• Glare testing (e.g., Brightness Acuity Tester)
  
• Contrast sensitivity (e.g., Bailey-Lovie and Pelli-Robson charts)

The Treatment

Cataract extraction with intraocular lens (IOL) implantation is appropriate if the cataract interferes with the patient’s activities of daily living. Surgery is also indicated if the cataract is obstructing examination of the posterior pole—for example, when the patient is under management for glaucoma or diabetic retinopathy.

Prior to surgery, a dilated fundus examination is necessary to rule out ocular pathology, which may contribute to reduced vision, such as macular disease. A-scan ultrasonography and keratometry are also required for calculating the power of the IOL implant. Specular microscopy is desirable for obtaining an endothelial cell count. An endothelial cell count of 1,000 cells/mm² or less is at moderate to high risk of developing postoperative corneal edema (see section later).

Phacoemulsification describes cataract removal by emulsifying the lens with ultrasonic energy. Also called “phaco,” this technique requires a small incision at the corneal limbus followed by a capsulorhexis, or creation of an opening through the anterior capsule. These entries allow a small ultrasonic probe to contact the cloudy lens material, breaking it up into small pieces that are concurrently irrigated and aspirated from the capsular bag. In place of the cloudy lens, the surgeon places a folded IOL through the corneal incision into the capsular bag, where the IOL is unfolded and properly positioned. Sutures are not usually necessary to close the small incision.

Phacoemulsification is currently the preferred form of cataract removal and has essentially replaced the older technique of extracapsular cataract extraction (ECCE), where the entire crystalline lens (except for the capsule) was removed in one piece through a larger incision. The use of a small selfsealing incision in phacoemulsification allows for a faster recovery with less patient discomfort. Small incisions also minimize any change in corneal curvature, which could negatively affect the postoperative refractive outcome. In selected cases, however, ECCE is still appropriate over phacoemulsification, including congenital cataracts and extremely hard and dense cataracts.

IOL Options

Figure 22-1. The Synchrony lens (Visiogen, Irvine, CA), a dual optics lens with a high plus anterior lens connected by a spring haptic to a low powered, static minus lens.

The toric IOLs (Alcon Arcysof Toric, Staar Toric) have powers that range from −1.50 to −3.00 giving them an effective power of up to −2.00 at the corneal plane. Higher amounts of astigmatism can be treated by limbal relaxing incisions. Accurate corneal cylinder measurements are required either from keratometry or IOL Master measurements. Patients who have an unstable capsular bag, including pseudoexfoliation and weak zonules may not be good candidates for these lenses as the lens may not remain stable in the capsular bag.

Two lenses use diffractive technology to obtain near and far vision. The first diffractive lens approved was the Alcon Acrysof ReStor 4.0 Multifocal IOL. Recently, Alcon received approval for a 3.0 version of the ReStor lens. The ReStor lens is a single-piece aspheric, ultraviolet and blue light blocking, diffractive lens. The lenses use a mathematical concept of apodization to produce a gradual blending of the diffractive steps in the lens. These steps can be as small as 0.2 μm. The difference between the 4.0 and the 3.0 is the add power. As expected, the 4.0 is a 4.0 D add yielding a 3.2 D add at the spectacle plane and the 3.0 D add yielding a 2.5 add at the spectacle plane.

The Tecnis Multifocal IOL (AMO-Irvince, CA) uses an aspheric optic design to offset the spherical aberration of the cornea. The lens has a prolate anterior surface with 0.27 μm of negative spherical aberrations and a posterior surface with diffractive rings to provide the near and distance images.

The principle side effect of diffractive lenses is glare and halos. This symptom is secondary to the two light foci within the patient’s eye. Additionally, these lenses cause a reduction in contrast sensitivity as a result of the separation in light energy into the two bundles.

The Crystalens HD (Baush and Lomb; Rochester, NY) is a plate haptic IOL with several unique features. The optic of the lens moves forward with the contraction of the ciliary muscle through an increase in vitreous cavity pressure. Secondarily, there is an “arching” of the lens centrally that results in an increase in negative spherical aberrations and coma. Finally, the HD version of the lens has a central asphericity that increases depth of focus resulting in improved near vision. A careful discussion regarding the limitations and potential complications of each of these lenses is important to have with each patient prior to surgery.

