Ординатура / Офтальмология / Английские материалы / Oxford American Handbook of Ophthalmology_Tsai, Denniston, Murray_2011

256 CHAPTER 9 Lens

Box 9.2 Recommendations for prophylaxis and treatment of endophthalmitis

Prophylaxis

Perform skin and conjunctival sac preparation with 5% aqueous povidone iodine at least 5 min before surgery. It is safe and effective in significantly reducing ocular surface flora. Additional benefit may be gained by postoperative instillation into the sac.

Identifying and treating risk factors such as blepharitis, conjunctivitis, or mucocoele is probably more useful than universal antibiotic prophylaxis. The use of antibiotics in irrigating solutions is controversial.

Treatment

•VA > LP: single-port vitreous biopsy via the pars plana should be performed using a vitreous cutting-suction device. The specimens are directly smeared for Gram stain etc. and plated for culture. Directly inject amikacin and vancomycin (or gentamicin and ceftazidime).

•VA < LP: three port pars plan vitrectomy and intravitreal antibiotics. High-dose systemic prednisone may be given (e.g., 60–80 mg daily), rapidly reducing dose to none over a week to 10 days. Steroids are contraindicated if there is a fungal infection.

If the clinical course warrants it, the biopsy and intravitreal antibiotic injection may be repeated after 48–72 hours.

POSTOPERATIVE CYSTOID MACULAR EDEMA 257

Postoperative cystoid macular edema

Irvine–Gass syndrome

Suspect

Suspect this if there is worsening vision (may decrease with pinhole), perifoveal retinal thickening and optic nerve leakage, ± cystoid spaces. There is increased risk in patients with diabetes mellitus, complicated surgery, postoperative uveitis, or previous CME (in the other eye post-routine surgery).

Diagnosis

Clinical appearance ± FA (typically dye leakage from both the optic disc as well as the parafovea into the cystoid spaces in a petalloid pattern) ± OCT demonstrates intraretinal cystic changes and thickening.

Prophylaxis

Consider adding a topical NSAID (e.g., ketorolac 0.3% 3x/day for 1 month) to the usual postoperative steroid regime for high-risk groups (patients with diabetes mellitus, uveitis, previous CME, or complicated surgery with vitreous loss).

Treatment

A step-wise approach is recommended. Review the diagnosis (e.g., OCT, FA) if atypical or slow to respond. One approach is as follows:

1.Topical: steroid (e.g., dexamethasone 0.1% 4x/day) + NSAID (e.g., ketorolac 0.3% 3x/day).

Review in 4–6 weeks. If CME is persistent, then continue as follows:

2.Periocular steroid (e.g., orbital floor/subtenons; methylprednisolone/ triamcinolone) and continue topical treatment.

Review in 4–6 weeks. If persistent, then continue as follows:

3.Consider repeating periocular or giving intravitreal steroid.

4.Anti–vascular endothelial growth factor (VEGF) agents (e.g., bevacizumab) or pars plana vitrectomy with peeling of internal limiting membrane may be necessary for recalcitrant cases.

258 CHAPTER 9 Lens

Abnormalities of lens size, shape, and position

Abnormalities of size, shape, and position (Table 9.9) may both affect the refractive power of the lens and increase optical aberration. In addition, most of these abnormalities are associated with lens opacity. Most common among this group are disorders of lens position (i.e., ectopia lentis).

Ectopia lentis

This may be complete (dislocation or luxation) or partial (displacement or subluxation). Do not neglect possible acquired causes of ectopia lentis.

Complications

•Refractive (edge effect, lenticular astigmatism, lenticular myopia, aphakic hypermetropia, diplopia).

•Anterior dislocation can cause glaucoma, corneal decompensation, or uveitis.

Treatment

•Refractive: contact lenses, eyeglasses.

•Dislocation into the posterior segment (followed by aphakic correction) by either 1) YAG zonulolysis or 2) mydriatics + lay the patient on his/ her back if lens is already dislocated anteriorly.

•Lensectomy (followed by aphakic correction, ACIOL, or suture-fixated PCIOL). Partially subluxed lenses may be more safely removed via phacoemulsification with the use of capsular tension rings with or without fixation loops (FDA approved) or with capsular tension segments (not FDA approved, but available through compassionate use).

