 mg b.i.d.).
If a fungus is found on smears and cultures, nystatin 1:20,000 drops t.i.d. and nystatin 1:20,000 solution irrigation several times per week may be effective. If evidence of herpes virus is found on smears, treat with trifluridine 1% drops five times per day. Silicone intubation along with appropriate antiviral therapy is sometimes required in viral canaliculitis.
Apply warm compresses to the punctal area q.i.d.

Follow-Up
Five to 7 days depending on severity. This is usually not an urgent condition.

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41
Q

Dacryocystitis

A

Treatment

Systemic antibiotics in the following regimen: Children older than 5 years and <40 kg:

Afebrile, systemically well, mild case, and reliable parent: Amoxicillin/clavulanate: 25 to 45 mg/kg/day p.o. in two divided doses for children, maximum daily dose of 90 mg/kg/day.
Alternative treatment: Cefpodoxime: 10 mg/kg/day p.o. in two divided doses for children, maximum daily dose of 400 mg.
Febrile, acutely ill, moderate-to-severe case, or unreliable parent: Hospitalize and treat with cefuroxime, 50 to 100 mg/kg/day intravenously (i.v.) in three divided doses in consultation with infectious disease specialist.

Adults:

Afebrile, systemically well, mild case, and reliable patient: Cephalexin 500 mg p.o. q6h.
Alternative treatment: Amoxicillin/clavulanate 500/125 mg t.i.d. or 875/125 mg p.o. b.i.d.
Febrile, acutely ill, or unreliable: Hospitalize and treat with cefazolin 1 g i.v. q8h. See 7.3.1, Orbital Cellulitis.
The antibiotic regimen is adjusted according to the clinical response and the culture/sensitivity results. The i.v. antibiotics can be changed to comparable p.o. antibiotics depending on the rate of improvement, but systemic antibiotic therapy should be continued for at least a full 10- to 14-day course.

Topical antibiotic drops (e.g., trimethoprim/polymyxin B q.i.d.) may be used in addition to systemic therapy. Topical therapy alone is not adequate.
Apply warm compresses and gentle massage to the inner canthal region q.i.d.
Administer pain medication (e.g., acetaminophen with or without codeine) p.r.n.
Consider incision and drainage of a pointing abscess.
Consider surgical correction (e.g., dacryocystorhinostomy with silicone intubation) only after the acute episode has resolved, particularly with chronic dacryocystitis.

Follow-Up
Daily until improvement confirmed. If the condition of an outpatient worsens, hospitalization and i.v. antibiotics are recommended.

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42
Q

Preseptal Cellulitis

A

Treatment

Antibiotic therapy

Mild preseptal cellulitis, older than 5 years (<40 kg), afebrile, reliable patient/parent:

Amoxicillin/clavulanate: 25 to 45 mg/kg/day p.o. in two divided doses for children, maximum daily dose of 90 mg/kg/day; 875/125 mg p.o. q12h for adults.

or

Cefpodoxime: 10 mg/kg/day p.o. in two divided doses for children, maximum daily dose of 400 mg; 200 mg p.o. q12h for adults.

or

Cefdinir: 14 mg/mg/day p.o. in two divided doses for children with maximum daily dose of 600 mg; 600 mg p.o. once daily for adults.

If the patient is allergic to penicillin, then

Trimethoprim/sulfamethoxazole: 8 to 12 mg/kg/day trimethoprim with 40 to 60 mg/kg/day sulfamethoxazole p.o. in two divided doses for children; 160 to 320 mg trimethoprim with 800 to 1,600 mg sulfamethoxazole (one to two double-strength tablets) p.o. b.i.d. for adults.

or

Moxifloxacin 400 mg p.o. daily (contraindicated in children).

If exposure to methicillin-resistant Staphylococcus aureus (MRSA) is suspected, then

Trimethoprim/sulfamethoxazole: 8 to 12 mg/kg/day trimethoprim with 40 to 60 mg/kg/day sulfamethoxazole p.o. in two divided doses for children; one to two tablets double strength trimethoprim-sulfamethoxazole 160/800 mg p.o. q12h for adults.

or

Doxycycline: 100 mg p.o. b.i.d (contraindicated in children, pregnant women, and nursing mothers).

or

Clindamycin: 10 to 30 mg/kg/day p.o. in three to four divided doses for children; 450 mg p.o. t.i.d. for adults. In addition to covering MRSA, this antibiotic also gives good coverage for streptococci and methicillin-sensitive S. aureus.

or

Linezolid: 20 to 30 mg/kg/day p.o. in two to three divided doses for children; 400 to 600 mg p.o. b.i.d. for adults. In addition to covering MRSA, this antibiotic also gives good coverage for streptococci. Limit use of this medication without infectious disease consultation so as to prevent resistance, and caution long-term therapy which can cause hematologic toxicity (e.g., thrombocytopenia, anemia).

Note
Patients with the following risk factors should be covered for MRSA: history of MRSA infection or colonization, recurrent skin infections, contact with someone known to have MRSA, admission to a healthcare or long-term care facility within the past year, placement of a permanent indwelling catheter, on hemodialysis, i.v. drug use, incarceration within the last 12 months, participation in sports that include skin-to-skin contact or sharing of equipment and clothing, poor personal hygiene.

Note
Oral antibiotics are maintained for 10 to 14 days.

Moderate-to-severe preseptal cellulitis, or any one of the following:

Patient appears toxic.
Patient may be noncompliant with outpatient treatment and follow-up.
Child 5 years or younger.
No noticeable improvement or worsening after 24 to 48 hours of oral antibiotics.

Admit to the hospital for i.v. antibiotics as follows:

Vancomycin: 10 to 15 mg/kg i.v. every 6 hours in children; 0.5 to 1 g i.v. q12h for adults. (Dose adjustment is needed in cases of impaired renal function.)

Plus one of the following:

Ampicillin/sulbactam: 300 mg/kg/day i.v. in four divided doses for children; 3.0 g i.v. q6h for adults.
Piperacillin–tazobactam: 240 mg/kg/day i.v. in three divided doses for children; 4.5 g i.v. q6h adults.
Ceftriaxone: 80 to 100 mg/kg/day i.v. in two divided doses for children with maximum of 4 g/day; 2 g i.v. q12h for adults.
Cefepime: 50 mg/kg q12h (max 2 g/dose) in children; 1 to 2 g i.v. q12h in adults.
Ceftazidime: 90 to 150 mg/kg/day i.v. in three divided doses for children; 1 g i.v. q8–12h in adults.

If the patient is allergic to penicillin, see 7.3.1, Orbital Cellulitis, for alternatives.

Note
Intravenous antibiotics can be changed to comparable oral antibiotics after significant improvement is observed. Systemic antibiotics are maintained for a complete 10- to 14-day course. See 7.3.1, Orbital Cellulitis, for alternative treatment. In complicated cases or patients with multiple allergies, consider consultation with infectious disease specialist for antibiotic management.

Warm compresses to the inflamed area t.i.d. p.r.n.
Polymyxin B/bacitracin ointment to the eye q.i.d. if secondary conjunctivitis is present.
Tetanus toxoid if needed. See Appendix 2, Tetanus Prophylaxis.
Nasal decongestants if sinusitis is present.
Orbital exploration and debridement is warranted if a fluctuant mass or abscess is present, or if a retained foreign body is suspected. Obtain Gram stain and culture of any drainage. Avoid the orbital septum if possible. A drain may need to be placed.
Consider an infectious disease consult in patients who have failed oral antibiotics and require i.v. treatment.

Follow-Up
Daily until clear and consistent improvement is demonstrated, then every 2 to 7 days until the condition has totally resolved. If a preseptal cellulitis progresses despite antibiotic therapy, the patient is admitted to the hospital and a repeat (or initial) orbital CT scan is obtained. For patients already on p.o. antibiotics, switch to i.v. antibiotics

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43
Q

Tumors of the Eyelid

A

Treatment

Basal cell carcinoma: Surgical excision with histologic evaluation of the tumor margins either by frozen sections or by Mohs techniques. The entire tumor should be excised with clean margins. Patients are informed about the etiologic role of the sun and are advised to avoid unnecessary sunlight exposure and to use protective sunscreens.

Sebaceous carcinoma: The approach is two-staged with stage 1 using map biopsies on the entire surface of the eye to ascertain the extent of Pagetoid spread or deep tumor. Stage 2 is performed after all biopsies are reviewed; Pagetoid spread is treated with cryotherapy whereas deep tumor requires excision. Reconstruction is then provided. Close follow-up of regional nodes is indicated. Exenteration is often required when orbital invasion is present. Referral to an oncologist or internist for systemic work-up and surveillance is important with attention to the lymph nodes, lungs, brain, liver, and bone.

Squamous cell carcinoma: Same as for basal cell carcinoma. Radiation therapy is the second best treatment after surgical excision. Patients are informed about the etiologic role of the sun. Referral to an oncologist or internist for regional and/or systemic work-up and surveillance is important.

Malignant melanoma: Treatment requires wide surgical excision. The margins must be free of tumor and require permanent sections. Sentinel lymph node biopsy may be required depending on the depth of the tumor. Referral to an oncologist or internist for regional and/or systemic work-up and surveillance is imperative.

Note
Because both melanoma and sebaceous carcinoma are difficult to diagnose by frozen section, multiple excisions utilizing permanent sectioning may be necessary until all surgical margins are free of tumor. The cornea and globe must be protected during this interim time with lubrication or temporary tarsorrhaphy.

Follow-Up
Initial follow-up is every 1 to 4 weeks to ensure proper healing of the surgical site. Patients are then reevaluated every 6 to 12 months, or more frequently, for more aggressive lesions. Patients who have had one skin malignancy are at greater risk for additional malignancies.

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44
Q

TED = Grave’s Disease

A
  • *eyelid lag on downward gaze = von Graefe sign
  • *IMSLO = order of muscle involvement (I = can’t elevate)

Treatment

Smoking cessation: All patients with TED who smoke must be explicitly told that continued tobacco use increases the risk of progression and the severity of the orbitopathy. This conversation should be clearly documented in the medical record.
Refer the patient to a medical internist or endocrinologist for management of systemic thyroid disease, if present. If TFTs are normal, the patient’s TFTs should be checked every 6 to 12 months. Not infrequently, a euthyroid patient with TED will have an elevated TSI.
Treat exposure keratopathy with artificial tears and lubrication or by taping eyelids closed at night. Goggles at night may be helpful. The use of topical cyclosporine drops for the treatment of ocular surface inflammation in TED is still under investigation, but is a reasonable long-term treatment option if dry eye syndrome is present.
Treat eyelid edema with cold compresses in the morning and head elevation at night. This management may not be very effective. Avoid diuretics.
Indications for orbital decompression surgery include: Optic neuropathy, worsening or severe exposure keratopathy despite adequate treatment, globe luxation, uncontrollably high IOP, morbid proptosis.
A stepwise approach is used for surgical treatment, starting with orbital decompression (if needed), followed by strabismus surgery (for significant strabismus, if present), followed by eyelid surgery. Alteration of this sequence may lead to unpredictable results. Note that only a minority of patients with TED will need to undergo the entire surgical algorithm.

The following recommendations are somewhat controversial:

Corticosteroids: During the acute inflammatory phase, prednisone 1 mg/kg p.o. daily, tapered over 4 to 6 weeks, is a reasonable temporizing measure to improve proptosis and diplopia in preparation for orbital decompression surgery. There is evidence that the use of pulsed intravenous corticosteroids followed by a course of oral corticosteroids may result in better long-term control of TED with fewer systemic side effects than oral corticosteroids and is a reasonable option to offer patients in the acute phase of TED; other experts questions the long-term efficacy of this regimen.
Selenium supplementation: Data from Europe has concluded that the use of selenium supplementation (an antioxidant) reduces the severity and progression of mild-to-moderate TED. It is reasonable to offer this therapy to women with mild-to-moderate, active TED at a dose of 100 μg p.o. b.i.d. Caution should be used in the use of selenium supplementation in men, especially with a family history of prostate cancer.

Visual loss from optic neuropathy: Treat immediately with prednisone 1 mg/kg/day with close monitoring. In cases of severe visual loss, admission for pulsed intravenous therapy may be indicated. Radiation therapy may be offered for mild-to-moderate optic neuropathy, with the understanding that there is typically a lag in the treatment effect. Posterior orbital decompression surgery (for mild-to-severe optic neuropathy), either medial or lateral, is essential and usually effective in rapidly reversing or stabilizing the optic neuropathy. Anterior orbital decompression is usually ineffective in treating TED optic neuropathy.

Follow-Up

Optic nerve compression requires immediate attention and close follow-up.
Patients with advanced exposure keratopathy and severe proptosis also require prompt attention and close follow-up.
Patients with minimal-to-no exposure problems and mild-to-moderate proptosis are reevaluated every 3 to 6 months. Because of the potential risk of optic neuropathy, patients with restrictive strabismus may be followed more frequently.
Patients with fluctuating diplopia or ptosis should be evaluated for myasthenia gravis
All patients with TED are instructed to return immediately with any new visual problems, worsening diplopia, or significant ocular irritation. All smokers with TED must be reminded to discontinue smoking at every office visit, and appropriate referral to their primary physician for a smoking cessation program is indicated.

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45
Q

Idiopathic Orbital Inflammatory Syndrome - Orbital pseudotumor

A

** painful, explosive onset, unilateral
Treatment

Prednisone 1 to 1.2 mg/kg/day as an initial dose in adults and children, along with gastric prophylaxis (e.g., ranitidine 150 mg p.o. b.i.d., omeprazole 40 mg p.o. daily). All patients are warned about potential systemic side effects and are instructed to follow up with their primary physicians to monitor blood sugar and electrolytes.
Low-dose radiation therapy may be used when the patient does not respond to systemic corticosteroids, when disease recurs as corticosteroids are tapered, or when corticosteroids pose a significant risk to the patient. Radiation therapy should only be used once orbital biopsy, if anatomically and medically feasible, has excluded other etiologies.
Steroid-sparing agents (e.g., methotrexate, cyclophosphamide, etc.) in cases that do not respond to or recur with corticosteroid therapy. Biopsy of affected tissue, when feasible, is indicated to rule out malignancy.
Biologic therapy may be considered in cases that fail other modalities. The efficacy of specific biologic agents (e.g., CD20 antibody, TNF antibody, etc.) in IOIS is not known.

Follow-Up
Reevaluate in 1 to 2 days. Patients who respond dramatically to corticosteroids are maintained at the initial dose for 3 to 5 days, followed by a slow taper to 40 mg/day over 2 weeks, and an even slower taper below 20 mg/day, usually over several weeks. If the patient does not respond dramatically to appropriate corticosteroid doses, biopsy should be strongly considered. Recurrences of IOIS are not uncommon, especially at lower corticosteroid doses.

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46
Q

Toxocariasis

A

**leukocoria
**nematode
**vitritis, vitreous traction
Treatment
Steroids (topical, periocular, or systemic routes may be used, depending on the severity of the inflammation).
Consider a surgical vitrectomy when vitreoretinal traction bands form or when the condition does not improve or worsens with medical therapy.
Consider laser photocoagulation of the nematode if it is visible.

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47
Q

Coat’s Disease

A

**leukocoria - from exudative RD

Treatment
Laser photocoagulation or cryotherapy to leaking vessels. Though associated with a poor outcome, surgery may be required for a retinal detachment. Consider anti-VEGF agents if significant exudate, subretinal or intraretinal fluid is present.

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48
Q

ROP

A

Treatment

Always based on severity and location. Therapeutic goal is ablation of immature, avascular zones of retina. Laser photocoagulation is preferred over cryotherapy. Treatment should be instituted within 48–72 hours. Use of intravitreal anti-VEGF agents is an emerging treatment modality, especially when photocoagulation is not available or in very posterior Zone 1 cases; however the long-term effects and potential risks of these medications in preterm infants have yet to be determined.

Type 1 ROP needs treatment.
- Defines high-risk eyes that meet the criteria for treatment:
Zone I (posterior pole), any stage with plus disease (2 quadrants of tortuous
vessels).
Zone I, stage 3 without plus disease.
Zone II (nasal periphery), stage 2 or 3 with plus disease.

Type 2 ROP should be followed closely.
- Defines less severely advanced eyes that should be monitored closely for
progression to Type 1 disease:
Zone I, stage 1 and 2 without plus disease.
Zone II, stage 3 without plus disease.
For stages 4 and 5: Surgical repair of retinal detachment by scleral buckling,
vitrectomy surgery, or both is recommended.

Follow-Up

A single ocular examination is sufficient only if it unequivocally shows full retinal vascularization in both eyes.
One week or less: immature vascularization, zone I, no ROP; immature retina localized to boundary of zone I and II; zone I, stage 1 or 2; zone II, stage 3; or any concern for aggressive posterior ROP.
One to 2 weeks: immature vascularization localized to posterior zone II; or zone II, stage 2; or zone I, regressing ROP.
Two weeks: immature vascularization localized to zone II, no ROP; zone II, stage 1; or zone II, regressing ROP.
Two to 3 weeks: zone III, stage 1 or 2; or zone III, regressing ROP.

Children who have had ROP have a higher incidence of myopia, strabismus, amblyopia, macular dragging, cataracts, glaucoma, and retinal detachment. An untreated fully vascularized fundus needs examination at age 6 months to rule out these complications.

Note
Because of the possibility of late retinal detachments and other ocular complications, ROP patients should be followed at yearly intervals for life.