Postoperative Cataract Management

For the uneventful cataract surgery, an acceptable course of postoperative management includes the following:

• Antibiotic drops (e.g., moxifloxacin HCl 0.5%, one drop four times a day for 1 week)
  
• Nonsteroidal anti-inflammatory drops (e.g., diclofenac sodium 0.1%, one drop four times a day for 1 week)
  
• Corticosteroid drops (e.g., prednisolone acetate 1.0%, one drop four times a day for 1 week, then one drop two times a day for 2 weeks)
  
• The patient should use nighttime protective goggles and avoid strenuous activity for 1 to 2 weeks following surgery. No hot tubs, saunas, or swimming for 2 weeks after surgery

• Postop 1 day. Unaided visual acuity, pinholed visual acuity, biomicroscopy, tonometry
  
• Postop 1 week. Unaided visual acuity, refraction, biomicroscopy, tonometry
  
• Postop 4 weeks. Unaided visual acuity, refraction, biomicroscopy, tonometry, prescribe eyewear
  
• Postop 3 months. Spectacle-corrected visual acuity, biomicroscopy, tonometry, dilated fundus examination, recheck in 3 to 6 months

Postoperative Cataract Complications

Jim Owen and Brian Chou

UVEITIS

ICD-9: 364.23—LENS-INDUCED IRIDOCYCLITIS

ICD-9: 364.04—SECONDARY IRIDOCYCLITIS, NONINFECTIONS

     THE DISEASE

Some inflammation in the anterior chamber is expected during the immediate postoperative recovery. However, an unusually severe degree of cell and flare early after surgery or the persistence of intraocular inflammation beyond 4 weeks is not typical and requires further investigation.

Etiology

There are multiple causes of abnormal intraocular inflammation following phacoemulsification. The differential diagnosis includes infectious endophthalmitis, phacoanaphylaxis to lens protein remnants, abrupt taper of corticosteroids, patient nonadherence in using corticosteroid drops, preexisting uveitis, epithelial down growth, use of prostaglandin-like ocular hypotensives, uveitis-glaucoma-hyphema (UGH) syndrome, and incarceration of vitreous or iris to the wound.

The Patient

Clinical Symptoms

The patient may complain of photosensitivity, eye pain, and blurred vision, each with a wide range of severity.

Clinical Signs

Biomicroscopy will show inflammatory cells and possibly flare (protein transudate) in the anterior chamber. Other findings may include keratic precipitates, ciliary injection, a miotic pupil, and an intraocular pressure that is lower in the affected eye. In severe cases, a hypopyon may be present with fibrin in the anterior chamber.

Ancillary Tests

If infectious endophthalmitis is suspected, perform cultures and sensitivities on samples of the aqueous and vitreous. Gonioscopy is sometimes useful for detecting vitreous or iris to the wound and detecting remnants of lens material in the anterior chamber.

The Treatment

CORNEAL EDEMA

ICD-9: 371.2—CORNEAL EDEMA

ICD-9: 371.20—CORNEAL EDEMA, UNSPECIFIED

ICD-9: 371.22—SECONDARY CORNEAL EDEMA

ICD-9: 371.23—BULLOUS KERATOPATHY

     THE DISEASE

Pseudophakic bullous keratopathy describes irreversible corneal edema following cataract surgery with IOL implantation. Surgical trauma and inflammation can damage the corneal endothelium, the layer of cells that regulates corneal hydration. The effect of mild corneal edema is limited to the stroma, while moderate to severe corneal edema also affects the epithelium. When the corneal epithelium is edematous, blisters or “bullae” form that substantially reduce vision.

Etiology

The corneal epithelium and endothelium are semipermeable membranes involved in regulating corneal hydration. The stroma lying in between contains proteoglycans that attract fluid into the collagen. Intraocular pressure also tends to drive fluid into the cornea. When the stroma imbibes fluid, the tissue swells. To prevent excess corneal swelling, the endothelium drives fluid out of the cornea by creating an osmotic gradient. If the endothelial pump is impaired by disease or trauma, steady-state hydration is lost, causing corneal edema.

