- •Contents
- •Foreword
- •Preface
- •List of Abbreviations
- •1. General Topics in Ophthalmology
- •Approach to the Patient: Exam and History
- •Embryology and Development
- •Emergencies
- •Epidemiology/Statistics
- •Genetics
- •Imaging: Computed Tomography (CT)
- •Imaging: Magnetic Resonance Imaging (MRI)
- •Optics
- •Pathology
- •Pregnancy
- •Radiation/Laser
- •Surgery
- •2. Orbit, Eyelids, and Ocular Adnexa
- •Anatomy and Physiology
- •Signs and Symptoms
- •Exam and Imaging
- •Congenital and Genetic Disease
- •Infectious Disease
- •Neoplastic, Eyelid: Benign Cystic Lesions
- •Neoplastic, Eyelid: Benign Growths
- •Neoplastic, Eyelid: Hair Follicle Tumors (‘‘Tricky’’ Tumors)
- •Neoplastic, Eyelid: Premalignant Lesions
- •Neoplastic, Eyelid: Malignant Lesions
- •Neoplastic, Eyelid and Orbital: Pigmented Lesions
- •Neoplastic, Orbital: Lacrimal Gland Tumors
- •Neoplastic, Orbital: Lymphoproliferative Lesions
- •Neoplastic, Orbital: Mesenchymal Tumors
- •Neoplastic, Orbital: Metastatic and Invasive Tumors
- •Neoplastic, Orbital: Neurogenic Tumors
- •Neoplastic, Orbital: Structural Lesions
- •Neoplastic, Orbital: Vascular Lesions
- •Metabolic and Degenerative Disease
- •Systemic and Vascular Disease
- •Physical Disease
- •Inflammatory and Immune Disease
- •Eyelid Surgery
- •Lacrimal Surgery
- •Orbital Surgery
- •Other Surgery
- •3. Cornea and Conjunctiva
- •Anatomy and Physiology
- •Signs and Symptoms
- •Exam and Imaging
- •Congenital and Genetic Disease
- •Infectious Disease
- •Neoplastic Disease: Benign Masses
- •Neoplastic: Malignant
- •Neoplastic: Melanocytic Lesions
- •Metabolic and Degenerative Disease
- •Physical Disease
- •Inflammatory and Immune Disease
- •Surgery
- •4. Glaucoma
- •Anatomy and Physiology
- •Signs and Symptoms
- •Exam and Imaging
- •Infantile and Pediatric Glaucoma
- •Primary Open-Angle Glaucoma
- •Secondary Open-Angle Glaucomas
- •Primary Angle-Closure Glaucoma
- •Secondary Angle-Closure Glaucoma
- •Surgery
- •Iris
- •Uveitis
- •Signs and Symptoms and Clinical Presentations of Uveitis
- •Anterior Uveitis Diagnosis and Work-Up
- •Anterior Uveitis Diseases
- •Intermediate Uveitis Diagnosis and Work-Up
- •Intermediate Uveitis Diseases
- •Posterior Uveitis Diagnosis and Work-Up
- •Posterior Uveitis Diseases
- •Panuveitis/Diffuse Uveitis
- •Surgery
- •6. Lens
- •Anatomy and Physiology
- •Signs and Symptoms
- •Congenital and Genetic Disease
- •Metabolic and Degenerative Disease
- •Systemic and Vascular Disease
- •Physical Disease
- •Cataract Surgery
- •Refractive Lens Surgery
- •7. Retina and Vitreous
- •Anatomy and Physiology
- •Signs and Symptoms
- •Exam and Imaging
- •Congenital and Genetic Disease
- •Hereditary Macular Disorders
- •Progressive Tapetoretinal Disorders
- •Stationary Tapetoretinal Disorders
- •Congenital and Genetic Vitreoretinopathies
- •Infectious Disease
- •Infectious Endophthalmitis
- •Neoplastic Disease
- •Metabolic and Degenerative Disease
- •Systemic and Vascular Disease
- •Physical Disease
- •Surgery: Laser
- •Surgery: Operative
- •8. Neurologic
- •Anatomy and Physiology
- •Signs and Symptoms
- •Exam and Imaging
- •Congenital and Genetic Disease
- •Infectious Disease
- •Neoplastic Disease
- •Metabolic and Degenerative Disease
- •Systemic and Vascular Disease
- •Physical Disease
- •Inflammatory and Immune Disease
- •Selected Cranial Nerve Abnormalities
- •Gaze Abnormalities
- •Nystagmus
- •Psychiatric Diseases
- •9. Pediatrics and Strabismus