Acute-phase ROP screening can be discontinued when any of the following signs is present, indicating that the risk of visual loss from ROP is minimal or passed:

  • Zone III retinal vascularization attained without previous zone I or II ROP. If there is doubt about the zone or if the postmenstrual age is <35 weeks, confirmatory examinations may be warranted.
  • Postmenstrual age of 50 weeks and no ROP disease equivalent to or worse than zone I, any stage or zone II, stage 3.
  • Full retinal vascularization in close proximity to the ora serrata (for cases treated with anti-VEGF therapy).

If treated with anti-VEGF, follow-up should be extended due to risk of ROP recurring after 45 weeks.

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49
Q

Familial Exudative Vitreoretinopathy (FEVR)

A

**Peripheral retinal capillary nonperfusion, most prominently temporally, and may be present for 360 degrees. Macular dragging temporally.
**AD
Treatment
Laser of peripheral nonperfused retina is sometimes considered if there is documented progression. Small, stable tufts of neovascularization can be observed. Scleral buckling and vitrectomy can be considered for retinal detachments. Often complicated by proliferative vitreoretinopathy. Treat amblyopia as needed. Genetic testing for common mutations may be considered.

Follow-Up
Asymptomatic patients should be followed every 6 to 12 months throughout life to monitor for progression.

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50
Q

Esotropia

A

Treatment
In all cases, correct refractive errors of +2.00 diopters or more. In children, treat any underlying amblyopia (see 8.7, Amblyopia).

Congenital esotropia: Almost always requires strabismus surgery. However, prescribe glasses and initiate treatment of any underlying amblyopia prior to surgical intervention as appropriate.

Accommodative esotropia: Glasses must be worn full time.

If the patient is <6 years, correct the hyperopia with the full cycloplegic refraction.
If the patient is >6 years, attempts should be made to give as close to the full-plus refraction as possible, knowing that some may not tolerate the full prescription. Attempts to push plus lenses during the manifest (noncycloplegic) refraction until distance vision blurs may be tried to give the most plus lenses without blurring distance vision. The goal of refractive correction should be straight alignment without sacrificing visual acuity.
If the patient’s eyes are straight at distance with full correction, but still esotropic at near fixation (high AC/A ratio), treatment options include the following:
- Bifocals (flat-top or executive type) +2.50 or +3.00 diopter add, with top of the bifocal at the lower pupillary border.
- Extraocular muscle surgery targeting the near deviation only may be indicated. This typically requires posterior fixation sutures to the muscle to modify the surgical effect for near only.
- Wearing full-plus distance glasses only.

Nonaccommodative, partially accommodative, or decompensated accommodative esotropia: Muscle surgery is usually performed to correct the nonaccommodative deviation or the significant residual esotropia that remains when glasses are worn.

Sensory-deprivation esotropia:

  • Attempt to identify and correct the cause of poor vision.
  • Amblyopia treatment.
  • Give the full cycloplegic correction (in fixing eye) if the patient is <6 years of age, otherwise give as much plus as tolerated during manifest refraction.
  • Muscle surgery to correct the manifest esotropia.
  • All patients with low vision in one eye need to wear protective polycarbonate lens glasses at all times.

Follow-Up
At each visit, evaluate for amblyopia and measure the degree of deviation with prisms (with glasses worn).

In the absence of amblyopia, the child is reevaluated in 3 to 6 weeks after a new prescription is given. If no changes are made and the eyes are straight, the patient should be followed several times a year when young, decreasing to annually when stable.
When a residual esotropia is present while the patient wears glasses, an attempt is made to add more plus power to the current prescription. Children <6 years should receive a new cycloplegic refraction; plus lenses are pushed without cycloplegia in older children. The maximal additional plus lens that does not blur distance vision is prescribed. If the eyes cannot be straightened with more plus power, then a decompensated accommodative esotropia has developed (see above in Section 8.4, Comitant OR Concomitant Esotropic Deviations).
Hyperopia often decreases slowly after age 5 to 7 years, and the strength of the glasses may need to be reduced so as not to blur distance vision. If the strength of the glasses must be reduced to improve visual acuity and the esotropia returns, then this is a decompensated accommodative esotropia.

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51
Q

Aplastic Anemia meds

A

Acetazolamide (diamox)
Methazolamide (Neptazane)
Chloramphenicol

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52
Q

Pseudotumor cerebri meds

A
CATS
contraceptives
accutane
tetracyclines
synthroid
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53
Q

Meds for MRSA tx

A

BCD - bacteria can’t decide
Bactrim
Clindamycin
Doxycyxline

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54
Q

Bone marrow suppression meds

A

TMP - treat marrow poorly
Trimethoprim
Methotrexate
Pyrimethamine

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55
Q

Cholinergic Agonists

A
Pilocarpine
MG meds
- Neostigmine
- Pyridostigmine
- Edrophonium
Ecothiophate

Systemic
- Donepezil

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56
Q

Cholinergic Antagonist

A

ASH CiTy

  • Atropine
  • Scopolamine
  • Homatropine
  • Cyclopentolate
  • Tropicamide
Systemic:
- Antianxiety
   Diazepam
- Antipsychotics
   Chlorpromazine
   Thioradazine
- Antidepressants
   Amitryptiline
   Imipramine
   Phenelzine
- Antihistamines
   Promethazine (phenergan)
   Bropheniramine
   Chlorpheniramine
   Dipheniramine
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57
Q

Adrenergic Agonist

A
Phenylephrine
a2 agonists
- Apraclonidine
- Brimonidine
Decongestant
- Naohazoline
- Tetrahydrozoline
Systemic:
- Clonidine
- Isoproterenol
- Asthma
   Salmeterol
   Albuterol
   Levalbuterol
   Terbutaline
   Metaproterenol
- Dopamine agonists
   Methylphenidate
   Dextroamphetamine
   Bromomcriptine
   Amantadine
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58
Q

Adrenergic Antagonist

A

B-blocker

  • Timolol
  • Carteolol
  • Metipranolol
  • Betaxolol
  • Levobunolol
Systemic
- BPH - a1 antagonists
   Tamsulosin
   Prazosin
   Terazosin
- B antagonists
   Labetolol
   Propranolol
- B1 antagonists
   Atenolol
   Metoprolol
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59
Q

Exotropia

A

Treatment
In all cases, correct significant refractive errors and treat amblyopia.

Exophoria:
- No treatment necessary unless it progresses to intermittent exotropia.

Intermittent exotropia:
Phase 1 (XT at D no N): Follow patient closely.
Phase 2 (XT at D some N): Muscle surgery may be considered to maintain normal binocular vision.
Phase 3 (XT at D and N): Muscle surgery is often indicated at this point. Bifixation or peripheral fusion can occasionally be attained.

Sensory-deprivation exotropia:

  • Correct the underlying cause, if possible.
  • Treat any amblyopia.
  • Muscle surgery may be performed for manifest exotropia.
  • When one eye has very poor vision, protective glasses (polycarbonate lens glasses) should be worn at all times to protect the good eye.

Congenital exotropia:
- Muscle surgery early in life, as in patients with congenital esotropia.

Consecutive exotropia: (post surgery)

  • Additional muscle surgery may be considered.
  • Prism correction in glasses can be used.
  • Over-minus or under-plus correction can stimulate accommodative convergence.

Dissociated horizontal deviation:
- Muscle surgery may be considered.

Convergence paralysis:

  • Base-in prisms at near to alleviate diplopia.
  • Plus lenses if accommodation is also weakened.

Follow-Up

If no amblyopia is present, then reexamine every 4 to 6 months. The parents and patient are asked to return sooner if the deviation increases, becomes more frequent, stays out longer, or if the patient begins to close one eye.

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60
Q

Amblyopia

A

Treatment

Patients younger than 12 years:

Appropriate spectacle correction (full cycloplegic refraction or reduce the hyperopia in both eyes symmetrically ≥1.50 diopters). If vision remains reduced after period of refractive adaptation (6 to 12 weeks), begin patching or penalization of fellow eye.
Patching: Patch the eye with better corrected vision 2 to 6 hours/day. Follow up visits should be scheduled for 1 week per year of age (e.g., 3 weeks for a 3 year old). Adhesive patches placed directly over the eye are most effective. Patches worn over glasses are not ideal due to the risk of children peeking. If a patch causes local irritation, use tincture of benzoin on the skin before applying the patch and use warm water compresses on the patch before removal.
Penalization with atropine: Atropine 1% once daily (used with glasses) has been shown to be equally effective as patching in mild-to-moderate amblyopia (20/100 or better). If vision does not improve, the effect of the atropine can be increased by removing the hyperopic lens from the glasses of the non-amblyopic eye. If the child is experiencing difficulty with school work with the use of atropine, he/she can wear full hyperopic correction with a +2.50 bifocal during school.
Optical degradation: Use a high plus lens (e.g., +9.00 diopters or an aphakic contact lens) to blur the image. If the child is highly myopic, may remove the minus lens from the preferred eye.

Continue patching until the vision is equalized or shows no improvement after three compliant cycles of patching. If a recurrence of amblyopia is likely, use part-time patching to maintain improved vision.
If occlusion amblyopia (a decrease in vision in the patched eye) develops, patch the opposite eye for a short period (e.g., 1 day per year of age), and repeat the examination.
In strabismic amblyopia, delay strabismus surgery until the vision in the two eyes is equal, or maximal vision has been obtained in the amblyopic eye.
If treatment of amblyopia fails or the patient presents outside of treatment age range, protective glasses should be worn to prevent accidental injury to the non-amblyopic eye. Any child who does not have vision improved to at least 20/40 needs to wear eye protection during sports (one-eyed athlete rule).
Treatment of media opacity: Remove the media opacity and begin patching the non-amblyopic eye.
Treatment of anisometropic amblyopia: Give the appropriate spectacle correction at the youngest age possible. If vision remains reduced after period of refractive adaptation (6 to 12 weeks), begin patching or penalization of fellow eye.

Follow-Up
Long-term follow-up depends on the age of the patient, the amount of prescribed patching, and the severity of the amblyopia.

61
Q

Ophthalmia Neonatorum

A

**24-36h = Toxic (meds)
**3-4d = Gonnorrhe
**1-2w = Chlamydia
Treatment
No information from stains, no particular organism suspected: Erythromycin ointment q.i.d. plus erythromycin elixir 50 mg/kg/day in four divided doses for 2 to 3 weeks.

Suspect chemical (e.g., silver nitrate) toxicity: Discontinue offending agent. No treatment or preservative-free artificial tears q.i.d. Reevaluate in 24 hours.

Suspect chlamydial infection: Erythromycin elixir 50 mg/kg/day orally in four divided doses for 14 days, plus erythromycin ointment q.i.d. Alternatively, azithromycin 20 mg/kg orally for 3 days can be used. Topical therapy alone is not effective. If confirmed by culture or immunofluorescent stain, treat the mother and her sexual partners with one of the following:
- Doxycycline 100 mg p.o. b.i.d. for 7 days (for women who are neither breast-feeding nor pregnant). If breast-feeding or pregnant, one of the following regimens may be used: azithromycin 1 g as a single dose, amoxicillin 500 mg p.o. t.i.d. for 7 days, or erythromycin 250 to 500 mg p.o. q.i.d. for 7 days.

Note
Inadequately treated chlamydial conjunctivitis in a neonate can lead to chlamydial otitis or pneumonia.

Suspect N. gonorrhoeae:

  • Saline irrigation of the conjunctiva and fornices until discharge gone.
  • Hospitalize and evaluate for disseminated gonococcal infection with careful physical examination (especially of joints). Blood and cerebrospinal fluid cultures are obtained if a culture-proven infection is present.
  • Ceftriaxone 25 to 50 mg/kg intravenously (i.v.) or intramuscularly (i.m.) (not to exceed 125 mg) as a single dose or cefotaxime 100 mg/kg i.v. or i.m. as a single dose. In penicillin- or cephalosporin-allergic patients, an infectious disease consult is recommended. If sensitivities are not initially available, ceftriaxone is the treatment of choice. Systemic antibiotics sufficiently treat gonococcal conjunctivitis, and topical antibiotics are not necessary.
  • Topical saline lavage q.i.d. to remove any discharge.
  • All neonates with gonorrhea should also be treated for chlamydial infection with erythromycin elixir 50 mg/kg/day in four divided doses for 14 days.
          Note
          If confirmed by culture, the mother and her sexual partners should be treated appropriately for both gonorrhea and chlamydia infections.

Gram-positive bacteria with no suspicion of gonorrhea and no corneal involvement: Bacitracin ointment q.i.d. for 2 weeks.

Gram-negative bacteria with no suspicion of gonorrhea and no corneal involvement: Gentamicin, tobramycin, or ciprofloxacin ointment q.i.d. for 2 weeks.

Bacteria on Gram stain and corneal involvement: Hospitalize, work-up, and treat as discussed

Suspect herpes simplex virus: The neonate (under 1 month of age), regardless of the presenting ocular findings, should be treated with acyclovir intravenously as well as with vidarabine 3% ointment five times per day or trifluridine drops nine times per day. Prompt initiation of intravenous acyclovir may prevent dissemination of the HSV infection and spread to the CNS. Topical therapy is optional when systemic therapy is instituted. In full-term infants, the dosage for acyclovir is 60 mg/kg/day divided into three doses. If infection is limited to the skin, eye, and mouth, it is administered intravenously for 14 days. Treatment duration is extended to 21 days if the disease is disseminated or involves the central nervous system. Consultation with a pediatric infectious disease specialist is recommended. For children with recurrent ocular lesions, oral suppressive therapy with acyclovir (20 mg/kg b.i.d.) may be of benefit.

Follow-Up
Initially examine daily as an inpatient or outpatient.
If the condition worsens (e.g., corneal involvement develops), reculture and hospitalize. Therapy and follow-up are tailored according to the clinical response and the culture results.

62
Q

Congenital Glaucoma

A

Treatment
Definitive treatment is usually surgical. Medical therapy is utilized as a temporizing measure before surgery and to help clear the cornea in preparation for possible goniotomy.
Medical:
- Oral carbonic anhydrase inhibitor (e.g., acetazolamide, 15 to 30 mg/kg/day in three or four divided doses): Most effective.
- Topical carbonic anhydrase inhibitor (e.g., dorzolamide or brinzolamide b.i.d.): Less effective; better tolerated.
- Topical beta-blocker (e.g., levobunolol or timolol, 0.25% if <1 year old or 0.5% if older b.i.d.).
- Prostaglandin analogs (e.g., latanoprost q.h.s.)

Note
Brimonidine is contraindicated in children under the age of 1 year because of the risk of apnea/hypotension/bradycardia/hypothermia. Caution should be used in children under 5 years old or <20 kg.

Surgical: Nasal goniotomy (incising the trabecular meshwork with a blade or needle under gonioscopic visualization) is the procedure of choice, although some surgeons initially recommend trabeculotomy. Miotics are sometimes used to constrict the pupil before a surgical goniotomy. If the cornea is not clear, trabeculotomy (opening the Schlemm canal from a scleral approach into the anterior chamber) or endoscopic goniotomy can be performed. If the initial goniotomy is unsuccessful, a temporal goniotomy may be tried. Trabeculectomy or tube shunt may be performed following failed angle-incision operations. Cyclophotocoagulation of the ciliary processes may also be an option to decrease aqueous production.

Note
Amblyopia is the most common cause of visual loss in pediatric glaucoma and should be treated appropriately. See 8.7, Amblyopia.

    Follow-Up Repeated examinations, under anesthesia as needed, to monitor corneal diameter and clarity, IOP, cup/disc ratio, and refraction/axial length.

These patients must be followed throughout life to monitor for progression.

Other forms of pediatric glaucoma in older children include uveitic glaucoma, traumatic glaucoma, juvenile open angle glaucoma (JOAG, autosomal dominant), and others.

63
Q

Congenital Syndrome Inheritance

A

Leber’s Congenital Amaurosis = AR (rod-cone disorder, abnormal ERG)
Congenital Stationary Night Blindness = AD, some AR and X (abnormal ERG)
Achromatopsia = AR (rod monochrome, abnormal photopic ERG)
Oculocutaneous Albinism = AR (tyrosinase deficient)
Ocular Albinism = X (

64
Q

Hepatitis types and transmission

A

A = animal

  • contaminated food
  • consuming aything that had infected fecal matter on it

B = blood

  • needle-stick
  • sharing items that had blood on them

C = crack
- intravenous drug use

65
Q

Glaucoma med contraidications

A

PGs:
with caution: patient with active uveitis, active CME
contraindicated: pregnant (or wishing to be) females

Beta-blockers:
contraindicated: asthma, COPD, heart block, bradyarrhythmia, unstable congestive heart failure, depression, or myasthenia gravis

a2 agonist:
contraindicated: taking monoamine oxidase inhibitors (risk of hypertensive crisis) relatively contraindicated: children under the age of 5 (risk for cardiorespiratory and CNS depression)

CAI:
with caution: sulfa allergy, patient with Fuch’s endothelial dystrophy or post-keratoplasty

Pilo:
with caution: <40yo (accom spasm), risk of RD
contraindicated: pt w/ retinal hole

66
Q

NTG

A
  • *paracentral scotoma
  • *more drance hemes

Treatment
Target IOPs are at least 30% lower than the level at which progressive damage was occurring. Therapies are those for POAG.
There is evidence that initial therapy with brimonidine 0.2% b.i.d. is superior to timolol 0.5% b.i.d. in preventing visual field progression in low tension POAG.

Ischemia to the optic nerve head may play a role in the pathogenesis of low tension POAG. Modification of cardiovascular risk factors is appropriate in managing general health, but has not proven beneficial in managing glaucoma. Refer to an internist for control of blood pressure, cholesterol, and optimal management of other comorbid conditions to maximize optic nerve perfusion. If possible avoid use of antihypertensive drugs at bedtime and use preferentially in the morning.