The Patient

Clinical Symptoms

Blurry and cloudy vision results with epithelial edema. The rupture of the epithelial bullae can cause pain, foreign body sensation, and photophobia.

Clinical Signs

Biomicroscopy will show folds in the corneal stroma, areas of microcystic epithelial edema, and epithelial bullae. Chronic cases may have corneal neovascularization. Endothelial guttata may be observable in cases of preexisting endothelial dystrophy (e.g., Fuchs).

Ancillary Tests

Although the clinical diagnosis of corneal edema is primarily made with biomicroscopy, specular microscopy and pachymetry can assist in the diagnosis. These measurements are also useful preoperatively for assessing the risk of persistent postoperative corneal edema.

• Specular microscopy. Imaging the endothelial layer provides a method for obtaining endothelial cell density. Normal densities may range from 2,000 to 3,500 cells/mm² depending on the age of the patient. Densities of 1,000 cells/mm² or less present an increased risk of problematic postoperative corneal edema.
  
• Pachymetry. The average central corneal pachymetry is approximately 550 µm, but in an edematous cornea, the tissue can swell substantially and result in increased corneal thickness of over 600 µm. This measurement is not diagnostic alone, since some individuals without corneal edema have thick corneas. However, within an individual, serial pachymetry can indicate diurnal fluctuations in corneal hydration or show longer term changes in corneal hydration because of endothelial damage.

The Treatment

When there is a rupture of epithelial bullae, a high dK bandage soft contact lens (e.g., lotrafilcon A) can control the discomfort until re-epithelialization. Since ruptured bullae create the potential for microbial entry, a broad spectrum antibiotic drop should be prescribed for prophylaxis (e.g., moxifloxacin 0.5% t.i.d.).

Corneal transplantation is reserved for severe corneal edema where hyperosmotics provide insufficient benefit.

INTRAOCULAR PRESSURE SPIKES

ICD-9: 365.04

     THE DISEASE

Increased intraocular pressure is commonly detected in the early postoperative cataract recovery. While a nonglaucomatous eye can sustain an IOP into the mid-20s mm Hg for a short duration without damage, higher IOPs require clinical action.

Etiology

Intraocular pressure spikes may result from a variety of causes:

• Retained viscoelastic. Viscoelastic is the thick cushioning solution used to “inflate” the anterior chamber during surgery and to protect the endothelium from mechanical insult. In some individuals, viscoelastic can significantly impede aqueous outflow, causing an IOP spike.
  
• Inflammatory material, hyphema, and dispersed pigment. The trabecular meshwork can become clogged with any of these components, leading to an IOP spike. Retained cortical fragments can incite an inflammatory response in proportion to the amount of cortical remnants. Uncommonly, an IOL may incarcerate an iris blood vessel, causing hemorrhage or rub against the iris dispersing pigment granules.
  
• Pupillary block. Formation of synechiae between the iris, and IOL can disrupt aqueous outflow and increase IOP. Pupillary block is rare and is seen mostly with anterior chamber IOLs where an iridectomy was not performed.
  
• Malignant glaucoma. This rare condition results when aqueous is misdirected into the vitreous cavity causing the iris to bow forward, causing a shallow anterior chamber. Unlike pupillary block, a peripheral iridotomy does not resolve the increased IOP.

The Patient

Clinical Symptoms

Patient symptoms generally do not signal elevated IOP when under 25 mm Hg. However, an acute rise of IOP over 35 mm Hg, as can happen with in pupillary block of malignant glaucoma, can be accompanied with redness, pain, and photophobia. Nausea and vomiting may also occur.

Clinical Signs

Elevated IOP is the primary indicator. Depending on etiology, biomicroscopy may show a flat anterior chamber, cortical remnants, hyphema, and so on.

Ancillary Tests

Not applicable.

The Treatment

In the case of pupillary block, a laser peripheral iridotomy should be performed if the cornea is clear enough to allow the treatment. However, if the cornea is steamy, instill a topical mydriatic agent (e.g., 1% cyclopentolate) to try breaking the synechiae. If the intraocular pressure is still not controlled, prescribe a topical β-blocker, oral carbonic anhydrase inhibitor, and/or oral hyperosmotic. Prednisolone acetate 1% q1h should also be instilled to control intraocular inflammation. As soon as the cornea clears, a peripheral iridotomy should be performed.