- •Anatomy and Physiology
- •Signs and Symptoms
- •Exam and Imaging
- •Congenital and Genetic Disease
- •Congenital Disease: Phakomatoses
- •Strabismus: Esotropia
- •Strabismus: Exotropia
- •Strabismus: Vertical Deviations
- •Surgery
- •Other
- •10. Medications
- •General
- •Antibacterials: Aminoglycosides
- •Antibacterials: Cephalosporins and Penicillins
- •Antibacterials: Fluoroquinolones
- •Antibacterials: Inhibitors of Cell Wall Function
- •Antibacterials: Inhibitors of Nucleic Acid Synthesis
- •Antibacterials: Inhibitors of Protein Synthesis
- •Antibacterials: Combinations
- •Antibacterial and Corticosteroid Combinations
- •Antifungal Agents
- •Anti-inflammatory: Allergy
- •Anti-inflammatory: Nonsteroidals
- •Antiseptics
- •Antiviral Agents
- •Glaucoma: Beta-Blockers
- •Glaucoma: Carbonic Anhydrase Inhibitors
- •Glaucoma: Hyperosmotics
- •Glaucoma: Miotics/Cholinergic, Direct Acting
- •Glaucoma: Miotics/Cholinergic, Indirect Irreversible
- •Glaucoma: Prostaglandin Analogues
- •Glaucoma: Sympathomimetics
- •Immunosuppressives: Antimetabolites
- •Immunosuppressives: Alkylating Agents
- •Immunosuppressives: Noncytotoxic
- •Miotics: Cholinergic, Indirect Reversible
- •Mydriatics and Cycloplegics: Anticholinergic
- •Mydriatics: Adrenergic
- •Neurologic Medications
- •Other Agents
- •Index
288 RETINA AND VITREOUS
found later: 12% initially, 30% by 1 month, 50% by 8 months, and 80% by 24 months.
Penetrating injuries usually have a retinal break opposite the injury, and proliferative vitreoretinopathy may cause a traction band away from the break.
For litiginous evaluation, may need to determine if trauma is causal: suspect traumatic cause if patient has unilateral pathology with dialysis or giant tear in a nonmyope <40 years old without otherwise prior history of trauma within 2 years.
VALSALVA RETINOPATHY Hemorrhagic detachment of ILM that is circumscribed, and juxtapapillary, from a sudden rise in the intrathoracic or abdominal pressure, with increased venous pressure and rupture of superficial capillaries. Also may have transient increased IOP (‘‘brass players’ glaucoma’’) from increased choroidal engorgement. Can occur with unrecognized Valsalva stress (e.g., intercourse). No treatment needed, and good prognosis can be expected, but if nonclearing, can consider YAG laser disruption of posterior hyaloid to drain hemorrhage into the vitreous.
WHIPLASH RETINOPATHY Immediate mild decreased VA (usually about 20/30) with gray swelling of the fovea. FA may show a tiny area of hyperfluorescence that may look like solar retinopathy. Typically resolves with little long-term changes.
Inflammatory and Immune Disease
See Chapter 5.
Surgery: Laser
FOCAL PHOTOCOAGULATION Used to ablate CNVM, tumors, vascular lesions (capillary or choroidal hemangioma, retinal artery macroaneurysm, etc.), parasites (DUSN, cysticercosis, etc.), destroy sick RPE in ICSR, create chorioretinal adhesions for retinal tears, or ‘‘wall off ’’ RD or necrotic CMV or ARN retina.
GRID PHOTOCOAGULATION, FOCAL MACULAR GRID (FMG) Used to treat macular edema for diabetic CSME (ETDRS) or after BRVO (BVOS). Settings usually use argon green, 100 mm, 0.1 second, and 100 mW (often begin lower). Light burns (for blond fundus, may begin at 50 mW), one burn width apart. Full grid for diffuse edema (‘‘doughnut’’-shaped ablation 500 mm around fovea) or partial laser over edema. Increased spot size increases cataract risk.