67
Q

OHTN

A

**>21mmHg on 2 visits

Treatment

If there are no suggestive optic nerve or visual field changes and IOP is <24 mm Hg, no treatment other than close observation is usually necessary.

Patients with an IOP >24 to 30 mm Hg but with normal examinations are candidates for IOP-lowering therapy (threshold varies per glaucoma specialist). A decision to treat a patient should be based on the patient’s choice to elect therapy and baseline risk factors such as age, CCT, initial IOP, optic nerve appearance, and family history. The results of the ocular hypertension treatment study (OHTS) showed that treatment reduced the development of visual field loss from 9.5% to 4.4% at 5 years, with a 20% average reduction of IOP. If treatment is elected, a therapeutic trial in one eye, as described for treatment of POAG, should be used. Some clinicians may elect to monitor these patients with close observation. Risk calculators have been developed to approximate the level of risk progression to glaucoma if left untreated.

Follow-Up
Close follow-up is required for patients being treated and observed. All patients should initially be followed similarly to POAG. If there is no progression in the first few years, monitoring frequency can be decreased to every 6 to 12 months. Stopping medication may be considered in patients who have been stable for several years to reassess the need for continued treatment.

68
Q

Angle closure glaucoma

A

Treatment
Depends on etiology of angle closure, severity, and duration of attack. Severe, permanent damage may occur within several hours. If visual acuity is hand motion or better, IOP reduction is usually urgent; therapeutic intervention should include all topical glaucoma medications, systemic (preferably intravenous) CAI, and in some cases intravenous osmotic agent (e.g., mannitol) as long as not contraindicated.

Compression gonioscopy is essential to determine if the trabecular blockage is reversible and may break an acute attack.
Topical therapy with β-blocker ([e.g., timolol 0.5%] caution with asthma or COPD), α-2 agonist (e.g., brimonidine 0.1%), prostaglandin analog (e.g., latanoprost 0.005%), and CAI (e.g., dorzolamide 2%) should be initiated immediately. In urgent cases, three rounds of these medications may be given, with each round being separated by 15 minutes.
Topical steroid (e.g., prednisolone acetate 1%) may be useful.
Systemic CAI (e.g., acetazolamide 250 to 500 mg i.v. or two 250-mg tablets p.o. in one dose if unable to give i.v.) if reduction in IOP is urgent or if IOP is refractory to topical therapy. Do not use in sulfonamide-induced angle closure.

Recheck the IOP in 1 hour. If IOP reduction is urgent or refractory to therapies listed above, repeat topical medications and give osmotic agent (e.g., mannitol 1 to 2 g/kg i.v. over 45 minutes [a 500 mL bag of mannitol 20% contains 100 g of mannitol]). Contraindicated in congestive heart failure, renal disease, and intracranial bleeding.

Note
Prior to initiation of systemic CAIs or osmotic agents, renal function should be tested.

When acute angle closure glaucoma is the result of:

  • Phakic pupillary block or angle crowding: Historically, pilocarpine, 1% to 2%, every 15 minutes for two doses was recommended but has fallen out of favor by some physicians due to adverse effects such as headache, accommodative spasm, associated increased risk for uveitis and retinal detachment, and potential for miosis-induced angle closure.
  • Aphakic or pseudophakic pupillary block or secondary closure of the angle: Do not use pilocarpine. Consider a mydriatic and a cycloplegic agent (e.g., cyclopentolate 1% to 2%, and phenylephrine 2.5% every 15 minutes for four doses) when laser or surgery cannot be performed because of corneal edema, inflammation, or both.
  • Topiramate- or sulfonamide-induced secondary angle closure: Do not use CAIs in sulfonamide-induced angle closure. Immediately discontinue the inciting medication. Consider cycloplegia to induce posterior rotation of the ciliary body (e.g., atropine 1% b.i.d. or t.i.d.). Consider hospitalization and treatment with intravenous hyperosmotic agents and intravenous steroids (methylprednisolone 250 mg i.v. every 6 hours) for cases of markedly elevated IOP unresponsive to other treatments. Cases involving large ciliochoroidal or choroidal effusions may benefit from intravenous corticosteroids, as inflammation may play a role in their formation. Peripheral iridotomy (PI) or iridectomy and miotics are not indicated.

In phacomorphic glaucoma, the lens should be removed as soon as the eye is quiet and the IOP controlled, if possible.
Address systemic problems such as pain and vomiting.
For pupillary block (all forms) or primary angle crowding: If the IOP decreases significantly, definitive treatment with laser (YAG) PI or surgical iridectomy is performed once the cornea is clear and the anterior chamber is quiet, typically 1 to 5 days after attack.

Note
If affected eye is too inflamed initially for laser PI, perform laser PI of the fellow eye first. An untreated fellow eye has a 40% to 80% chance of acute angle closure in 5 to 10 years. Repeated angle closure attacks with a patent PI may indicate plateau iris syndrome.

Patients are discharged on a regimen of maintenance dose IOP-lowering drops and oral medications (described above). Close monitoring with IOP measurement each day is necessary immediately after an angle closure attack. Once the IOP has been reasonably reduced, follow-up frequency is guided by overall clinical response and stability.

Note
If IOP does not decrease after two courses of maximal medical therapy, a laser (YAG) PI should be considered if there is an adequate view of the iris. If IOP still does not decrease after more than one attempt at laser PI, then a laser iridoplasty or surgical PI is needed. If all preceding treatments are unsuccessful or refractory, a guarded filtration procedure should be considered.

For secondary angle closure: Treat the underlying problem. Consider argon laser gonioplasty to open the angle, particularly in plateau iris syndrome or nanophthalmos. Goniosynechiolysis can be performed for chronic angle closure of <6 months’ duration. Systemic steroids may be required to treat serous choroidal detachments secondary to inflammation.

Follow-Up
After definitive treatment, patients are reevaluated in weeks to months initially, and then less frequently. Visual fields and stereo disc photographs are obtained for baseline purposes.

Note

Cardiovascular status and electrolyte balance must be considered when contemplating osmotic agents, CAIs, and β-blockers.
The corneal appearance may worsen when the IOP decreases.
Worsening vision or spontaneous arterial pulsations are signs of increasing urgency for pressure reduction.
Since one-third to one-half of first-degree relatives may have occludable angles, patients should be counseled to alert relatives to the importance of screening.
Angle closure glaucoma may be seen without an increased IOP. The diagnosis should be suspected in a patient who had episodes of pain and reduced acuity and is noted to have:
- An edematous, thickened cornea.
- Normal or markedly asymmetric pressure in both eyes.
- Shallow anterior chambers in both eyes.
- Occludable anterior chamber angle in the fellow eye.

69
Q

Angle recession glaucoma

A

**10-20 years after initial trauma/hyphema

Treatment
Same as Primary Open Angle Glaucoma.
However, miotics (e.g., pilocarpine) may be ineffective or even cause increased IOP as a result of a reduction of uveoscleral outflow. ALT and SLT are rarely effective in this condition. Surgical therapy may be necessary if uncontrolled with medications.

Follow-Up
Both eyes are monitored closely because of high incidence of delayed open angle glaucoma. Patients with angle recession without glaucoma are examined yearly. Those with glaucoma are examined as POAG

70
Q

Inflammatory/ Uveitis Glaucoma

A

Treatment

Topical steroid (e.g., prednisolone acetate 1%) q1–6h, depending on the severity of the anterior chamber inflammation.
Mydriatic/cycloplegic (e.g., cyclopentolate 1% t.i.d.).
One or more of the following pressure-reducing agents can be used in addition to the other treatments, depending on the IOP and the status of the optic nerve:
- Topical β-blocker (e.g., timolol 0.5% daily or b.i.d.) if not contraindicated (e.g., asthma, COPD).
- Topical α-2 agonist (e.g., brimonidine 0.1% to 0.2% b.i.d. to t.i.d.).
- Topical CAI (e.g., dorzolamide 2% t.i.d.) or oral CAI (e.g., methazolamide 25 to 50 mg p.o. b.i.d. to t.i.d. or acetazolamide 500 mg sequel p.o. b.i.d.).
- Hyperosmotic agent when IOP is acutely increased (e.g., mannitol 20% 1 to 2 g/kg i.v. over 45 minutes).
- Anterior chamber paracentesis if reduction in IOP is urgent or if IOP is refractory to topical therapy.

Note
Topical steroids are not used, or are used with extreme caution, in patients with an infectious process.

Manage the underlying problem.
If IOP remains dangerously elevated despite maximal medical therapy, glaucoma filtering surgery may be indicated. Trabeculectomy surgery has high rates of failure in cases of inflammatory glaucoma. Tube shunt is often the preferred alternative.
If HSV suspected, start antiviral coverage (e.g., acyclovir 400 mg p.o. 5× daily or valacyclovir 500 mg p.o. t.i.d.).

Note
Prostaglandin agonists (e.g., latanoprost 0.005%) and miotics (e.g., pilocarpine) should be used with caution in active inflammatory glaucoma but may be considered once the eye is quiet.

Follow-Up

Patients are seen every 1 to 7 days at first. Higher IOP and more advanced glaucomatous cupping warrant more frequent follow-up.
Antiglaucoma medications are discontinued as IOP returns to normal. Steroid-response glaucoma should always be considered if IOP remains high when inflammation has subsided. IOP elevation in the presence of significant uveitis suggests the need for more, not less, steroids and additional or alternative pressure lowering therapy.

71
Q

Posner-Schlossman aka Glaucomatocyclitic crisis

A

**unilateral IOP 40-60 w/ mild pain

Treatment
Tends to be very responsive to topical steroids and aqueous suppressants.

Topical β-blocker (e.g., timolol 0.5% daily or b.i.d.), topical α-2 agonist (e.g., brimonidine 0.1% to 0.2% b.i.d. to t.i.d.), topical CAI (e.g., dorzolamide 2% b.i.d. to t.i.d.).
Short course (1 week) of topical steroids (e.g., prednisolone acetate 1% q.i.d.) may decrease inflammation. Longer use may cause an elevation in IOP. Oral indomethacin (e.g., 75 to 150 mg p.o. daily) or topical nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., ketorolac q.i.d.) may also be effective.
Consider a systemic CAI (e.g., acetazolamide 500 mg sequel p.o. b.i.d.) if IOP is significantly increased and unresponsive to topical therapy (rare).
Hyperosmotic agents (e.g., mannitol 20% 1 to 2 g/kg i.v. over 45 minutes) or anterior chamber paracentesis can be considered when the IOP is determined to be dangerously high for the involved optic nerve
Consider a cycloplegic agent (e.g., cyclopentolate 1% t.i.d.) if the patient is symptomatic.

Follow-Up

Patients are seen every few days at first and then weekly until the episode resolves. Attacks usually subside within a few hours to a few weeks.
Medical or surgical therapy may be required, depending on the baseline IOP between attacks.
If the IOP decreases to levels not associated with disc damage, no treatment is necessary.
Steroids are tapered rapidly if they are used for 1 week or less and slowly if they are used for longer.
Both eyes are at risk for the development of chronic open angle glaucoma. Patients should be followed as if the diagnosis is POAG.

72
Q

Steroid Induced glaucoma

A

**2-4 weeks after initiation

Treatment
Any or all of the following may be necessary to reduce IOP:
- Determine if steroid use (in any form) is truly needed. If not needed, stop or taper steroids.
- Reduce the concentration or dosage of the steroid.
- Change to a steroid with lesser propensity for IOP elevation (e.g., fluorometholone, loteprednol, or rimexolone).
- Switch to a topical NSAID (e.g., ketorolac 0.4% or 0.5%, diclofenac 0.1%).
- Start antiglaucoma therapy.
- Consider anterior chamber paracentesis when the IOP is determined to be dangerously high for the involved optic nerve
- Laser trabeculoplasty (e.g., SLT) may be effective in treating some patients.

For sustained IOP elevation after steroid cessation or in patients at risk of glaucoma progression, treat like POAG, including appropriate surgical options.

Note
For inflammatory glaucoma, if the inflammation is moderate to severe, increase the steroids initially to reduce the inflammation while initiating antiglaucoma therapy.

If a medically uncontrollable dangerously high IOP develops after a depot steroid injection, the steroid may need to be excised. After intravitreal steroid injection, options include glaucoma filtering surgery or a pars plana vitrectomy to remove the steroid.
Steroid-induced glaucoma after LASIK may be difficult to detect using applanation tonometry due to falsely low readings caused by either reduced corneal thickness or interface fluid between the flap and the stromal bed.

Follow-Up
Dependent on the severity of pressure elevation and glaucomatous damage. Follow patients as if they have POAG.

73
Q

Plateau Iris Syndrome

A

Treatment

If Acute Angle Closure is Present:

Treat medically. Max medical therapy + oral CAI + Mannitol (as needed)
A laser PI is performed within 1 to 3 days if the angle closure attack can be broken medically. If the attack cannot be controlled, a laser or surgical PI may need to be done as an emergency procedure. Consider a laser iridoplasty to break an acute attack not responsive to medical treatment and PI.
One week after the laser PI, gonioscopy should be repeated prior to dilating the eye with a weak mydriatic (e.g., tropicamide 0.5%). If the IOP increases or a spontaneous angle closure episode occurs, plateau iris syndrome is diagnosed and should be treated with an iridoplasty. Second-line therapy includes chronic instillation of a weak miotic agent (e.g., pilocarpine 0.5% to 1% t.i.d. to q.i.d.).
If the patient’s IOP does respond to a laser PI (e.g., plateau iris configuration), then a prophylactic laser PI may be indicated in the contralateral eye within 1 to 2 weeks.

If Acute Angle Closure is Not Present:

Laser PI to relieve any pupillary block component; also done to prove pupillary block is not the primary mechanism.
Check gonioscopy every 4 to 6 months to evaluate the angle.

Perform iridoplasty if new PAS or further narrowing of the angle develops.
Most do well with close observation alone and earlier cataract extraction. Can consider ECP at the time of phacoemulsification to shrink ciliary processes.
If the angle continues to develop new PAS or becomes narrower despite iridoplasty, then consider lens extraction. If uncontrolled IOP treat as CACG

Follow-Up

Similar to performing a PI in acute angle closure. Reevaluate in 1 week, 1 month, and 3 months, and then yearly if no problems have developed.
Patients with a plateau iris configuration without previous acute angle closure are examined every 6 months.
Every examination should include IOP measurement and gonioscopy looking for PAS formation, narrowing angle recess, or increasing angle closure. The PI should be examined for patency. Dilation should cautiously be performed periodically (approximately every 2 years) to ensure that the PI remains adequate to prevent angle closure. If the patient needs more frequent dilation due to retinal pathology, consider cataract surgery to help open the angle.
Ophthalmoscopic disc evaluation is essential

74
Q

pupil quiz
aniso > in lit room
pilo 0.125% causes constriction

A

Adie’s tonic pupil –> post-ganglionic iris sphincter denervation

  • *Acute dilated
  • *deep tendon reflexes affected
75
Q

pupil quiz
aniso > in lit room
pilo 0.125% doesn’t cause change
check w/ 1% pilo

A

constricts w/ 1% pilo = 3rd nerve palsy

doesnt constrict w/ 1% pilo = pharmacological dilation

76
Q

pupil quiz
aniso > in dark room
no dilation lag
cocaine 10% causes dilation

A

Physiologic aniso

77
Q
pupil quiz 
aniso > in dark room
dilation lag of smaller pupil
0.5% apraclonidine = causes reversal of aniso (small pupil is now big)
10% cocaine = no dilation of small pupil
A

Horner’s syndrome –> oculosympathetic pathway lesion

hydroxyamphetamine test

  • YES dilation = pre-gang or central
  • NO dilation = post-gang
78
Q

Medication causing thrombocytopenia, leucopenia and folate deficiency

A

Pyrimethamine
- TMP

T.gondii med

79
Q

Infections to report to CDC

A

Syphillis, chlamydia, gonorrhea

80
Q

CN 3 isolated Palsy

A
  • eye down and out
  • pupil-involving = likely compression from PCA aneurysm
  • not pupil involving = likely microvascular –> NEVER get aberrant regen
    monitor - fnxn should return in 3 mo
81
Q

CN 4 isolated palsy

A
  • vertical diplopia, do Park’s 3 step
  • The involved eye is higher (hypertropic) in primary gaze. The hypertropia increases when looking in the direction of the uninvolved eye or tilting the head toward the ipsilateral shoulder. The patient often maintains a head tilt toward the contralateral shoulder to eliminate diplopia.
  • etiology: Trauma, vascular infarct (often the result of underlying diabetes or hypertension), congenital, idiopathic, or demyelinating disease.
  • F/U: If the work-up is negative, the lesion is presumed vascular or idiopathic and the patient is reexamined in 1 to 3 months. If the palsy does not resolve in 3 months or if an additional neurologic abnormality develops, appropriate imaging studies of the brain are indicated.
82
Q

CN 6 isolated palsy

A
  • horizontal diplopia, lack of abduction
  • etiology adult: Vasculopathic (e.g., diabetes, hypertension, other atherosclerotic risk factors), trauma, idiopathic
  • etiology child: Benign and usually self-limited after viral infection or vaccination, trauma, increased intracranial pressure
  • F/U: Reexamine every 6 weeks after the onset of the palsy until it resolves. MRI of the head is indicated if any new neurologic signs or symptoms develop, the abduction deficit increases, or the isolated sixth nerve palsy does not resolve in 3 to 6 months.
83
Q

CN 7 isolated palsy

A
  • Weakness or paralysis of one side of the face, inability to close one eye, excessive drooling
  • etiology: central (inferior side of face involved) or peripheral lesion (full side of face involved)
  • F/U: Recheck all patients at 1 and 3 months and more frequently if corneal complications arise.
    If not resolved after 3 months, order MRI of brain to rule out mass lesion.
    In nonresolving facial palsy with repeatedly negative work-up, consider referral to neurosurgeon or plastic surgeon for facial nerve graft, cranial nerve reanastomosis, or temporalis muscle transposition for patients who desire improved facial motor fnxn
84
Q

Myasthenia Gravis

A
  • *worsening ptosis throughout day, diplopia
  • *ask: difficulty swallowing/ heiwng, weakness?
  • *blood test for AcH receptor antibodies or MUSK
  • *chest X-Ray/CT cuz increased risk of thymoma

Treatment
Refer to a neurologist familiar with this disease.