Causes

Congenital

•Familal ectopa lentis (AD): unior bilateral superotemporal lens subluxation; no systemic abnormality.

•Ectopia lentis et pupillae (AR): superotemporal dislocation with pupil displacement in the opposite direction; no systemic abnormality.

•Marfan syndrome (AD, Ch15, fibrillin): bilateral superotemporal lens subluxation with some preservation of accommodation, lattice degeneration, retinal detachment, anomalous angles, glaucoma, keratoconus, blue sclera, axial myopia; musculoskeletal (arachnodactyly, disproportionately long-limbed, joint laxity, pectus

excavatum, kyphoscoliosis, high arched palate, herniae); cardiovascular (aortic dilatation, aortic regurgiation, aortic dissection, mitral valve prolapse).

•Weill–Marchesani syndrome (AR): bilateral anteroinferior lens subluxation, microspherophakia, retinal detachment, anomalous angles; musculoskeletal (short stature, brachydactyly); neurological (reduced IQ).

260CHAPTER 9 Lens

•Homocystinuria (AR, cystathionine synthetase abnormality l homocysteine and methionine accumulation): bilateral inferonasal lens subluxation, myopia, glaucoma; skeletal (knock-kneed, marfanoid habitus, osteoporosis); hematological (thromboses, especially

associated with general anesthesia); characteristic facies (fine, fair hair); neurological (low IQ).

•Hyperlysinemia (AR, lysine A-ketogluatarate reductase): lens subluxation, microspherophakia; musculoskeletal (joint laxity, hypotonia); neurological (epilepsy, low IQ).

•Sulphite oxidase deficiency (AR): lens subluxation; neurological (hypertonia, low IQ); life expectancy less than 5 years.

Acquired

These include trauma, high myopia (hyper)mature cataract, pseudoexfoliation, buphthalmos, and ciliary body tumor.

Glaucoma

Anatomy and physiology 262

Glaucoma: assessment 264

Ocular hypertension (OHT) 267

Primary open-angle glaucoma (POAG) 269

Normal-tension glaucoma (NTG) 271

Primary angle-closure glaucoma (PACG) 273

Pseudoexfoliation (PXF) syndrome 275

Pigment dispersion syndrome (PDS) 277

Neovascular glaucoma (NVG) 279

Inflammatory glaucoma: general 281

Inflammatory glaucoma: syndromes 283

Lens-related glaucoma 284

Other secondary open-angle glaucomas 286

262 CHAPTER 10 Glaucoma

Anatomy and physiology

Glaucoma has classically been described as a progressive optic neuropathy with characteristic changes in the optic nerve head and corresponding loss of visual field. In many cases, optic nerve damage is identified clinically or with imaging technologies prior to visual field loss.

In some cases of “glaucoma,” the optic nerve and visual fields are normal but the intraocular pressure (IOP) is at such a high level that glaucomatous damage is considered imminent or inevitable. Glaucoma represents a final common pathway for a number of conditions, for most of which raised IOP is the most important risk factor.

In Western countries, glaucoma is present in 1% of those over 40 and 3% in those over 70 years old. It is the second leading cause of irreversible blindness worldwide. In the United States, glaucoma is estimated to affect nearly 3 million individuals and will increase to 3.6 million by 2020. African Americans are three times more likely than white Americans to have glaucoma.

Anatomy

•Anterior chamber angle extends from Schwalbe’s line (the termination of Descemet’s membrane on the peripheral cornea) posteriorly to the trabecular meshwork (TM), scleral spur, or ciliary body (depending

on the angle configuration) where an acute angle is formed with the peripheral iris.

•Trabecular meshwork is a reticulated band of fibrocellular sheets, with a triangular cross-section and base toward the scleral spur.

•Schlemm’s canal is a circumferential septate drain with an inner wall of endothelium containing giant vacuoles and an outer wall obliquely punctuated by collector channels that drain into the episcleral veins.

•Scleral spur is a firm fibrous projection from the sclera, with Schlemm’s canal at its base and the longitudinal portion of the ciliary muscle inserting into its posterior surface.