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PANRETINAL PHOTOCOAGULATION (PRP) Used to cause regression of NV, destroy ischemic tissue that is producing VEGF, or improve oxygenation from the choroid such as for PDR, sickle cell retinopathy, NV following BRVO, or NVI after CRVO. Settings often about 200 mW, 0.2 seconds, 200 mm spot. Power density, and thus tissue damage, increases as the spot size is decreased, wattage is increased, or time is decreased. Partial PRP usually leaves two laser spots between burns; in contrast, extensive PRP tightens the pattern to one spot separating burns. Usually deliver argon PRP <900 spots per session, in two or three sessions, and complete PRP is around 2000 spots. Treat inferior retina first; focally treat NVE. If FMG is needed, complete it first.
Complications: 11% of patients lose one line of VA. May also have nyctalopia (especially warn diabetic patients) and field constriction (rare complaint with PDR, as the peripheral retina is already ischemic). With extramacular treatment, the patient will have a negative scotoma that is not noticed as much as a positive scotoma, which occurs with a macular lesion. Also may have CME (treat the temporal ‘‘C’’ last and avoid temporal retina within 2 DD of the fovea), foveal traction, choroidal rupture (apply gentle pressure on globe if any bleeding is seen), and serous choroidal detachment (avoid by delivering in several sessions). May also have posterior synechia if iris is burned when treating the retinal periphery, cornea or lens burns, CNVM or foveal burns, transient retinal edema (improves after 3 weeks), retinal thinning, and holes (especially in high myopes). Persistent mydriasis and paresis of accommodation have been reported from ciliary nerve damage (the 3 and 9 o’clock location in the retina).
PHOTODYNAMIC THERAPY (PDT) Intravenous photosensitizing agent (e.g., verteporfin or Visudyne, peak sensitivity at 690 nm) accumulates in proliferating neoplastic or NV tissue (possibly from LDL receptors on proliferating cells), which is then activated by irradiation at wavelength specific for the molecule’s peak absorption. Photochemical reaction (not photocoagulation) produces tissue damage by free radical formation (type 1 injury) and reactive singlet oxygen molecules (type 2 injury) that causes vascular endothelial damage and thrombus formation.
TRANSPUPILLARY THERMOTHERAPY (TTT) Subthreshold laser to ‘‘cook’’ vascular lesions, such as CNVM and melanomas. Laser wavelength is 810 nm (choriocapillaris level), usually with 3.0 mm spot size, 60 seconds, and 820 mW. Several sessions needed.
Surgery: Operative
GASES AND FLUIDS USED INTRAOPERATIVELY Used to maintain vitreous space and pressure (Table 7–4).
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290 |
RETINA AND VITREOUS |
|
|
|
TABLE 7–4 |
|
|
|
|
Expansile Gas Properties |
|
|
|
|
|
|
|
|
Nonexpansile |
Gas |
|
Duration |
Expansion |
Concentration |
|
|
|
|
|
Air |
|
1–3 days |
0 |
NA |
SF6 (sulfur hexafluoride) |
10 days–2 weeks |
2 |
20% (can rapidly |
|
|
|
|
|
increase IOP) |
C2F6 (perfluoroethane) |
4 weeks |
3 |
NA |
|
C3F8 (perfluoropropane) |
6 weeks–2 months |
4 |
16% |
|
NA, not applicable.
Intraocular gases: specific gravity of the gases are much less than water.
Also, blood nitrogen diffuses into the gas; thus, do not use N2 with inhalational anesthetics during surgery.
Perfluorocarbons (PFCs): used in proliferative vitreoretinopathy, giant retinal tears, retinopathy of prematurity, and to remove posteriorly displaced lens fragments or IOL. Characterizewd by high specific gravity, with transparency, high surface tension, and low viscosity. Potential toxicity seen in subretinal space and anterior segment with retained intraocular PFC. Four PFCs commonly in use, most com-
monly perfluoro-N-octane (PFO), which has a relatively low viscosity (0.8 Cs at 25 C) and a high vapor pressure (50 mmHg at 37 C). Low viscosity allows for easy injection and aspiration via a 20-gauge needle, and high vapor pressure allows evaporation of small droplets of residual PFO during air–fluid exchange.