If the patient is having difficulty swallowing or breathing, urgent hospitalization for plasmapheresis, intravenous immunoglobulin (IVIG), and respiratory support may be indicated.
If the condition is mild, purely ocular, and is not disturbing to the patient, therapy need not be instituted (the patient may patch one eye as needed).
If the condition is disturbing or more severe, an oral anticholinesterase agent such as pyridostigmine should be given (often starting with 30 mg p.o. t.i.d. gradually increasing to an approximate dose of 60 mg p.o. q.i.d. for an adult). The dosage must be adjusted according to the response.
If symptoms persist, consider systemic steroids. There is no uniform agreement concerning the dosage. One option is to start with prednisone 20 mg p.o. daily, increasing the dose slowly until the patient is receiving 100 mg/day. These patients may require hospitalization for several days when a high-dose regimen of steroids is employed.

Note
Steroid use in myasthenia may precipitate respiratory crisis in the first 2 weeks of treatment. Therefore, in patients with systemic symptoms, hospitalization to begin steroids is required.

Azathioprine (2 to 3 mg/kg/day) may be helpful in older patients. Other medications include mycophenolate mofetil and cyclosporine. Some patients with systemic myasthenia are treated with regularly scheduled IVIG or plasmapheresis.
Treat any underlying thyroid disease or infection.
Surgical removal of the thymus can be performed. This is indicated for anyone with thymoma. It may also improve symptoms in patients with generalized myasthenia without thymoma.

Follow-Up

If systemic muscular weakness is present, patients need to be monitored every 1 to 4 days by an appropriate medical specialist until improvement is demonstrated.
Patients who have had their isolated ocular abnormality for an extended time (e.g., months) should be seen every 4 to 6 months and if proven to be stable, every 6 to 12 months.
Patients should always be warned to return immediately if swallowing or breathing difficulties arise. After isolated ocular myasthenia has been present for 2 to 3 years, progression to systemic involvement is unlikely.

Note
Newborn infants of myasthenic mothers should be observed carefully for signs of myasthenia because acetylcholine receptor antibodies may cross the placenta. Poor sucking reflex, ptosis or decreased muscle tone may be seen.

85
Q

Internuclear Ophalmoplegia (INO)

A
  • *MLF lesion - check for MS of brainstem stroke/mass
  • *Weakness or paralysis of adduction, with horizontal jerk nystagmus of the abducting eye.

Treatment
REFER

86
Q

Optic Neuritis

A
  • *vision loss, pain w eye movement, 18-45yo
  • *Relative afferent pupillary defect in unilateral or asymmetric cases; decreased color vision; central, cecocentral, arcuate, or altitudinal visual field defects
  • *idiopathic, MS or viral

Treatment
If patient seen acutely with no prior history of MS or optic neuritis:
- If MRI reveals at least one typical area of demyelination, offer pulsed intravenous steroid in the following regimen within 14 days of decreased vision:
- Methylprednisolone 1 g/day i.v. for 3 days, then
- Prednisone 1 mg/kg/day p.o. for 11 days, then
- Taper prednisone over 4 days (20 mg on day 1, 10 mg on days 2 through 4).

Antiulcer medication (e.g., omeprazole 20 mg p.o. daily or ranitidine 150 mg p.o. b.i.d.) for gastric prophylaxis.

Note
The Optic Neuritis Treatment Trial (ONTT) found steroid treatment reduced initial progression to clinically definite multiple sclerosis (CDMS) for 3 years. Steroid therapy only increases the rapidity of visual return but does not improve final visual outcome.

If MRI shows two or more characteristic demyelinating lesions, treat with the aforementioned steroid regimen. Refer to neurologist or neuro-ophthalmologist for possible treatment with interferon-beta, glatiramer acetate, fingolimod, dimethyl fumarate, or teriflunomide. Patients with one or more typical signal changes on MRI have a 72% chance of developing CDMS over 15 years.

Note
NEVER use oral prednisone as a primary treatment because of increased risk of recurrence found in ONTT. Interferon-beta and glatiramer acetate as well as some of the new oral immunomodulatory agents have been shown to reduce probability of progression to CDMS in high-risk patients.

With a negative MRI, the risk of MS is low, 25% at 15 years. Pulsed intravenous steroid may still be used to hasten visual recovery, though may be withheld unless the contralateral eye has pre-existing visual compromise or the patient requests treatment and understands the risks, benefits, and alternatives. Repeat MRI in 3 to 6 months and periodically after that.

In a patient with a diagnosis of prior MS or optic neuritis:
- Observation.

Follow-Up

Reexamine the patient approximately 4 to 6 weeks after presentation and then every 3 to 6 months.
Patients at high risk for CDMS, including patients with CNS demyelination on MRI or a positive neurologic examination, should be referred to a neurologist or neuro-ophthalmologist for evaluation and management of possible MS.

87
Q

IICP / Pseudotumor Cerebri

A
  • *Must have: Papilledema due to increased intracranial pressure. Negative MRI/MRV of the brain. Increased opening pressure on LP with normal CSF composition.
  • *Assoc with CATS: contraceptives, accutane, tetracyclines and synthroid (also cyclosporine, sulfa meds)

Treatment
Idiopathic intracranial hypertension may be a self-limited process. Treatment is indicated in the following situations:
- Severe, intractable headache.
- Evidence of progressive decrease in visual acuity or visual field loss.
- Some ophthalmologists suggest treating all patients with papilledema.

Methods of treatment include the following:

  • Weight loss if overweight.
  • Acetazolamide 250 mg p.o. q.i.d. initially, building up to 500 to 1,000 mg q.i.d. if tolerated. Use with caution in sulfa-allergic patients.
  • Discontinuation of any causative medication.
  • Consider short course of systemic steroids, especially if any plans for surgical intervention.

If treatment by these methods is unsuccessful, consider a surgical intervention:

  • A neurosurgical shunt (ventriculoperitoneal or lumboperitoneal) or venous sinus stenting procedure should be considered if intractable headache is a prominent symptom.
  • Optic nerve sheath decompression surgery or neurosurgical shunt (ventriculoperitoneal or lumboperitoneal) is often effective if vision is threatened.

Special Circumstances

  • Pregnancy: Incidence of idiopathic intracranial hypertension does not increase during pregnancy beyond what would be expected from the weight gain. No increased risk of fetal loss. Acetazolamide may be used after 20 weeks gestation (in consultation with OB/GYN). Intense weight loss is contraindicated during pregnancy. Without visual compromise, close observation with serial visual fields is recommended. With visual compromise, consider steroids, optic nerve sheath decompression, shunting, or repeat LPs.
  • Children/adolescents: A secondary cause is identifiable in 50% patients.
      Follow-Up If acute, patients can be monitored every 3 months in the absence of visual field loss. If chronic, initially follow patient every 3 to 4 weeks to monitor visual acuity and visual fields, and then every 3 months, depending on the response to treatment. In general, the frequency of follow-up depends on the severity of visual loss. The more severe, the more frequent the follow-up
88
Q

AION (GCA)

A

**must: Afferent pupillary defect; visual loss (often counting fingers or worse); pale, swollen disc, at times with flame-shaped hemorrhages. Later, optic atrophy and cupping occurs as the edema resolves. The ESR, CRP, and platelets may be markedly increased

Treatment

Systemic steroids should be given immediately once GCA is suspected. Methylprednisolone 250 mg i.v., q6h for 12 doses, and then switch to prednisone 80 to 100 mg p.o. daily. A temporal artery biopsy specimen should be obtained within 1 week of systemic steroid initiation.
If the temporal artery biopsy is positive for GCA (or clinical presentation/therapeutic response warrants continued therapy), the patient must be maintained on prednisone, about 1 mg/kg initially. Oral steroids are tapered on an individual basis with the goal of using the lowest required dose necessary for disease suppression (see below).
If the biopsy is negative on an adequate (2 to 3 cm) section, the likelihood of GCA is small. However, in highly suggestive cases, biopsy of the contralateral artery is performed.
Steroids are usually discontinued if the disease is not found in adequate biopsy specimens, unless the clinical presentation is classic and a response to treatment has occurred.

Note
Without steroids (and occasionally on adequate steroids), the contralateral eye can become involved within 1 to 7 days.
Concurrent antiulcer (e.g., proton-pump inhibitor [e.g., omeprazole 20 mg p.o. daily] or histamine type 2 receptor blocker [e.g., ranitidine 150 mg p.o. b.i.d.]) should be used for gastrointestinal prophylaxis while on steroids.
A medication to help prevent osteoporosis should be used as directed by an internist, particularly given the long-term need for steroids.

Follow-Up
Patients suspected of having GCA must be evaluated and treated immediately.
After the diagnosis is confirmed by biopsy, the initial oral steroid dosage is maintained until the symptoms resolve and lab values normalize. The dosage is then tapered slowly, repeating bloodwork with each dosage change and/or monthly (whichever appropriate based on disease stability) to ensure that the new steroid dosage is enough to suppress the disease.
If the ESR or CRP increase or symptoms return, the dosage must be increased.
Treatment should last at least 6 to 12 months. The smallest steroid dose that suppresses disease is used

89
Q

NAION

A

**must: Afferent pupillary defect, pale disc swelling (often segmental), flame-shaped hemorrhages, normal ESR and CRP

Treatment

Observation.
Cardiovascular risk factor modification.
Consider avoiding blood pressure medication at bedtime to help avoid nocturnal hypotension. Also avoid sildenafil/verdenafil

Follow-Up

One month.
Up to 40% of patients show mild improvement in vision over 3 to 6 months in some studies. Optic nerve edema resolves within 8 weeks.
Patients should be counseled of risk to the contralateral eye (variable).

90
Q

Leber’s Hereditary Optic Neuropathy

A
  • *Painless progressive visual loss in one and then the other eye within days to months of each other. Visual loss is bilateral at onset in approximately 25% of cases.
  • *young men aged 15 to 30 years
  • *Mild swelling of optic disc progressing over weeks to optic atrophy
  • *mitchondrial mutation

Treatment

Idebenone is used in Canada and the United Kingdom but is not available in the United States. Studies thus far have shown variable results regarding its effectiveness.
Tobacco and alcohol avoidance are recommended.
Genetic counseling should be offered.
Consider cardiology consult because of increased incidence of cardiac conduction defects.

91
Q

Life or Vision-threatening causes of HAs

A

Life or Vision Threatening

  • GCA: Age ≥55 years. May have high ESR, CRP, and platelets.
  • Acute angle closure glaucoma: Decreased vision, painful eye, fixed mid-dilated pupil, high intraocular pressure. .
  • Ocular ischemic syndrome: Periorbital eye pain.
  • Malignant hypertension: Marked increase of blood pressure, often accompanied by retinal cotton–wool spots, hemorrhages, and, when severe, optic nerve swelling. Headaches typically are occipital in location.
  • Increased intracranial pressure: May have papilledema and/or a sixth cranial nerve palsy. Headaches usually worse in the morning and with Valsalva.
  • Infectious CNS disorder (meningitis or brain abscess): Fever, stiff neck, mental status changes, photophobia, neurologic signs.
  • Structural abnormality of the brain (e.g., tumor, aneurysm, arteriovenous malformation): Mental status change, signs of increased intracranial pressure, or neurologic signs during, and often after, the headache episode.
  • Subarachnoid hemorrhage: Extremely severe headache, stiff neck, mental status change; rarely, subhyaloid hemorrhages seen on fundus examination, usually from a ruptured aneurysm.
  • Epidural or subdural hematoma: Follows head trauma; altered level of consciousness; may produce anisocoria.

**A “sinus” headache may be a serious headache in diabetic patients and immunocompromised hosts given the possibility of zygomycosis infection (e.g., mucormycosis).

92
Q

PVD

A

**Approximately 8% to 10% of all patients with acute symptomatic PVD have a retinal break

No treatment

Follow-Up

The patient should be given a list of RD symptoms (an increase in floaters or flashing lights, worsening vision, or the appearance of a persistent curtain or shadow anywhere in the field of vision) and told to return immediately if these symptoms develop. The timing of symptoms could be anywhere from days to years later.

Patients should be informed that they will also likely develop a PVD in their fellow eye.

If no retinal break or hemorrhage is found, the patient should be scheduled for repeat examination with scleral depression in 2 to 4 weeks, 2 to 3 months, and 6 months after the symptoms first develop.

If no retinal break is found, but mild VH or peripheral punctate retinal hemorrhages are present, repeat examinations are performed 1 week, 2 to 4 weeks, 3 months, and 6 months after the event.

If no retinal break is found but significant VH or anterior pigmented vitreous cells are present, repeat examination should be performed the next day by a retina specialist because of the high likelihood of a retinal break.

93
Q

Retinal Tear

A

Treatment
In general, laser therapy or cryotherapy is required within 24 to 72 hours for acute retinal breaks, and only rarely for chronic breaks. However, each case must be individualized (e.g., superior breaks pose greater risk of progression to detachment than inferior breaks). We follow these general guidelines:

Treatment recommended:

Acute symptomatic break (e.g., a horseshoe or operculated tear).
Acute traumatic break (including a dialysis).

Treatment to be considered:

Asymptomatic retinal break that is large (e.g., ≥1.5 mm), above the horizontal meridian, or both, particularly if there is no PVD.
Asymptomatic retinal break in an aphakic or pseudophakic eye, an eye in which the involved or the contralateral eye has had an RD, or in a highly myopic eye.

Follow-Up

Patients with predisposing conditions or retinal breaks that do not require treatment are followed every 6 to 12 months.
Patients treated for a retinal break are reexamined in 1 week, 1 month, 3 months, and then every 6 to 12 months.
RD symptoms (an increase in floaters or flashing lights, worsening visual acuity, or the appearance of a curtain, shadow, or bubble anywhere in the field of vision) are explained and patients are told to return immediately if these symptoms develop.
94
Q

Retinal Detachment

A

Treatment

Patients with an acute RRD that threatens the fovea should have surgical repair performed urgently. The visual prognosis is significantly worse in detachments that progress to involve the fovea. Surgical options include laser photocoagulation, cryotherapy, pneumatic retinopexy, vitrectomy, and/or scleral buckle.

All RRDs that are macula-off, or tractional retinal detachments that involve the macula, should be repaired but are not necessarily urgent. Multiple studies suggest that visual outcomes for macula-off detachments do not change if surgery is performed within 7 to 10 days of the onset.

Chronic macula-off RDs are treated within one week if possible.

For exudative RD, successful treatment of the underlying condition often leads to resolution of the detachment.

Follow-Up
Patients treated for RD are reexamined as per the retinal specialist, often at 1 day, 1 week, 1 month, 2 to 3 months, then ever 6 to 12 months.

95
Q

Juvenile Retinoschisis

A
  • *X-linked recessive
  • *Foveal schisis seen as stellate maculopathy: Cystoid foveal changes with retinal folds that radiate from the center of the fovea (petaloid pattern). Unlike the cysts of cystoid macular edema (CME), they do not stain or leak on IVFA
  • *inferiotemporal most common

Treatment

No definitive treatment for stellate maculopathy. Topical carbonic anhydrase inhibitors have been shown to decrease foveal thickness and improve visual acuity in some patients.
For nonclearing VH, consider vitrectomy.
Surgical repair of an RD should be performed.
Superimposed amblyopia may be present in children younger than 11 years of age when one eye is more severely affected, and a trial of patching should be considered.

Follow-Up
Every 6 months; more frequently if treating amblyopia.

96
Q

Age-related Retinoschisis

A

**absolute scotoma in area of schisis

Treatment

Surgery is indicated when a clinically significant RD develops.
A small RD walled off by a demarcation line is usually not treated. This may take the form of pigmentation at the posterior border of outer layer breaks.

Follow-Up
Every 6 months. RD symptoms (an increase in floaters or flashing lights, blurry vision, or the appearance of a curtain or shadow anywhere in the field of vision) are explained to all patients, and patients are told to return immediately if these symptoms develop.

97
Q

CRAO

A
  • *marked RAPD
  • *sudden unilateral vision loss
  • *cherry red spot, box-carring of vessels
  • *caused by embolus or thrombus maybe GCA

Treatment

If an embolus is seen, refer to an internist or neurologist immediately for stroke management, complete work-up as above, and treatment of any underlying disorders.
If GCA suspected.
For specific management of ocular signs and symptoms, there are anecdotal reports of improvement after the following treatments, if instituted within 90 to 120 minutes of the occlusive event. None of these treatments have been proven effective in randomized, controlled clinical trials, and should not be considered the standard of care.
- Immediate ocular massage with fundus contact lens or digital massage.
- Anterior chamber paracentesis
- IOP reduction with acetazolamide, 500 mg i.v. or two 250-mg tablets p.o. or a topical beta-blocker (e.g., timolol or levobunolol, 0.5% daily or b.i.d.).