•Ciliary body comprises the ciliary muscle and ciliary epithelium, arranged anatomically as the pars plana and pars plicata (containing the ciliary processes). Contraction of the ciliary muscle permits accommodation and increases trabecular outflow. The ciliary epithelium is a cuboidal bilayer arranged apex to apex with numerous gap junctions. The inner layer is nonpigmented, with high metabolic activity, and posteriorly is continuous with the neural retina. The outer layer is pigmented and posteriorly is continuous with the RPE.

Physiology

Aqueous production

Aqueous humor is a clear, colorless, plasma-like balanced salt solution produced by the ciliary body. It is a structurally supportive medium providing nutrients to the lens and cornea. It differs from plasma in having lower glucose (80% of plasma levels), low protein (assuming an intact blood aqueous barrier), and high ascorbate.

It is formed at around 2.5 μL/min by a combination of active secretion (70%), ultrafiltration (20%), and osmosis (10%). Active secretion is

ANATOMY AND PHYSIOLOGY 263

complex, involving the maintenance of a transepithelial potential by the Na+K+ pump, ion transport by symports and antiports (including the important Na+/K+/2Cl– symport), calciumand voltage-gated ion channels, and carbonic anhydrase.

Aqueous outflow

While the trabecular route is the major outflow, the uveoscleral contribution may be as much as 30%. The outflow capacity through the trabecular route and uveoscleral route varies and has been demonstrated to decrease with age.

Trabecular (conventional) route

Most aqueous humor leaves the eye by this passive, pressure-sensitive route. Around 75% of outflow resistance is due to the trabecular meshwork itself, the major component being the outermost (juxtacanalicular) portion of the trabecular meshwork. This comprises several layers of endothelial cells embedded in ground substance that appears to act as a filter, which is continually cleaned by endothelial cell phagocytosis.

Further transport into Schlemm’s canal is achieved via pressure-dependent transcellular channels (seen as giant vacuoles of fluid crossing the endothelium) and paracellular pores. Aqueous is then transported via collector channels to the episcleral veins and on to the general venous circulation.

Uveoscleral (unconventional) route

The aqueous passes across the iris root and ciliary body into the supraciliary and suprachoroidal spaces from where it escapes via the choroidal circulation.

Intraocular pressure (IOP)

Flow in = Flow out = C (IOP – Pv) + U

where C is the pressure-sensitive outflow facility (via trabecular meshwork), U is the pressure-independent outflow (via uveoscleral route), and Pv is the episcleral venous pressure.

Typical values are as follows:

Flow in =C (IOP − Pv) +U

2.5 μL/min = 0.3 μL/min/mmHg (16 – 9 mmHg) + 0.4 μL/min

Variation in IOP

Within the population

Based on population studies, normal IOP is generally taken to be mean IOP (16 mmHg) ± 2 SD (2 x 2.5 mmHg), i.e., a range of 11–21 mmHg. However, there is a positive skew to this distribution.

Within the individual

Mean diurnal variation is approximately 5 mmHg in normal patients but may fluctuate from 10 to 15 mmHg in primary open-angle glaucoma (POAG). In most individuals, IOP tends to peak early morning upon awakening. Pulse pressure, respiration, extremes of blood pressure, and season also have an effect on IOP variation.

264 CHAPTER 10 Glaucoma

Glaucoma: assessment

At initial consultation (Table 10.1) consider 1) evidence for glaucoma (Table 10.2) vs. normal variation or alternative pathology (Table 10.3); 2) evidence for underlying cause (i.e., type of glaucoma—steroid responsive, pigmentary); 3) factors influencing treatment (age, vision, comorbidities).

Be cautious of interpreting any one abnormality in isolation—e.g., apparent field defects may be artifactual and disappear with repeated testing because of the “learning effect”; a patient with a normal IOP one day may have a high IOP another day.

Table 10.1 An approach to assessing possible glaucoma

The ISNT rule describes the normal contour of the disc rim, being thickest inferiorly, followed by the superior and nasal quadrants, with the temporal region being thinnest.

Table 10.3 A short differential diagnosis of the glaucoma triad