Silicone oil (SiO): surface tension is less than for gases, and SiO is buoyant in fluid-filled eye (inferior peripheral iridectomy is needed). Use for long-term tamponade, especially with recurrent RD, when 180 degree retinotomy is performed, air travel is anticipated, etc.
INTRAVITREAL INJECTION Useful for antibiotic and steroid delivery, for subfoveal hemorrhage >1 mm (may inject TPA), and for pneumatic displacement.
Endophthalmitis tap and inject: usually place retrobulbar block, then use empty tuberculin syringe or other small syringe with 23 gauge needle placed 3 mm posterior to limbus, observing through the pupil (indirect light works well) as the needle is advanced about 1 cm, and aspirate about 0.5 mL. Then use a new site and 30 gauge needle on TB syringe to inject 0.1 cc of antibiotics in the midvitreous.
RETINAL DETACHMENT SURGERY Goal is to find the retinal holes and close them, then relieve vitreoretinal traction. Three common errors: failure
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to find the hole, failure to find the other holes, and failure to close them. If macula is on and RD is peripheral, then do surgery within a few days. If RD is near macula, then perform surgery as early as possible, and within hours if macula is threatened or giant retinal tear is present (>1 quadrant). If macula is off, then can wait 1 or 2 days if history suggests that the RD is recent or up to 1 or 2 weeks if it is a chronic RD.
Pneumatic retinopexy: best for single break or group no larger than 1 clock hour within the superior 8 clock hours. Intraocular gas temporarily closes the break and displaces the retina toward the eye wall; holes are treated with cryotherapy or laser. Successful in 75% of cases.
Scleral buckle procedure: conjunctival peritomy, pass bridle suture around each rectus muscle, and inspect sclera. Scleral depress and localize all breaks, and mark externally on sclera. Create chorioretinal adhesion with laser or cryotherapy (most commonly used), with cryoreactions touching each other without a gap, ‘‘toe in’’ (avoid indenting eye with shaft), do not cryotherapy in middle of flap tear, surround each tear with 2–3 mm of cryotherapy, and treat the entire lattice lesion if applicable. Apply the buckle to indent the sclera and choroid toward the retina, relieve vitreous traction, and displace SRF. Then place sutures to anchor the exoplant. Drain SRF if needed, where the RD is most elevated usually, anterior to the equator and superior or inferior to the horizontal rectus muscles; expose choroid by radial scleral incision and peforate choroid with a 27 gauge needle diagonally (ensure IOP is not elevated; relieve tension on traction sutures). Tighten the buckle, and irrigate with Marcaine for pain relief. Carefully close conjunctiva and Tenon’s capsule.
Complications: scleral rupture from cryotherapy, retinal perforation, retinal incarceration (do not try to push back in; put gas or air into eye to flatten out), redetachment, buckle exposure, anterior segment ischemia, strabismus, and induced myopia. Proliferative vitreoretinopathy is most common cause for failure (5–10% for RRD); PVR is usually an ‘‘inferior disease’’ (gravity dependent).
Eighty to 90% scleral buckle success for RD, with permanent support of the vitreous base and less proliferative vitreoretinopathy. Ten to 20% require more than one surgery. Eighty-five percent of patients who present with 20/20 VA keep that following surgery, and 15% have decreased VA usually from CME or ERM. If macula is on preoperative, then 80 to 85% of patients are 20/50 or better following surgery. If macula is off preoperative, then there is only a 20 to 40% chance of 20/50 VA or better (one third will be 20/200 or worse).
Vitrectomy with gas: used for posterior breaks.
Vitrectomy with scleral buckle: used for complicated RD, such as with proliferative vitreoretinopathy, traction RD, and giant tears.
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292 RETINA AND VITREOUS
VITRECTOMY Performed for nonclearing VH with severe PDR in insulindependent diabetes, complicated RD, removal of ERM or other posterior segment lesions, and CME (vitreous holds cytokines against macula, blocks medications getting to macula, and is a reservoir for antigens and cells). The microvitreoretinal (MVR) blade passes through the sclera, stroma of pars plana, pigmented then non-pigmented epithelium, sometimes zonules, and into the vitreous base. If a VH occurs after vitrectomy, consider anterior hyaloid vascular proliferation around the sclerotomy site.
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