Follow-Up

Follow as directed by managing internist and/or neurologist.
Repeat eye examination in 1 to 4 weeks, checking for neovascularization of the iris/disc/angle/retina (NVI/NVD/NVA/NVE), which develops in up to 20% of patients, at a mean of 4 weeks after onset. If neovascularization develops, perform panretinal photocoagulation (PRP) and/or administer an anti-vascular endothelial growth factor (anti-VEGF) agent

98
Q

CRVO

A

**etiology: HTN, glaucoma, Atherosclerosis of the adjacent central retinal artery: The artery compresses the central retinal vein in the region of the lamina cribrosa, secondarily inducing thrombosis in the lumen of the vein.

Types

Ischemic CRVO: Multiple CWSs (usually ≥6), extensive retinal hemorrhage, and widespread capillary nonperfusion on IVFA. RAPD often present and visual acuity is typically 20/400 or worse with visual field constriction. ERG shows decreased b-wave amplitude.
Nonischemic CRVO: Mild fundus changes. No RAPD is present, and acuity is often better than 20/400.

Treatment

Discontinue oral contraceptives; change diuretics to other antihypertensive medications if possible.
Reduce IOP if increased in either eye.
Treat underlying medical disorders.
If NVI or NVA is present, perform PRP promptly. Consider PRP if NVD or retinal neovascularization is present. Prophylactic PRP for non-perfusion is usually not recommended unless follow-up is in doubt. Intravitreal VEGF inhibitors are very effective in temporarily halting or reversing anterior and posterior segment neovascularization. They may be a useful adjunct to PRP, particularly when rapid reversal of neovascularization is needed.
Aspirin 81 to 325 mg p.o. daily is often recommended, but no clinical trials have demonstrated efficacy to date, and it may increase the risk of hemorrhage.

CRVO-Related Macular Edema

Intravitreal ranibizumab 0.5 mg and aflibercept 2 mg are U.S. Food and Drug Administration (FDA)-approved for treating RVO-related macular edema (ME). Intravitreal bevacizumab has been used off-label in a similar fashion. Risks of intravitreal injections are low, but include VH and endophthalmitis, among others.
Ozurdex, a biodegradable 0.7 mg dexamethasone implant, is FDA-approved for the treatment of ME associated with retinal vein occlusion. Off-label intravitreal steroid (e.g., triamcinolone 40 mg/mL, injecting 1 to 4 mg) can also be considered and has been effective in both improving vision and reducing vision loss in patients with ME secondary to CRVO. Complications include cataract formation and elevated IOP.

Note
In a large, prospective, randomized trial (SCORE-CRVO), a 1 mg dose of intravitreal triamcinolone was found to be equally as effective as a 4 mg dose, but with fewer side-effects (elevated IOP and cataract formation).

Follow-Up

Every month initially, with gradual interval taper based on vision, presence of macular edema, and response to treatment.
At each follow-up visit, evaluate anterior segment for NVI and assess presence/absence of NVA with undilated gonioscopy, followed by careful dilated fundus examination looking for NVD or other retinal neovascularization. Evidence of early NVI or NVA should prompt immediate PRP and/or anti-VEGF therapy and monthly follow-up until stabilized or regressed.
Patients should be informed that there is an 8% to 10% risk for the development of a BRVO or CRVO in the fellow eye.

99
Q

Ocular Ischemic Syndrome

A
  • *men>women, 50-80
  • *unilateral
  • ** retinal arterioles are narrowed. Associated findings include midperipheral retinal hemorrhages (80%), iris neovascularization (66%), and posterior segment neovascularization (37%)
  • *etiology: carotid stenosis >90%

Treatment
Often unsuccessful.

Carotid endarterectomy for significant stenosis. Refer to neurovascular surgeon.
Consider PRP and anti-VEGF agents in the presence of neovascularization.
Manage glaucoma if present. See 9.14, Neovascular Glaucoma.
Control HTN, diabetes, and cholesterol. Refer to internist.
Lifestyle modification (e.g., smoking cessation).

Follow-Up
Depends on the age, general health of the patient, and the symptoms and signs of disease. Surgical candidates should be evaluated urgently.

100
Q

CSME Definitions

A
  1. Retinal thickening within 500 μm (one-third of disc diameter) of the foveal center.
  2. Hard exudates within 500 μm of the foveal center, if associated with thickening of the adjacent retina.
  3. Retinal thickening greater than one disc area in size, part of which is within one disc diameter of the center of the fovea.
101
Q

Diabetic Retinopathy - diabetic macular edema

A

Treatment
Diabetic Macular Edema
1. Anti-VEGF therapy with FDA-approved ranibizumab and aflibercept as well as off-label bevacizumab are first line therapy for center-involving diabetic macular edema.
2. Focal or grid laser treatment should be considered in patients with clinically significant macular edema. Patients with enlarged foveal avascular zones on IVFA are treated lightly, away from the regions of foveal ischemia, if they are treated at all. Patients with extensive foveal ischemia are poor laser candidates. Younger patients and diet-controlled diabetic patients tend to have a better response.
3. Those who are nonresponsive to these treatments can consider corticosteroid therapy with FDA-approved Ozurdex (dexamethasone) or Iluvien (fluocinolone acetonide) vitreous implants. Off-label intravitreal steroid (e.g., triamcinolone 40 mg/mL, inject 1 to 4 mg) can also be considered. Complications include cataract formation and elevated IOP.
4. Patients with diffuse or extensive ME, ME in the presence of foveal ischemia, or those with poor response to prior focal/grid laser may benefit from intravitreal anti-VEGF or corticosteroid therapy, either alone or in combination with laser.

102
Q

Diabetic Retinopathy - Proliferative DR

A

Treatment
PRP is indicated for any one of the following high-risk characteristics
1. NVD greater than one-fourth to one-third of the disc area in size.
2. Any degree of NVD when associated with preretinal hemorrhage or VH.
3. NVE greater than one-half of the disc area in size when associated with a preretinal hemorrhage or VH.
4. Any NVI or neovascularization of the angle.

Anti-VEGF therapy can be utilized as an adjunct to PRP with or without pars plana vitrectomy. Ranibizumab (lucentis) was shown to be a reasonable initial therapy when compared to PRP, at least through two years. Caution must be used in the presence of retinal traction.

Note
Some physicians treat NVE or any degree of NVD without preretinal hemorrhage or VH, especially in unreliable patients.

Indications for Vitrectomy
Vitrectomy may be indicated for any one of the following conditions:
- Dense VH causing decreased vision, especially when present for several months.
- Traction RD involving and progressing within the macula.
- Macular epiretinal membranes (ERMs) or recent-onset displacement of the macula.
- Dense premacular hemorrhage.
- Chronic ME not responsive to other treatment.
- Severe retinal neovascularization and fibrous proliferation that is unresponsive to laser photocoagulation.

Note
Young patients with juvenile type 1 diabetes are known to have more aggressive PDR and therefore may benefit from earlier vitrectomy and laser photocoagulation. B-scan US may be required to rule out tractional detachment of the macula in eyes with dense VH obscuring a fundus view.

Follow-Up

Diabetes without retinopathy. Annual dilated examination.

  • Mild NPDR. Dilated examination every 6 to 9 months.
  • Moderate to severe NPDR. Dilated examination every 4 to 6 months.
  • PDR (not meeting high-risk criteria). Dilated examination every 2 to 3 months.
  • Diabetes and pregnancy. Changes that occur during pregnancy have a high likelihood of postpartum regression.

Note
The Diabetes Control and Complications Trial showed that strict control of blood sugar with insulin (in type 1 diabetes) decreases the progression of diabetic retinopathy, as well as nephropathy and neuropathy.

103
Q

Vitreous Hemorrhage

A

**causes: PDR, EARMD, BRVO, retinal tear, RD, PVD, sickle cell, trauma

Treatment

If the etiology of the VH is not known and a retinal break or an RD or both cannot be ruled out (i.e., there is no known history of one of the diseases mentioned previously, there are no changes in the contralateral eye, and the fundus is obscured by a total VH), the patient is monitored closely as an outpatient.
No heavy lifting, no straining, no bending. Keep head of bed elevated. This reduces the chance of recurrent bleeding and allows the blood to settle inferiorly, permitting a view of the superior peripheral fundus, a common site for responsible retinal breaks.
Eliminate aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and other anticlotting agents unless medically necessary.
The underlying etiology is treated as soon as possible (e.g., retinal breaks are sealed with cryotherapy or laser photocoagulation, detached retinas are repaired, and proliferative retinal vascular diseases are treated with laser photocoagulation).
Surgical removal of the blood (vitrectomy) is usually performed for:
- VH accompanied by RD or RT on B-scan US.
- Nonclearing VH, usually persisting ≥3 to 6 months. However, two-thirds of patients with an idiopathic, fundus-obscuring hemorrhage will have retinal tears or an RD. Thus, early vitrectomy should be carefully considered.
- VH with neovascularization of the iris.
- Hemolytic or ghost cell glaucoma.

Note
Vitrectomy for isolated VH (e.g., without RD) may be considered earlier than 3 months for diabetic patients or those with bilateral VH, depending on their visual needs.

Follow-Up
The patient is evaluated daily for the first 2 to 3 days. If a total VH persists, and the etiology remains unknown, the patient is followed up with B-scan US every 1 to 3 weeks to rule out an RD.

104
Q

Cystoid Macular Edema

A
  • *most common 6-10wks post-cataract removal = Irvine Gass
  • *other causes: DR, RVO, uveitis, RP, ERM, juvenile x-linked schisis, meds (Epinephrine, dipivefrin, and prostaglandin analog), etc.

Treatment
Treat the underlying disorder if possible.

Topical NSAID (e.g., ketorolac 0.5% q.i.d., bromfenac 0.09% or nepafenac 0.3% daily) often in conjunction with topical steroids (e.g., prednisolone acetate 1% q.i.d.).
Discontinue topical epinephrine, dipivefrin, or prostaglandin analog drops and medications containing nicotinic acid.
Other forms of therapy that have unproven efficacy but are often used include:
- Subtenon steroid (e.g., triamcinolone 40 mg/mL, inject 0.5 to 1.0 mL).
- Intravitreal steroid (e.g., triamcinolone 40 mg/mL, inject 1 to 4 mg).
- Intravitreal anti-VEGF therapy (e.g., bevacizumab 1.25 mg in 0.05 mL).
- Systemic steroids (e.g., prednisone 40 mg p.o. daily for 5 days and then taper over 2 weeks).
- Systemic NSAIDs (e.g., indomethacin 25 mg p.o. t.i.d. for 6 weeks).

CME with or without vitreous incarceration in a surgical wound may be improved by vitrectomy or yttrium aluminum garnet (YAG) laser lysis of the vitreous strand.

Follow-Up
Postsurgical CME is not an emergency condition. Other forms of CME may require an etiologic work-up and may benefit from early treatment (e.g., elimination of nicotinic acid–containing medications).

105
Q

Central Serous Chorioretinopathy (CSCR)

A

**Type A (high cortisol level), 25-50yo men, steroid users

Treatment

Observation: Prognosis for spontaneous recovery of visual acuity to at least 20/30 is excellent. Worse prognosis for patients with recurrent disease, multiple areas of detachment, or prolonged course.
Laser therapy: Accelerates visual recovery. Does not improve final visual outcome. May increase risk of CNV formation. Given the CNV risk, use low laser intensity. Consider laser for:
- Persistence of a serous detachment for several months.
- Recurrence of the condition in an eye that sustained a permanent visual deficit from a previous episode.
- Occurrence in the contralateral eye after a permanent visual deficit resulted from a previous episode.
- Patient requires prompt restoration of vision (e.g., occupational necessity).

Stop steroids, if possible, including topical skin preparations and nasal sprays.
If CNV develops, consider anti-VEGF therapy.
Chronic CSCR may respond to treatment with photodynamic therapy (PDT).
In small, uncontrolled observational case series, treatment with mineralocorticoid receptor antagonists (e.g., eplerenone) have been associated with improved anatomic and visual outcomes in chronic CSCR.

Follow-Up

Examine patients every 6 to 8 weeks until resolution.

106
Q

Dry ARMD

A

Treatment
Patients with intermediate dry ARMD (one large druse [125 microns] and/or ≥20 medium drusen [63 to 125 microns]), or advanced dry or exudative ARMD in one eye but not the other eye, are at high risk for the development of advanced stages of ARMD. The original Age-Related Eye Disease Study (AREDS) report demonstrated that treatment with a high-dose combination of vitamin C (500 mg), vitamin E (400 IU), beta-carotene (15 mg), zinc (80 mg), and cupric oxide (5 mg) reduces the risk of progression to advanced ARMD by approximately 25% over 5 years and reduces the risk of vision loss caused by advanced ARMD by approximately 19% by 5 years. A second study (AREDS2), evaluated the role of increased intake of different carotenoids (lutein and zeaxanthin) as well as two specific omega-3 long-chain polyunsaturated fatty acids (docosahexaenoic acid [DHA] + eicosapentaenoic acid [EPA]). The addition of lutein + zeaxanthin, DHA + EPA, or both to the original AREDS formulation did not further reduce risk of progression to advanced AMD but was found to be equally effective.

Note
Beta-carotene (in the original AREDS formula) should be withheld in past or present smokers because of increased risk of lung cancer. The AREDS2 formulation (with lutein + zeaxanthin) is preferred as it does not contain beta-carotene.

In addition, recommend consumption of green leafy vegetables if approved by primary care physician (intake of vitamin K decreases effectiveness of warfarin) and fish/fish oils containing high levels of omega-3 fatty acids.

Low-vision aids may benefit some patients with bilateral loss of macular function.

Refer to an internist for management of presumed risk factors: HTN, hypercholesterolemia, smoking cessation, etc.

Those at high risk for progressing to exudative AMD may benefit from home monitoring technology for earlier detection (ForseeHome). Although this technology is in its infancy, early detection of CNV increases the likelihood of better visual acuity results after intravitreal anti-VEGF therapy is initiated.

Certain genetic mutations confer an increased risk for ARMD (e.g., Y402H mutation of the complement factor H gene) and may influence response to treatment. Genetic screening in ARMD patients is not routinely performed.

Follow-Up
Every 6 to 12 months, watching for signs of the exudative form. Daily use of Amsler grid with instructions to return promptly if a change is noted.

107
Q

Wet ARMD

A
  • *patients with wet ARMD in one eye have a 10% to 12% risk per year of developing a CNV in the fellow eye. The risk increases for eyes with multiple or confluent soft drusen with RPE clumping.
    • CNVM in CH BALA –> choroidal rupture, Histo, Best, Angioid streaks, lacquer cracks and AMD

Treatment
Subfoveal CNV
- Ranibizumab (Lucentis): Anti-VEGF antibody fragment injected intravitreally that is FDA-approved for all subfoveal CNV subtypes. In the original phase 3 efficacy trials (MARINA and ANCHOR), ranibizumab was given monthly to patients with close to 40% of patients in both studies gaining three or more lines of visual acuity at 1 year. While the best visual results may occur with monthly dosing, prn dosing using OCT guidance (PrONTO study) had similar 1 year visual results with half the number of injections.
- Aflibercept (Eyelea): Anti-VEGF fusion protein that binds all isoforms of VEGF-A and placental growth factor. FDA-approved as intravitreal injection for the treatment of neovascular ARMD. Phase 3 studies showed similar efficacy at 1 year to monthly intravitreal ranibizumab with aflibercept dosed q8 weeks after a 12-week monthly induction phase.
- Bevacizumab (Avastin): Full-length anti-VEGF antibody. FDA-approved for colon cancer. Off-label use as intravitreal injection at a dose of 1.25 mg is effective in treating all types of neovascular ARMD. It is cost-effective and commonly used in place of ranibizumab. The Comparison of Age-related Macular Degeneration Treatments Trial (CATT) study demonstrated the noninferiority of bevacizumab as compared to ranibizumab at 1 year, when monthly or prn dosing was used.
- Pegaptanib (Macugen): Anti-VEGF aptamer injected intravitreally every 6 weeks for 1 to 2 years. FDA-approved for all subfoveal CNV subtypes. Pegaptanib reduces the risk of vision loss, but rarely improves visual acuity. Now rarely used.
- PDT: FDA-approved intravenous infusion of photosensitizing dye (verteporfin) followed by nondestructive (cold) laser application to activate the dye within the CNV. PDT can be performed as often as every 3 months for 1 to 2 years. Small, classic subfoveal CNV responds best, but small occult or minimally classic subfoveal CNV may also respond. PDT decreases vision loss, but does not improve vision as monotherapy. Now rarely used.

Nonsubfoveal CNV

  • Anti-VEGF agents are the treatment of choice for nonsubfoveal CNV. See above for details.
  • Thermal laser photocoagulation: Results are best for extrafoveal CNV (≥200 mm from fovea) or peripapillary CNV. Laser photocoagulation treatment is complicated by high CNV recurrence rates. Uncommonly used.

Follow-Up
Depends on the treatment algorithm used, but typically monthly follow-up until the CNV lesion is inactive based on IVFA and/or OCT. Patients receiving anti-VEGF therapy need indefinite follow-up, though the follow-up frequency depends on treatment response and treatment algorithm. Patients receiving intravitreal injections should be given warning symptoms for endophthalmitis and RD.

