- •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
CHAPTER 4
Glaucoma
Anatomy and Physiology
LIMBUS-ANGLE STRUCTURES (FIG. 4–1) From anterior to posterior: Schwalbe’s ring (Descemet’s termination), trabecular meshwork (TM), scleral spur (SS), and ciliary body (CB).
TRABECULAR MESHWORK, THREE DIVISIONS Uveal (iris processes), corneoscleral (from SS to Schwalbe’s, lined by endothelium; engulf debris), and juxtacanalicular (greatest resistance to outflow; uses micropinocytosis and transcellular vacuoles to move aqueous fluid across the endothlium; likely site of primary open-angle glaucoma pathology; steroids increase GAG here).
Endothelial cells lining trabecular beams are phagocytic and act as a ‘‘self-cleaning filter.’’ Pigment can overwhelm the endothelial cells, which also cannot phagocytize exfoliative material. Red blood cells also pliably squeeze through the TM (except ghost cells) and pass into vacuoles or are phagocytized.
Posterior TM is more pigmented and overlies Schlemm’s canal, which drains to the aqueous veins of Ascher, then to laminated veins of the conjunctiva, then the episcleral vein, and finally into the superior orbital vein. More external collector channels are inferior and nasal.
AQUEOUS FLUID OUTFLOW The Goldmann equation shows that IOP ¼
(Fformation / Cfacility) þ EVP. The equation can be rearranged to show that aqueous outflow is directly proportional to the net forward aqueous pressure
(IOP – EVP) and inversely proportional to outflow resistance: Fformation ¼ (IOP – EVP) / R, where R is resistance. The equation is missing
uveoscleral outflow.
Tonography: measures resistance; the inverse of resistance is known
as facility |
(C), and |
is normally 0.2–0.3 mL/minute/mmHg. |
Low |
C ¼ high |
resistance |
and pressure; for example, age-related |
loss |
of endothelial cells leads to decreased outflow and thus increased IOP.
Some determinants of IOP: increases with age, female sex, AfricanAmerican race, family history, high blood pressure, obesity, posture,
143
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Figure 4–1 Gonioscopic view of a wide-open anterior chamber angle.
144
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ANATOMY AND PHYSIOLOGY |
145 |
myopia, exercise, lid closure, inflammation, water imbibition, cycloplegics, steroids, ketamine, and succinylcholine. IOP is decreased with inhalational anesthesia, alcohol, and marijuana. Diurnal peak in morning from endogenous corticosteroids.
An acute increase in the EVP (normally about 9 mmHg) increases the IOP in a 1:1 ratio (chronic EVP increases the IOP less).
Diurnal variation: the net forward aqueous flow pressure (P) is the result of pressure in the eye minus venous pressure: Poutflow ¼
PIOP – PEVP, and is normally about 5 mmHg (14 – 9). If inflow doubles (as with diurnal variation), the outflow pressure
also doubles. For example, if IOP were 14 mmHg and the inflow
doubles (Poutflow that was 5 doubles to 10), then the IOP would increase to 19 mmHg (10 þ 9) because the EVP remains
constant. Glaucoma is characterized by large diurnal fluctuations (e.g., 22 mmHg may increase to 35 when diurnal production doubles).
TM outflow: responsible for 80% of outflow; increased with elevated IOP, pilocarpine, epinephrine, dipivefrin, ALT, and trabeculotomy. Outflow is passive bulk flow through the TM due to hydrostatic pressure gradient. Parasympathetic tone keeps the TM open (thus cycloplegics cause TM collapse and may increase IOP).
Uveoscleral outflow: responsible for about 20% of outflow, through the ciliary body face into the suprachoroidal space. Ouflow increases with atropine, epinephrine, alpha-2 agonists, and prostaglandin analogues, as well as a cyclodialysis cleft. Uveoscleral outflow is decreased with pilocarpine from ciliary muscle contraction and closure of spaces between muscle fibers. Unlike the TM, uveoscleral outflow is pressureindependent (if IOP < EVP, all outflow is uveoscleral).
CILIARY BODY Composed of two divisions: the pars plicata, which is the anterior 2 mm (approximately 3 mm posterior to limbus) and has 70 to 80 ciliary processes, and the pars plana, which is the posterior flat 4 mm of the CB (thus, for a vitrectomy, usually enter 3.5 mm posterior to the limbus to avoid the ciliary processes). The CB forms the aqueous, vitreous MPS, affects outflow, forms and supports the zonules, is responsible for accommodation, and is the attachment for the anterior vitreous base.
Ciliary processes have a double epithelium. The outer, pigmented, cuboidal layer of cells is a continuation of the RPE and is contiguous with the posterior (inner) iris epithelium. The inner, nonpigmented, columnar layer is a contination of the neurosensory retina and is the site of aqueous production (apigmented ¼ aqueous). The blood– aqueous barrier is formed by tight junctions of the inner epithelium and the nonfenestrated iris vessels.
Three ciliary muscles:
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146GLAUCOMA
Longitudinal (meridional): attaches SS/TM to the ora serrata (thus, miotics may cause RD). Contracture opens the TM and increases outflow and decreases uveoscleral outflow (thus, pilocarpine and Xalatan counteract each other).
Circular (sphincteric): contraction reduces the diameter of the ciliary ring and thus relaxes zonular tension (accommodation).
Oblique (radial): lies between the longitudinal and circular muscles. Contraction increases uveoscleral outflow and shallows the AC by pulling the lens diaphragm forward (thus increased risk of
angle closure with miotics).
Vasculature: major arterial circle is poorly defined and is more vascular in the anterior ciliary body (more hyphemas in the anterior chamber). It is formed from the two long posterior ciliary arteries and seven anterior ciliary arteries (two from each rectus muscle except the LR; thus, there is a risk of anterior segment ischemia with multiple muscle surgery).
AQUEOUS FLUID The aqueous provides a clear medium and nourishment (more glucose in the posterior chamber, more lactate in AC, acidic pH of 7.2, and decreased protein but 15 more ascorbate than serum) and maintains IOP (to prevent pthisis). Volume is about 200–300 mL and is produced at 2–3 mL/minute; thus, there is a complete turnover every
100minutes.
Produced by active transport (Naþ, Cl , HCO3 pumped across basal cell surface, and H2O follows), ultrafiltration (H2O and soluble products), and diffusion (lipid solubles pass via osmosis).
Glaucoma is caused by outflow obstruction, not hypersecretion, as would be needed to increase production 8 to get IOP to 40 mmHg. Production decreases with age, surgery, and inflammation. Measure production with fluorophotometry.
OPTIC NERVE See Chapter 8. The optic disk is a vertical oval and is smaller in Caucasian versus African-American patients. Rim thickness normally follows the ISNT rule: inferior rim broadest, then superior, followed by nasal and temporal. This creates an optic cup that is normally a horizontal oval (becomes more vertical in glaucoma, which does not follow the ISNT rule, and inferior and superior nerve fiber layer axons are preferentially lost). The lamina cribrosa is stacked fenestrated collagen (type IV) and laminin plates, with larger openings and thinner walls superiorly and inferiorly (possibly less supportive and more easily damaged).
DEFINITION AND PATHOGENESIS OF GLAUCOMA Optic neuropathy characterized by nerve head cupping with associated loss of visual field. Diagnosis is typically made if two of three conditions are present: increased
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