108
Q

Idiopathic Polypoidal Choroidal Vasculopathy

A
  • *sudden or gradual central VA decrease
  • *Subretinal red-orange, polyp-like lesions of the choroidal vasculature. Can be macular (more symptomatic) or peripapillary
  • *appearance of a network of branching choroidal vessels with terminal, polyp-like aneurysmal dilations.
  • *females, african/asian, HTN

Treatment
Asymptomatic lesions may be observed and may resolve spontaneously. IPCV with exudation and/or hemorrhagic complications has been treated with PDT, anti-VEGF agents, or a combination of both. A multicenter randomized control trial (EVEREST) showed combination therapy with PDT and ranibizumab resulted in better visual acuity and less retinal hemorrhage than monotherapy. Thermal laser photocoagulation, feeder vessel treatment, submacular surgery, macular translocation, steroid injection, and pneumatic displacement of large submacular hemorrhage have also been used.

Follow-Up
The prognosis of IPCV is generally better than for neovascular ARMD. Symptomatic or macular IPCV is followed every 1 to 2 months with repeat OCT, IVFA, and ICG as needed for new developments. Consider treatment, or retreatment, if symptomatic, persistent, or new leakage occurs.
**Depending on the extent of area involved prognosis is generally good. Even in patients with longer chronicity of disease, studies have shown halting of visual decline. Evidence supports that symptomatic patients with PCV can have complete regression without severe vision loss with PDT and anti-VEGF treatment

109
Q

Retinal Arterial Macroaneurysm (RAMA)

A
  • *Acute hemes in multiple layers - seb-retinal, intra-retinal, pre-retinal
  • *if chronic will have hard exudates
  • *Hx of HTN!
  • *female>males

Treatment
Observation.
Bleeding is typically not treated since it usually only occurs once secondary to thrombosis and spontaneous involution. Consider laser treatment if edema and/or exudate threatens central vision. Caution must be taken when treating arterioles that supply the central macula since distal thrombosis and obstruction can occur. Laser can also cause aneurysmal rupture resulting in retinal and vitreous hemorrhage.

Follow-Up
Frequency based on the amount and location of exudate and hemorrhage.

110
Q

Sickle Cell

A
  • *Sea-fan (periph ret neo), salmon patch (superficial intra-ret heme), black sunbursts (midperiph pigmented lesions)
  • *Retinopathy is most common with HbSC (most severe) and HbS-Thal
  • *proliferative disease has stages
  • Stage 1: Peripheral arteriolar occlusions. Salmon patch, coma sign
  • Stage 2: Peripheral arteriovenous anastomoses. Sunbursts
  • Stage 3: Neovascular proliferation. Seafan neo
  • Stage 4: Vitreous hemorrhage.
  • Stage 5: Retinal detachment. Usually tractional

Treatment summary

  • non-proliferative = observation every 6 mo
  • proliferative = Low-intensity scatter laser photocoagulation to areas of capillary non-perfusion & Pars plana vitrectomy for non-clearing vitreous hemorrhage and/or retinal detachment

Treatment
There are no well-established indications or guidelines for treatment. Isolated retinal neovascularization is not an indication. Neovascularization with associated VH is an indication for PRP to the avascular area anterior to the neovascularization. Retinal detachment and VH may be best treated with vitrectomy. Anti-VEGF agents may be beneficial, but caution should be used in cases with significant traction.

Follow-Up
No retinopathy: Annual dilated fundus examinations.
Retinopathy present: Repeat dilated fundus examination every 3 to 6 months, depending on severity.

111
Q

Valsalva Retinopathy

A
  • *heavy lifting, coughing, vomiting, constipation, straining –> increase in intraocular venous pressure leading to rupture of superficial capillaries in macula
  • *1+ sub-ILM hemes

Treatment
Prognosis is excellent. Most patients are observed as sub-ILM hemorrhage usually resolves after a few days to weeks. Occasionally laser is used to permit the blood to drain into the vitreous cavity thereby uncovering the macula. Vitrectomy rarely considered, typically only for nonclearing VH.

Follow-Up
May follow-up every 2 weeks for the initial visits to monitor for resolution, then follow-up routinely

112
Q

Angioid streaks

A
  • *PEPSI –> Associations with angioid streaks
  • Pseudoxanthoma elasticum - most common, check Serum alkaline phosphatase and urine calcium levels, skin/scar biopsy
  • Ehlers Danlos
  • Paget’s disease - bone disease
  • Sickle cell disease
  • Idiopathic
  • *ANgioid –> At Nerve

Treatment

Anti-VEGF therapy is now used for angioid streak-associated CNV, as focal laser photocoagulation and PDT have discouraging outcomes.
Management of any underlying systemic disease by an internist.
Recommend wearing one-piece polycarbonate safety glasses for sports because there is an increased risk of subretinal hemorrhage and choroidal rupture from minor trauma.

Follow-Up

Fundus examination every 6 months, monitoring for CNV.
Instruct patient to check Amsler grid daily and return immediately if changes are noted.

113
Q

Ocular Histoplasmosis (presumed)

A

**fungus from Ohio–Mississippi River Valley, 20-50yo
**Classic triad. Need two of the three to make the diagnosis:
1. Yellow-white, punched-out round spots usually <1 mm in diameter, deep to the retina in any fundus location (histo-spots). Pigment clumps in or at the margin of the spots may be seen.
2. A macular CNV appearing as a gray-green patch beneath the retina, associated with detachment of the sensory retina, subretinal blood or exudate, or a pigment ring evolving into a disciform scar.
3. Peripapillary atrophy or scarring, sometimes with nodules or hemorrhage. There may be a rim of pigment separating the disc from the area of atrophy or scarring.
NO VITRITIS

Treatment

Antifungal treatment is not helpful.
Intravitreal anti-VEGF therapy for CNV. PDT for subfoveal CNV and focal laser photocoagulation for extrafoveal CNV may be used as well. Submacular surgery may be considered in the setting of medically unresponsive subfoveal CNV if vision is <20/100.

Follow-Up

Instruct all patients to use an Amsler grid daily and return immediately if any sudden visual change is noted.
Patients treated with anti-VEGF injections are generally seen every 4 to 6 weeks, depending on the clinical response to therapy. Patients treated with PDT or focal laser are typically seen at 2 to 3 weeks, 4 to 6 weeks, 3 months, and 6 months after treatment, and then every 6 months thereafter.
A careful macular examination and OCT is performed at each visit. IVFA may be repeated whenever renewed neovascular activity is suspected.
Patients without CNV are seen every 6 months when macular changes are present in one or both eyes and yearly when no macular disease is present in either eye

114
Q

Macular Hole / VMT

A
  • *women, 60-80yo
  • *stages
    1. Stage 1: An impending hole, yellow spot, or ring in fovea.
    2. Stage 2: Small full-thickness hole.
    3. Stage 3: Full-thickness hole with cuff of SRF, no PVD.
    4. Stage 4: Full-thickness hole with cuff of SRF, with complete PVD.

Treatment

Fifty percent of VMT (previously stage 1 premacular holes) resolve spontaneously.
Ocriplasmin is a recombinant protease with activity against components of the vitreoretinal interface (fibronectin and laminin). It is FDA-approved for the treatment of symptomatic VMA, VMT, and macular hole.
For symptomatic macular holes, pars plana vitrectomy with membrane peel remains the gold standard for treatment. It is preferable to operate within the first 6 months of onset for highest chance of visual recovery. The risk of RD is small; however, symptoms of an RD (e.g., sudden increase in flashes and floaters, abundant “cobwebs” in the vision, or a curtain coming across the field of vision) should be explained to patients, particularly those with high myopia.

Follow-Up

Follow-up intervals vary depending on symptoms, examination, and surgical management.
Patients with high myopia are usually seen at least twice a year.
All patients are seen sooner if RD symptoms develop.
Because there is a small risk that the condition may develop in the contralateral eye, patients are given an Amsler grid for periodic home monitoring.

115
Q

Choroidal Effusion/ Detachment

A
  • *causes
  • Serous choroidal detachment: Low IOP (often <6 mm Hg), shallow anterior chamber with mild cell and flare, positive transillumination. post glauc surgery
  • Hemorrhagic choroidal detachment: High IOP (if detachment is large), shallow anterior chamber with mild cell and flare, no transillumination. rupture of SPCAs

Treatment
General Treatment

Cycloplegic (e.g., atropine 1% t.i.d.).
Topical steroid (e.g., prednisolone acetate 1% four to six times per day).
Consider oral steroids.
Surgical drainage of the suprachoroidal fluid may be indicated for a flat or progressively shallow anterior chamber, particularly in the presence of inflammation (because of the risk of peripheral anterior synechiae), corneal decompensation resulting from lens–cornea touch, or “kissing” choroidals (apposition of two lobules of detached choroid).

Specific Treatment: Repair the Underlying Problem

Serous
Wound or filtering bleb leak: Patch for 24 hours, decrease steroids and add aqueous suppressants, suture the site, use cyanoacrylate glue, place a bandage contact lens on the eye, or a combination of these.
Cyclodialysis cleft: Laser therapy, diathermy, cryotherapy, or suture the cleft to close it.
Uveitis: Topical cycloplegic and steroid as discussed previously.
Inflammatory disease: See the specific entity.
RD: Surgical repair. Proliferative vitreoretinopathy after repair is common.

Hemorrhagic:
Drainage of the choroidal detachment with or without vitrectomy is performed for severe cases with retina or vitreous to the wound. More successful if hemorrhage is liquefied, which occurs 7 to 10 days after the initial event. Otherwise use general treatment.

Follow-Up
In accordance with the underlying problem

116
Q

RP

A
  • *reduced ERG
  • *night blindness + triad (bony spicules, attenuation and ON waxy pallor)
  • *AR most common, AD least severe, X-linked R

Treatment
Some evidence supports that diets high in vitamin A (15,000 IU/day) and lutein (12 mg/day) may help slow midperipheral visual field loss in nonsmokers with RP, but the literature remains inconclusive. If high-dose vitamin A therapy is initiated, monitor liver function tests and vitamin A levels. Both epiretinal and subretinal microchip implants have been used with moderate success to improve vision in patients with advanced RP. Clinical trials are ongoing with a variety of designs to determine the safety and efficacy of retinal implant technology. In addition, research in gene therapy for specific types of RP is underway, though not yet clinically available.

117
Q

Gyrate Atrophy

A
  • *nyctalopia, AR
  • *highh plasma onithine, very poor ERG, constricted VF

Treatment

Reduce dietary protein consumption and substitute artificially flavored solutions of essential amino acids without arginine (e.g., arginine-restricted diet). Monitor serum ammonia levels.
Supplemental vitamin B6 (pyridoxine). The dose is not currently established; consider 20 mg/day p.o. initially and increase up to 500 mg/day p.o. if there is no response. Follow serum ornithine levels to determine the amount of supplemental vitamin B6 and the degree to which dietary protein needs to be restricted. Serum ornithine levels between 0.15 and 0.2 mmol/L are optimal.

118
Q

Stargardt’s

A
  • *In early stages, vision declines before visible macular changes develop.
  • *AR
  • *pisciform flecks, beaten bronze (atrophic mac degen)
  • *late stages triad: 20/200 vision, beaten bronze mac, salt and pepper fundus

Treatment
Ultraviolet light-blocking glasses when outdoors may be beneficial. Low-vision aids, services dedicated to helping the visually handicapped, and genetic counseling are helpful

119
Q

Best’s Disease

A
  • *normal ERG, abnormal EOG
  • *AD
  • *stages
    1. Stage I (Previtelliform): normal vision, normal or only subtle RPE changes (tiny, central honeycomb structure centrally) with abnormal EOG.
    2. Stage II (Vitelliform): classic “egg-yolk” lesion. 30% have ectopic lesions. Normal vision or mild vision loss.
    3. Stage III (Pseudohypopyon): layering of lipufuscein. Vision similar to stage II.
    4. Stage IV (Vitelleruptive): breakup of material gives “scrambled egg” appearance. Vision may be similar or mildly decreased from stage I/II.
    5. Stage V (Atrophic): Central RPE and retinal atrophy. Vision may range from 20/30 – 20/200.
    6. Stage VI (CNV): This complication occurs in about 20% of patients. Vision often decreased to 20/200 or worse.

Treatment
There is no effective treatment for the underlying disease. Treatment for CNV is controversial because it may heal without devastating visual loss. Laser should be considered for well-defined CNV outside the foveal center. Subfoveal CNV treatment options include PDT and intravitreal anti-VEGF agents.

Follow-Up
Patients with CNV should be treated promptly. Otherwise, there is no urgency in seeing patients with this disease. Patients are given an Amsler grid, instructed on its use, and told to return immediately if a change is noted.

120
Q

Chloroquine/ Hydroxychloroquine Toxicity

A
  • *bull’s eye maculopathy
  • *abnormal ERG and EOG

Treatment
Discontinue medication. Chloroquine >300mg, HydroC >400mg (variable)

Follow-Up
After the baseline examination, annual screening with HVF and either multifocal ERG, FAF, or SD-OCT should begin after 5 years of medication use. These tests should be acquired sooner if any concern for toxicity exists or patients are at high risk.

Note
Once ocular toxicity develops, it usually does not regress even if the drug is withdrawn. In fact, new toxic effects may develop, and old ones may progress even after the chloroquine/hydroxychloroquine has been discontinued.

121
Q

Optic Pit

A

Treatment

Isolated optic pit: No treatment required.
Optic pit with a serous macular detachment: Laser photocoagulation to the temporal margin of the optic disc is used in most cases. Vitrectomy with intravitreal gas with laser may be used in refractory cases.

Follow-Up

Isolated optic pits: Yearly examination including IOP check, dilated fundus examination, and visual field testing if indicated; sooner if symptomatic. Patients should be given an Amsler grid. See Appendix 4, Amsler Grid.
Optic pits with serous macular detachment: Reexamine 3 to 4 weeks after treatment to check for resorption of SRF. Monitor for and treat amblyopia if present.

122
Q

Solar Retinopathy

A

**Acute findings include a yellow-white spot in the fovea with or without surrounding granular grey pigmentation. Classic late finding is a red, sharply demarcated, cyst-like lesion in the fovea.

Treatment

Observation. Eyes with better visual acuities on initial examination tend to recover more vision. Long-term significant reduction in visual acuity is rare. However, central or paracentral scotomata may persist despite improvement in visual acuity.

123
Q

Risk factors of chororidal nevus conversion to MM

A

“To Find Small Ocular Melanoma”
T: Thickness >2 mm.
F: Fluid (subretinal).
S: Symptoms (typically flashes or floaters).
O: Orange pigment over the lesion.
M: Margin of tumor ≤3 mm from the optic disc.

Note
If three or more factors are present, the lesion has a >50% chance to show growth and is likely to be a small choroidal melanoma.

124
Q

Keratitic Precipitates in Uveitis

A

Stellate –> herpes (S and Z), CMV, Fuch’s iridocyclitis
Fine, non-G –> UCRAP, Posner-Schlossman, trauma, JIA
Granulomatous –> sarcoid, syphillis, TB, VKH

125
Q

Anterior Uveitis

A

Treatment

Cycloplegic (e.g., cyclopentolate 1% t.i.d. for mild to moderate inflammation; atropine 1% b.i.d. to q.i.d. for severe inflammation).
Topical steroid (e.g., prednisolone acetate 1%) q1-6h, depending on severity of inflammation. Most cases of moderate to severe acute uveitis require q1–2h dosing initially. Difluprednate (Durezol) 0.05% may allow less frequent dosing than prednisolone acetate. Consider a loading dose (prednisolone acetate 1% one drop every minute for 5 minutes) or fluorometholone 0.1% ophthalmic ointment at night. If the anterior uveitis is severe, unilateral, and is not responding to topical steroids, then consider periocular repository steroids (e.g., 0.5 to 1.0 mL subtenon injection of triamcinolone 40 mg/mL). 

Note
Periocular use of triamcinolone is off-label and must be discussed with patients. A trial of topical steroids at full strength for several weeks may help identify patients at risk of a significant IOP increase from steroids. Additionally, periocular depot steroids should be used with extreme caution in patients with scleritis because of possible scleral melting.

If there is no improvement on maximal topical and repository steroids, or if the uveitis is bilateral and severe, consider systemic steroids, or immunosuppressive therapy. Consider referral to a uveitis specialist and rheumatologist.

Note
Prior to initiating systemic steroids or periocular depot steroids, it is important to rule out infectious causes.

Treat secondary glaucoma with aqueous suppressants. Avoid pilocarpine. Glaucoma may result from:

  • Cellular blockage of the trabecular meshwork.
  • Secondary angle closure from synechiae formation.
  • Neovascularization of the iris and angle.
  • Steroid-response.

If an exact etiology for the anterior uveitis is determined, then additional ocular and/or systemic management may be indicated.

  • Ankylosing spondylitis: Often requires systemic anti-inflammatory agents (e.g., NSAIDs such as naproxen). Consider consulting rheumatology, physical therapy, and cardiology (increased incidence of cardiomegaly, conduction defects, and aortic insufficiency).
  • Inflammatory bowel disease (IBD): Often benefits from systemic steroids, sulfadiazine, or other immunosuppressive agents. Obtain a medical or gastrointestinal consult.
  • Reactive arthritis (previously known as Reiter syndrome): If urethritis is present, then the patient and sexual partners are treated for chlamydia (e.g., single dose azithromycin 1 g p.o.). Obtain medical and/or rheumatology or urology consult.
  • Psoriatic arthritis: Consider a rheumatology and/or dermatology consult.
  • Glaucomatocyclitic crisis
  • Lens-induced uveitis: Usually requires removal of lens material.
  • Herpetic uveitis: Herpes simplex typically requires topical or oral antivirals and steroid drops for non-epithelial corneal disease. Herpetic iridocyclitis benefits from topical steroids and systemic antiviral medications (e.g., acyclovir/valacyclovir); topical antivirals are ineffective for uveitis due to poor intraocular penetration.
  • UGH syndrome
  • Behçet disease
  • Lyme disease
  • JIA: Steroid dosage is adjusted according to the degree of anterior chamber cells, not flare. Prolonged cycloplegic therapy may be required. Consult rheumatology or pediatrics as systemic steroid therapy or immunomodulatory therapy is often needed. Regular follow-up is essential as flares may be asymptomatic; recurrent or chronic disease can lead to irreversible damage and various sequelae including synechiae, glaucoma, CME, and cataract formation.

Note
Cataract surgery in patients with JIA-associated uveitis has a high complication rate. Avoid cataract surgery if possible until patient is inflammation-free for at least 3 months. An IOL may be placed in select circumstances.

  • Chronic iridocyclitis of children: Same as JIA.
  • FHIC: Usually does not respond to or require steroids (a trial of steroids may be attempted, but they should be tapered quickly if there is no response); cycloplegics are not necessary.

Note
Patients with FHIC usually do well with cataract surgery, however they may develop a hyphema (i.e., Amsler sign).

  • Sarcoidosis
  • Syphilis
  • Tuberculosis: Refer the patient to an internist, infectious disease specialist, or public health officer for consideration of systemic treatment. Patients with ocular TB frequently have no pulmonary disease but still require systemic four-drug antituberculous therapy. Concomitant oral steroids may be necessary.

Follow-Up

Every 1 to 7 days in the acute phase, depending on the severity; every 1 to 6 months when stable.
At each visit, the anterior chamber reaction and IOP should be evaluated.
A vitreous and fundus examination should be performed for all flare-ups, when vision is affected, or every 3 to 6 months. Macular edema is a frequent cause of decreased vision even after the uveitis is controlled; optical coherence tomography (OCT) can be very useful diagnostically.
If the anterior chamber reaction has resolved, then the steroid drops can be slowly tapered with intermittent examinations to ensure that the inflammation does not return during the taper (usually one drop per day every 3 to 7 days [e.g., q.i.d. for 1 week, then t.i.d. for 1 week, then b.i.d. for 1 week, etc.]). Steroids are usually discontinued following the taper when the anterior chamber does not have any cellular reaction. Occasionally, long-term low-dose steroids every day or every other day are required to keep the inflammation from recurring. Punctal occlusion techniques may increase potency of drug and decrease systemic absorption. The cycloplegic agents also can be tapered off as the anterior chamber reaction improves and no new posterior synechiae are noted.

126
Q

Intermediate Uveitis

A
  • *snowbanking
  • *bilateral, 15-40yo
  • *70% idiopathic, other etiologies: MS, Sarcoid, Lyme, Syphillis, Toxocariasis

Treatment
Treat all vision-threatening complications (e.g., CME, vitritis) in symptomatic patients with active disease. Mild vitreous cell in the absence of symptoms or vision loss may be observed.
Topical prednisolone acetate 1% or difluprednate 0.05% q1–2h. Consider subtenon steroid (e.g., 0.5 to 1.0 mL injection of triamcinolone 40 mg/mL). May repeat the injections every 6 to 8 weeks until the vision and CME have stabilized. Slowly taper the frequency of injections. Subtenon steroid injections must be used with caution in patients with steroid-induced glaucoma.
If minimal improvement after three subtenon steroid injections 1 to 2 months apart, consider systemic steroids (e.g., prednisone 40 to 60 mg p.o. daily for 4 to 6 weeks).

Note
In bilateral cases, systemic steroid therapy may be preferred to periocular injections. However, in children and adolescents, growth suppression (in addition to the usual complications of long-term systemic steroids) is a major concern.

Transscleral cryotherapy to the area of snowbanking should be considered in patients who fail to respond to either oral or subtenon corticosteroids and who have neovascularization.

Pars plana vitrectomy may be useful in cases refractory to systemic steroids or to treat vitreous opacification, tractional retinal detachment, ERM, and other complications. Additionally, vitreous biopsy through a pars plana vitrectomy may be indicated in cases of suspected masquerade syndromes, especially intraocular lymphoma.

Note
Some physicians delay steroid injections for several weeks to observe whether the IOP increases on topical steroids (steroid response). If a marked steroid response is found, depot injections should be avoided.

Topical NSAIDs are usually not effective in patients with uveitic CME.

Cataracts are a frequent complication of intermediate uveitis. If cataract extraction is performed, the patient should ideally be free of inflammation for 3 months preceding the operation. Consider starting the patient on oral prednisone 60 mg daily 5 days prior to surgery and tapering the prednisone over the next month. Consider a combined pars plana vitrectomy at the time of cataract surgery if significant vitreous opacification is present.

Follow-Up
In the acute phase, patients are reevaluated every 1 to 4 weeks, depending on the severity of the condition.
In the chronic phase, reexamination is performed every 3 to 6 months. Monitor for neo

127
Q

HLA-B27 Uveitis - UCRAP

A
  • *Recurrent, unilateral (or alternating bilateral) nongranulomatous anterior uveitis
  • *reactive arthritis - do chlamydia swab

Treatment
Cyclo + Steroid –> see anterior uveitis

128
Q

Toxoplasmosis

A
  • *New, unilateral white retinal lesion often associated with an old pigmented chorioretinal scar. There is a moderate to severe focal vitreous inflammatory reaction directly over the lesion.
  • *raw meat or cat poop
  • *parasitic protozoan

TREATMENT Summary
Start antibiotic regimen together with topical cycloplegic and corticosteroid drops
At least 24-48 hours later may begin oral steroid (i.e. 60mg Prednisone orally daily for a week, then taper slowly over many weeks) - maintain antibiotics until conclusion of steroid taper
“Classic” therapy is 5-6 weeks of oral pyrimethamine, sulfadiazine, and folinic acid
Pyrimethamine - 2 loading doses of 50mg q12h, then 25mg orally twice daily thereafter
Sulfadiazine - 2g loading dose, then 1g PO QID
Folinic acid, 3 to 5 mg (or equivalent) 2x/week to prevent thrombocytopenia and leukopenia
Alternatively trimethoprime-sulfamethoxazole, double-strength (Bactrim DS, 800/160) 1 tablet, orally twice daily
with or without clindamycin (i.e. 300 mg orally four times a day)
An intravitreal dose of clindamycin (1 mg in 0.1 ml)

Treatment

Mild peripheral retinochoroiditis.
- Self-limited in immunocompetent patients. May consider observation only for peripheral lesions.
- Treat elevated IOP with antiglaucoma medications and anterior uveitis with topical cycloplegic (e.g., cyclopentolate 1% to 2% t.i.d.) with or without topical steroid (e.g., prednisolone acetate 1% q2h).
-
Treatment usually recommended for lesions in the macula, within 2 to 3 mm of the disc, threatening a large retinal vessel, associated with severe vitritis causing decreased vision, or disease in an immunocompromised patient. Immunocompromised patients may require extended treatment.
- Classic first-line triple therapy (for 4 to 6 weeks):
Pyrimethamine, 200 mg p.o. load (or two 100 mg doses p.o. 12 hours apart), and then 25 to 50 mg p.o. daily. Do not give pyrimethamine to pregnant or breast-feeding women. (Spiramycin 1 g p.o. t.i.d. for women who seroconvert in pregnancy.)
Folinic acid 10 mg p.o. every other day (to minimize bone marrow toxicity of pyrimethamine).
Sulfadiazine 2 g p.o. load and then 1 g p.o. q.i.d. Expensive and difficult to obtain; trimethoprim/sulfamethoxazole 160 mg/800 mg (Bactrim DS) twice daily may be substituted as described below.
Prednisone may be added 20 to 60 mg p.o. daily beginning at least 24 hours after initiating antimicrobial therapy and tapered 10 days before stopping antibiotics. Periocular steroids should not be given.

Systemic steroids should only rarely be used in immunocompromised patients. Before systemic steroid use, evaluation of fasting blood sugar/hemoglobin A1C and studies to rule out tuberculosis are prudent.

Note
Due to potential bone marrow suppression, a CBC must be obtained once per week while a patient is taking pyrimethamine. If the platelet count decreases below 100,000, then reduce the dosage of pyrimethamine and increase the folinic acid. Patients taking pyrimethamine should not take vitamins that contain folic acid. The medication should be given with meals to reduce anorexia.

Alternate regimens:

  • Clindamycin 150 to 450 mg p.o. t.i.d. to q.i.d. (maximum 1.8 g/day) may be used alone, with pyrimethamine as alternative therapy (if the patient is sulfa allergic), or as an adjunct (quadruple therapy). Patients on clindamycin should be warned about pseudomembranous colitis, and the medication should be stopped if diarrhea develops. Intravitreal injection of clindamycin (0.1 mg/0.1 mL) can be effective for macular-threatening cases, or when the patient is intolerant to systemic medication. Combined intravitreal clindamycin (0.1 mg/0.1 mL) and dexamethasone (0.4 mg/0.1 mL) have been reported helpful.
  • Atovaquone 750 mg p.o. q.i.d., used as alternative similar to clindamycin.
  • Trimethoprim/sulfamethoxazole (160 mg/800 mg) one tablet p.o. b.i.d., with or without clindamycin and prednisone.
  • Azithromycin loading dose 1 g (day 1) then 250 to 500 mg daily. May be used alone or in combination with pyrimethamine (50 mg daily)
  • Spiramycin 400 mg p.o. t.i.d. may be considered in cases of pregnancy, but must be obtained from CDC.

Vitrectomy has been used for nonclearing dense vitritis or other complications.

Maintenance therapy (if patient is immunosuppressed)
- Trimethoprim/sulfamethoxazole 160 mg/800 mg one tablet p.o. three times a week.
or
- If sulfa-allergic (common in HIV-infected patients), may use clindamycin 300 mg p.o. q.i.d.

Prophylaxis: In a patient with a history of toxoplasmosis undergoing cataract or refractive surgery, consider using trimethoprim/sulfamethoxazole b.i.d. during the perioperative period.

Follow-Up
In 3 to 7 days for blood tests and/or ocular assessment, and then every 1 to 2 weeks on therapy.

Special Consideration In Immunocompromised Patients
Vitritis usually much less prominent. Adjacent retinochoroidal scars may not be present. The lesions may be single or multifocal, discrete or diffuse, and unilateral or bilateral. CNS imaging is essential because of high association with CNS disease (e.g., toxoplasmic encephalopathy in HIV patients). Diagnostic vitrectomy may be necessary because of the multiple simulating entities and the variability of laboratory diagnostic tests. Systemic steroids for ocular toxoplasmosis should be used very cautiously in patients with AIDS.

129
Q

Sarcoidosis

A
  • *Iris nodules, large mutton-fat KP (especially in a triangular distribution on the inferior corneal endothelium), sheathing along peripheral retinal veins (candlewax drippings).
  • *20-50yo, Africans and Scandinavians
  • *Uveitis, secondary glaucoma, cataracts, and CME are the most common vision-threatening complications of ocular sarcoidosis
  • *chest radiography, ACE, tissue biopsy

Treatment
Refer patients to an internist or pulmonologist for systemic evaluation and medical management. Consider early referral to a uveitis specialist in complicated cases. A poor visual outcome has been reported with posterior uveitis, glaucoma, delay in definitive treatment, or presence of macula-threatening conditions such as CME.

Anterior uveitis:

Cycloplegic (e.g., atropine 1% b.i.d. or cyclopentolate 1% t.i.d.).
Topical steroid (e.g., prednisolone acetate 1% q1–6h).

Posterior uveitis:

Supplement calcium with Vitamin D (e.g., 600 mg with 400 iU) once or twice daily and consider a histamine type 2 receptor (H2) blocker (e.g., ranitidine 150 mg p.o. b.i.d.) or proton pump inhibitor (e.g., pantoprazole 40 mg daily).
Periocular steroids (e.g., 0.5 to 1.0 mL injection of triamcinolone 40 mg/mL) may be considered instead of systemic steroids, especially in unilateral or asymmetric cases. Can repeat injection every 3 to 4 weeks. 

Immunosuppressives (e.g., methotrexate, azathioprine, mycophenolate mofetil, cyclosporine, cyclophosphamide, infliximab) have been used effectively as steroid-sparing agents. Decisions regarding therapy should be individualized given known side effect profiles of each regimen.

Note
Topical steroids alone are inadequate for treatment of posterior uveitis.

Retinal neovascularization: May require panretinal photocoagulation.
Orbital disease is managed with systemic steroids as described previously.
Optic nerve granulomas require consultation with neuro-ophthalmology and treatment with systemic steroids.
Pulmonary disease, facial nerve palsy, CNS disease, and renal disease require systemic steroids and management by an internist or neurologist.

Follow-Up

Patients are reexamined in 1 to 7 days, depending on the severity of inflammation. The steroid dosages are adjusted in accordance with the treatment response. Slowly taper the steroids and cycloplegic agent as the inflammation subsides. Monitor IOP and reevaluate the fundus at each visit.
Patients with quiescent disease are seen every 3 to 6 months.
Patients being treated with steroids or systemic immunosuppression are monitored every 2 to 6 weeks, pending clinical response.
Poor response to steroid treatment should prompt a work-up for other causes of uveitis or referral to a subspecialist.

130
Q

Behcets Disease

A
  • *systemic: mouth ulcers, erythema nodosum, genital ulcers
  • *anterior and posterior uveitis, periphlebitis, shifting hypopyon
  • *25-40yo middle eastern/japanese, no gender predilection

Treatment
If untreated, bilateral blindness often develops within 3 to 4 years. Death may result from CNS involvement. Proper referral for immunosuppressive therapy is critical.

Topical corticosteroids (e.g., prednisolone acetate 1% q1–6h depending on severity of inflammation) and cycloplegics (e.g., atropine 1% b.i.d.) for anterior inflammation.
Systemic corticosteroids should be started (prednisone 1 mg/kg p.o. daily or intravenous methylprednisolone sodium succinate 1 g daily for three days, followed by prednisone). Steroids delay the onset of blindness but do not alter the long-term outcome. Prior to systemic therapy, it is important to rule out syphilis and tuberculosis.
All patients with Behçet disease and posterior uveitis should be referred to a specialist for initiation of immunosuppressive therapy. TNF-antagonists such as infliximab are now considered first-line therapy for Behçet disease. Calcineurin inhibitors (tacrolimus, cyclosporine) and antimetabolites (e.g., mycophenolate mofetil, methotrexate, azathioprine) can be used but take 1 to 2 months to achieve full effect.

Follow-Up
Daily during acute episode to monitor inflammation and IOP. Refer to uveitis specialist for further f/u

**prognosis: Approximately 25% of patients with chronic ocular involvement have 20/200 vision or less due to macular edema, vasculitis, retinal detachment, vitreous hemorrhage, neovascularization, atrophy of the optic nerve, or glaucoma. Even with treatment, up to 75% of patients lose useful vision after a 6-10 year period following the onset of ocular symptom

131
Q

Lyme Disease

A
  • *ELISA and western blot for testing
  • *tick bite –> Borrelia burgdorferi = spirochete bacteria
  • *CN7 palsy commonly assoc

Treatment
Doxycyline (100mg BID), tetracycline (500mg BID), amoxicillin 500mg TID-QID x2-3 weeks
- children, pregnant, breastfeeding - erythromycin 500mg QID

Treatment
Early Lyme Disease (Including Lyme-Related Uveitis, Keratitis, or Facial Nerve Palsy)

Doxycycline 100 mg p.o. b.i.d. for 10 to 21 days.
In children, pregnant women, and others who cannot take doxycycline, substitute amoxicillin 500 mg p.o. t.i.d., cefuroxime axetil 500 mg p.o. b.i.d., clarithromycin 500 mg p.o. b.i.d., or azithromycin 500 mg p.o. daily.

Patients with Neuro-ophthalmic Signs or Recurrent or Resistant Infection

Ceftriaxone 2 g intravenously daily for 2 to 3 weeks.
Alternatively, penicillin G, 20 million units intravenously daily for 2 to 3 weeks.

Follow-Up
Every 1 to 3 days until improvement is demonstrated, and then weekly until resolved.

132
Q

Acute Retinal Necrosis (ARN)

A
  • *The American Uveitis Society criteria include: one or more foci of retinal necrosis with discrete borders in the peripheral retina, rapid progression of disease in the absence of antiviral therapy, circumferential spread, evidence of occlusive vasculopathy with arterial involvement, and prominent inflammatory reaction in the anterior chamber and vitreous. If untreated, circumferential progression of necrosis may become confluent and spread posteriorly. The macula is typically spared early in the disease course.
  • *clinical syndrome caused by the herpes virus family: varicella zoster virus (older patients), herpes simplex virus (younger patients), or rarely, CMV or EBV

Treatment

Note
All patients with ARN should be referred to a specialist.

Prompt inpatient or outpatient treatment. The goal is to decrease the incidence of the disease in the fellow eye. Treatment does not reduce the rate of retinal detachment in the first eye.
Oral antivirals (valacyclovir 1 to 2 g t.i.d. or famciclovir 500 mg t.i.d. preferred; acyclovir 800 mg five times per day second-line option as it achieves lower intravitreal levels) with supplemental intravitreal injections with foscarnet (2.4 mg/0.1 mL) or ganciclovir (2 mg/0.1 mL) given one to two times per week. Alternative therapy includes intravenous acyclovir 10 mg/kg t.i.d. for 5 to 14 days (requires dose adjustment for renal insufficiency) with supplemental intravitreal injections as noted above, followed with oral valacyclovir 1 g t.i.d. or acyclovir 400 to 800 mg five times per day. Either of these regimens is maintained for up to 14 weeks from the onset of infection. Involvement of the second eye typically starts within 6 weeks of initial infection. Published literature suggests that primary treatment with oral antivirals in conjunction with the above intravitreal injections has similar efficacy as intravenous therapy. Stabilization and early regression of retinitis is usually seen within 4 days. The lesions may progress during the first 48 hours of treatment.
Topical cycloplegic (e.g., atropine 1% t.i.d.) and topical steroid (e.g., prednisolone acetate 1% q2–6h) in the presence of anterior segment inflammation.
Systemic steroids may be considered, particularly when the optic nerve is thought to be involved. Steroids are usually delayed at least 24 hours after the initiation of antiviral therapy, or when regression of retinal necrosis is evident. A typical oral corticosteroid regimen is prednisone 60 to 80 mg/day for 1 to 2 weeks followed by a taper over 2 to 6 weeks. Subtenon injection of triamcinolone (40 mg/1 mL) can be considered after adequate loading of antiviral therapy but may interfere with clearance of virus by the eye.
Consider prophylactic barrier laser photocoagulation posterior to active retinitis to wall off or prevent subsequent RRD (efficacy unclear).
Pars plana vitrectomy, with long-acting gas or silicone oil, is the best way to repair the associated complex RRD. Proliferative vitreoretinopathy is common.

Follow-Up

Patients are seen daily initially and are examined every few weeks to months for the following year; examination of both eyes is essential.
A careful fundus evaluation is performed at each visit to rule out retinal holes that may lead to a detachment. If barrier laser demarcation has been done and the retinitis subsequently crosses the posterior margin, consider applying additional laser therapy.
Pupillary evaluation should be performed, and optic neuropathy should be considered if the retinopathy does not explain the amount of visual loss

133
Q

Progressive Outer Retinal Necrosis(PORN)

A
  • *immunocompromised pt
  • *Rapidly progressive retinitis characterized by clear vitreous and sheet-like opacification deep to normal-looking retinal vessels, and occasional spontaneous vitreous hemorrhage. PORN is usually found in immunocompromised individuals and frequently leads to rapid bilateral blindness due either to the infection itself or to secondary retinal detachment, making prompt diagnosis and treatment essential. Unlike ARN, pain and vitritis are minimal and macular involvement occurs early.
134
Q

CMV Retinitis

A

**patients with CD4+ counts <100 cells/mm3 should be seen at least every 3 to 6 months

Treatment
Oral therapy with valganciclovir 900 mg p.o. b.i.d. for induction (21 days), followed by 900 mg p.o. daily for maintenance. Alternatively, intravenous ganciclovir 5 mg/kg b.i.d. or foscarnet 90 mg/kg b.i.d. (adjusting for renal function) may be used, followed by oral therapy valganciclovir (900 mg p.o. b.i.d. to complete 3-week induction, then 900 mg p.o. daily). Patients with progression of retinitis despite induction or who have disease that threatens the macula may benefit from intravitreal antiviral injections, but systemic therapy is still necessary to prevent involvement of the fellow eye. The goal of treatment is quiescent retinitis: nonprogressive areas of RPE atrophy with a stable opacified border.
Under the direction of an internist or infectious disease specialist, HAART should be initiated or optimized; immune recovery with sustained CD4+ counts >200 cells/mm3 results in decreased risk of retinal detachment, second-eye involvement, antiviral resistance, and mortality.
Small, macula-sparing RRDs may be treated with laser demarcation. Pars plana vitrectomy with silicone oil is indicated for detachments involving the macula.
Primary prophylaxis with oral valganciclovir in high-risk patients is not recommended because of potential toxicity.

Follow-Up

Ganciclovir resistance (reflected by positive blood or urine CMV cultures) may occur at any point during treatment.
All currently available anti-CMV therapy is virostatic, not virocidal, and almost all patients eventually relapse if not treated with HAART. Serial fundus photographs are quite useful. Relapse is defined as recurrent or new retinitis, movement of opacified border, or expansion of the atrophic zone.
Relapse does not necessarily indicate drug resistance. Reinduction with the same medication is the first line of treatment. Subtherapeutic intraocular drug levels may occur in patients on maintenance therapy and allow for relapse.

Discontinuation of anti-CMV maintenance therapy may be considered in select patients receiving HAART who have CD4+ counts >100 cells/mm3 for greater than 6 months and completely quiescent CMV retinitis. In these patients, whose immune system can control CMV, stopping maintenance therapy may prevent drug toxicity and drug-resistant organisms. In iatrogenically immunosuppressed patients, cessation or reduction in dosage of immunosuppressive drugs may be required for long-term control of CMV retinitis.
Immune recovery uveitis (IRU): Occurs in previously immunocompromised patients (HIV/iatrogenic) with CMV after the CD4+ count or immune system reconstitutes. In the presence of a functioning immune system, the CMV antigens elicit an inflammatory response that is predominantly posterior (e.g., vitritis, papillitis, CME, ERM). Treatment may require topical, periocular, or intraocular steroids. Antivirals should be continued to avoid reactivation of CMV in cases of borderline CD4+ counts.

135
Q

Vogt-Koyanagi-Harada

A
  • *20-50 female with pigmented skin
  • *phases - Systemic (4 phases):
    1. Prodromal: loss of high-frequency hearing, tinnitus, meningismus, encephalopathy, hypersensitivity of skin to touch.
    2. Uveitic: acute ocular findings - granulomatous
    3. Convalescent: alopecia, vitiligo, poliosis, “sunset glow” fundus (yellow-orange appearance of the fundus due to depigmentation of the RPE and choroid).
    4. Chronic recurrent: recurrence of anterior uveitis, subretinal fibrosis, neovascularization, glaucoma, cataract.

Treatment
Inflammation is initially controlled with steroids; the dose depends on the severity of the inflammation. In moderate to severe cases, the following regimen can be used. Steroids are tapered very slowly as the condition improves.

Topical steroids (e.g., prednisolone acetate 1% q1h).
Systemic steroids (e.g., prednisone 60 to 80 mg p.o. daily or intravenous methylprednisolone sodium succinate 1 g daily for three days followed by oral therapy) with concurrent calcium/vitamin D supplementation and antiulcer prophylaxis.
Topical cycloplegic (e.g., atropine 1% b.i.d. or cyclopentolate 1% t.i.d.).
Treatment of any specific neurologic disorders (e.g., seizures or coma).
For patients who cannot tolerate or are unresponsive to long-term oral steroids, consider immunosuppressive agents (e.g., antimetabolites, calcineurin inhibitors, cytotoxic agents, TNF-alpha inhibitors).

Follow-Up

Initial management may require hospitalization if intravenous corticosteroids initiated.
Weekly, then monthly reexamination is performed, watching for recurrent inflammation and increased IOP.
Steroids are tapered very slowly, and most patients should be transitioned to steroid-sparing immunosuppressants for long-term management. Inflammation may recur up to 9 months after the steroids have been discontinued. If this occurs, steroids should be reinstituted.

136
Q

Syphillis

A

**stages w/ ocular involvement
Primary: A chancre may occur on the eyelid or conjunctiva.
Secondary: Uveitis (mixed anterior and intermediate most common), optic neuritis, active chorioretinitis, retinitis, retinal vasculitis, conjunctivitis, dacryoadenitis, dacryocystitis, episcleritis, scleritis, monocular interstitial keratitis, and others
Tertiary: Optic atrophy, old chorioretinitis, interstitial keratitis, chronic iritis, Argyll Robertson pupil
**pathognomonic for syphilis include the following: patchy hyperemia of the iris with fleshy, pink nodules near the iris sphincter; acute placoid macular chorioretinitis; and punctate inner retinitis.

Treatment

Neurosyphilis (positive FTA-ABS in the serum and either cell count >5 white blood cells/mm3, protein >45 mg/dL, or positive CSF VDRL on lumbar puncture): Aqueous crystalline penicillin G 2 to 4 million U i.v. q4h for 10 to 14 days, followed by benzathine penicillin 2.4 million U intramuscularly (i.m.) weekly for 3 weeks (1.2 million U in each buttock). Many experts believe that any ocular involvement, especially retinal or optic nerve, should be considered as neurosyphilis and treated accordingly.

Anterior and/or intermediate syphilitic uveitis: Benzathine penicillin 2.4 million U i.m. weekly for 3 weeks.

If anterior segment inflammation is present, treatment with a cycloplegic (e.g., cyclopentolate 1% t.i.d.) and topical steroid (e.g., prednisolone acetate 1% q2h) may be beneficial.

Note
Incomplete response of uveitis to i.m. penicillin may occur but a full course of i.v. therapy is virtually always effective; therefore, only the latter is considered definitive therapy.

Treatment for chlamydial infection with a single dose of azithromycin 1 g p.o. is typically indicated.

Therapy for penicillin-allergic patients is not well established and should be managed in consultation with an infectious disease specialist. Ceftriaxone 2 g i.v./i.m. for 10 to 14 days is usually the first-choice alternative, but is contraindicated with severe allergy. Tetracycline 500 mg p.o. q.i.d. for 30 days is used by some for both late syphilis and neurosyphilis. Some believe that using penicillin is critical in neurosyphilis and merits ICU admission and desensitization in penicillin-allergic patients.

Follow-Up
Neurosyphilis: Management by infectious disease specialist mandatory. Repeat lumbar puncture every 6 months for 2 years, less frequently if the cell count returns to normal sooner. The cell count should decrease to a normal level within this period, and the CSF VDRL titer should decrease fourfold within 6 to 12 months. An increased CSF protein decreases more slowly. If these indices do not decrease as expected, retreatment may be indicated.

Other forms of syphilis: Repeat the VDRL/RPR testing at 3 and 6 months after treatment. If a titer of 1:8 or more does not decline fourfold within 6 months, if the titer increases fourfold at any point, or if clinical symptoms or signs of syphilis persist or recur, lumbar puncture and retreatment are indicated. If a pretreatment VDRL/RPR titer is <1:8, retreatment is indicated only when the titer increases or when signs of syphilis recur (as in some patients treated with i.m. penicillin).

Congenital Syphilis
Ocular signs include bilateral interstitial keratitis, secondary cataracts, salt-and-pepper chorioretinitis, and iridocyclitis. Hutchinson triad of congenital syphilis includes peg-shaped widely spaced incisors, interstitial keratitis, and deafness. Serologic testing is similar to acquired syphilis above. Standard treatment is with penicillin G, but dosing should be managed by a pediatrician or infectious dise

137
Q

Sympathetic Ophthalmia

A

**4-6weeks after surgery or penetrating trauma to fellow eye

Treatment

Prevention: Enucleation of a blind, traumatized eye before a sympathetic reaction can develop (usually considered within 14 days of the trauma). Once sympathetic ophthalmia develops, enucleation of the sympathizing eye appears to have no benefit.
Topical steroids (e.g., prednisolone acetate 1% q1–2h or difluprednate 0.05% q2h). Topical steroids are tapered slowly as condition improves.
Periocular or intravitreal steroids (e.g., subconjunctival triamcinolone acetate 40 mg in 1 mL).
Systemic steroids (e.g., prednisone 60 to 80 mg p.o. daily) with calcium/vitamin D supplementation and antiulcer prophylaxis.
Slow-release intravitreal steroid implants (e.g., dexamethasone 0.7 mg intravitreal implant; fluocinolone acetonide 0.19 or 0.59 mg intravitreal implant) are alternatives to oral steroids.
Cycloplegic (e.g., atropine 1% b.i.d.).
Long-term systemic immunosuppression with corticosteroid-sparing agents is essential in most cases. Choice of immune suppression should be made in conjunction with a uveitis specialist and individualized for each patient.

Follow-Up

Every 1 to 7 days initially, to monitor the effectiveness of therapy and IOP.
As the condition improves, the follow-up interval may be extended to every 3 to 4 weeks.
Steroids should be maintained for 3 to 6 months after all signs of inflammation have resolved and should be tapered slowly. Because of the possibility of recurrence, periodic checkups are important.
The long-term prognosis in patients treated with immunosuppressive therapy can be good, with up to 75% of eyes seeing ≥20/40 at 1yr f/u

138
Q

Lens dislocation

A
  • *Marfan’s –> up and out
  • AD and heart problems
  • *Homocysteinuria –> down and in
  • AR and bone problems
139
Q

Vitamin A deficiency

A
  • *night blindness, Bitot’s spots, dry eye, corneal liquefaction, decreased ERG
  • *assoc with cirrhosis, Occurs in the developed world from malnutrition, malabsorption from bowel or bariatric surgery, and poor vitamin metabolism from liver disease

TREATMENT
Oral vitamin A 10,000-20,000 IU daily
Intramuscular vitamin A for severe cases

140
Q

MEWDS (multiple evanescent white dot syndrome)

A
  • *~20s female, possible Hx of viral infection
  • *sudden painless monocular decrease in VA
  • *Orange-yellow granularity to the RPE underlying the fovea
  • *Small, transient white dots at the level of the RPE
  • *Small relative afferent pupillary defect possible

TREATMENT
None—resolves spontaneously
Most patients achieve normal acuity and fields in weeks to months
Photopsia, scotomas, dyschromatopsia may rarely persist
Recurrence is unusual
No systemic workup is necessary

141
Q

Cat-scratch Disease

A
  • *perinaud’s oculoglandular conjunctivitis + neuroretinitis + focal chorioretinitis
    • Bartonella Henselae

TREATMENT
patients will almost always get better on their own
several treatments to shorten the duration of symptoms have been described (doxycycline, erythromycin, rifampin, azithromycin, ciprofloxacin, and steroids later in the course)
doxycycline (i.e. 100 mg PO 2x/day) or erythromycin with or without rifampin (300 mg PO 2x/day) is likely sufficient

Conjunctivitis:
Cat-scratch disease: Generally resolves spontaneously in 6 weeks. Consider azithromycin 500 mg p.o. q.i.d., then 250 mg daily for four doses (for children, 10 mg/kg q.i.d., then 5 mg/kg daily for four doses); alternatives include trimethoprim/sulfamethoxazole (160/800 mg b.i.d.) or ciprofloxacin 500 mg p.o. b.i.d. Duration should be individualized. Use a topical antibiotic (e.g., bacitracin/polymyxin B ointment or gentamicin drops q.i.d.). The cat does not need to be removed.

142
Q

Familial Drusen

A
  • *Malattia Leventinese –> AD
  • *RPE drusen in a radial pattern over the macula, start ~20s
  • *vision good until 30-40yo, then metamorphopsia, paracentral scotoma and possible CNVM

TREATMENT
Molecular diagnosis may aid in definitive diagnosis
Genetic counseling and discussion with patient
If CNVM develops, consider treating according to current treatment recommendations applied to more common causes of macular degeneration (Note: no specific study can currently comment on the predicted effectivity in Malattia Leventinese of treatments developed for age-related macular degeneration)

143
Q

Perphipheral Ulcerative Keratitis

A
  • *assoc w/ rehum condition
  • *onset y trauma/surgery/infection
  • *assoc with necrotizing scleritis
  • *assoc with wegener’s granulomatosis –> test ANCA

Treatment summary
TREATMENT
Local
- Aggressive lubrication and eyelid hygiene
- Topical antibiotics
- Topical cyclosporine 0.05%
- Bandage contact lens
Systemic
- Oral doxycycline
- Systemic corticosteroids for acute control
- Additional systemic immunomodulatory agents are often required for associated autoimmune disease
Surgical
Cyanoacrylate adhesive; Penetrating keratoplasty; Lamellar keratoplasty ; Conjunctival resection; Tarsorrhaphy

Treatment
Primary treatment for acute disease control is systemic corticosteroids, often started at 0.5-1 mg/kg/d with a maximum dose of 60-80 mg daily. Patients with imminent vision loss may be started initially on pulsed methylprednisolone 1 g/d for 3 days and then transitioned to oral steroids. The steroids are tapered in accordance with the activity of the disease. Usually, prednisone is given at a high dose for 2-4 weeks then tapered over the course of several months
First-line for rheumatoid arthritis-associated PUK is often methotrexate (5-25 mg once weekly)
Local therapy should include aggressive lubrication and eyelid hygiene, possibly incorporating the use of punctal plugs
Oral doxycycline can assist in ocular surface lubrication through its effects on the Meibomian gland secretions and also has anti-inflammatory effects. Topical cyclosporine 0.05% (Restasis) has been reported to be successful for non-healing ulcers, likely due to its anti-inflammatory action

144
Q

Allergy Types

A

1 –> immediate (IgE), super fast
ex. anaphylaxis

2–> cytotoxic (IgM, IgD), mins to hours
ex. pemphigoid, rheumatic fever

  1. immune modulated (antibody antigen), hours
    ex. RA, SLE, staph marginal keratitis
  2. delayed (T lymphocyte) days, years
    ex. GPC, contact dermatitis, phlyctenule
145
Q

Meds causing NAION

A

Viagra (sildenafil)
Imitrex (sumatriptan)
Amiodarone
- also causes corneal verticillata and anterior lens opacities

146
Q

4 factors indicating AMD will progress from wet to dry

A

smoking
hypertension
focal hyperpigmentation
confluent soft drusen

147
Q

Lasers and their uses (unfinished slide)

A
PRP --> PDR, NVI = PRP to retina
sector laser --> sickle cell neo
grid laser
laser photocoagulation --> coats
PDT w/ vertaporfin? --> Histo
148
Q

Unilateral disc edema causes

A

compressive: thyroid, meningioma
ischemic: AAION, NAION
ophthalmic: CRVO, hypotony
inflammatory:
- infection: syphilis, TB
- non-infectious: sarcoid, lupus
- other: neuritis