CYSTOID MACULAR EDEMA

ICD-9: 362.53

     THE DISEASE

CME refers to thickening of the retina around the fovea with or without small fluid-filled cysts. CME can occur in diabetic retinopathy, retinal vein occlusions, and many other conditions. When it occurs after cataract surgery, the condition is also referred to as Irvine-Gass’ syndrome. Approximately 3% of patients undergoing cataract surgery experience vision loss as a result of CME within the first postoperative year. The peak incidence occurs 6 to 10 weeks following surgery.

Etiology

CME results from leaky perifoveal capillaries. There are several specific elements that may cause these capillaries to leak after cataract surgery:

• Intraocular inflammation where inflammatory mediators including prostaglandins cause vasodilation of the perifoveal capillaries
  
• Vitreal-retinal traction because of surgery or vitreal prolapse
  
• Use of epinephrine (or the prodrug, dipivefrin) eye drops
  
• Ultraviolet light

The Patient

Clinical Symptoms

Gradual and painless decrease in vision.

Clinical Signs

Using a 78 D or similar lens while viewing with an optic section will show retinal thickening and fluid cysts using an optic section. Resolution of the edema is best using a contact lens to view the macula.

Ancillary Tests

Fluorescein angiography shows leakage of the perifoveal capillaries during the early phase and a petal-shaped hyperfluorescence over the macula during the late phase. Optical coherence tomography has been demonstrated to detect retinal thickening even before angiographic evidence of CME.

The Treatment

Postoperative CME often resolves spontaneously within 6 months. However, resolution can be hastened with a topical nonsteroidal anti-inflammatory (NSAID, e.g., diclofenac sodium 0.1% q.i.d. for 1 to 3 months). By inhibiting the cyclooxygenase pathway, prostaglandin synthesis is disrupted, which in turn is thought to reduce the perifoveal capillary leakage. There are also anecdotal reports that carbonic anhydrase inhibitors (e.g., acetazolamide, 250 mg p.o. b.i.d.) help clear macular edema. About 90% of pseudophakic CME with posterior chamber IOLs eventually regain acuity of 20/40 or better.

POSTERIOR CAPSULE OPACIFICATION (PCO)

ICD-9: 366.5—AFTER-CATARACT

ICD-9: 366.50—AFTER-CATARACT, UNSPECIFIED

ICD-9: 366.52—OTHER AFTER-CATARACT, NOT OBSCURING VISION

ICD-9: 366.53—AFTER-CATARACT, OBSCURING VISION

     THE DISEASE

Etiology

PCO is characterized by a proliferation of equatorial lens epithelial cells along the posterior capsular surface. The result is thickening and clouding of the posterior capsule.

The Patient

Clinical Symptoms

Patients complain of decreased vision and glare.

Clinical Signs

Biomicroscopy shows a fibrotic membrane over the posterior capsule, most easily seen with the pupil dilated.

Ancillary Tests

Not applicable.

The Treatment

When PCO causes visual impairment, Nd:YAG (neodymium: yttrium-aluminum garnet) capsulotomy is indicated. YAG treatment creates an opening in the posterior capsule by photodisrupting the opaque membrane. This procedure is routine and relatively safe. However, potential complications include intraocular inflammation, CME, IOP spikes, and retinal detachment.

Recent studies show that the incidence of PCO can be minimized through surgical techniques with capsular tension rings and square-edge IOL implants.

RETINAL DETACHMENT

ICD-9: 361.0

     THE DISEASE

The incidence of rhegmatogenous retinal detachment after uncomplicated cataract surgery is estimated at 0% to 3%, with approximately half of cases occurring within the first year of surgery. Loss of vitreous during the surgery is a significant risk factor because of resulting vitreo-retinal traction. There are conflicting reports on whether YAG capsulotomy increases the risk of retinal detachment.

Lasik Management

Jim Owen and Brian Chou

     THE PROCEDURE

LASIK, laser-assisted in situ keratomileusis, is the most widely performed refractive surgery. It is used to treat varying degrees of myopia and hyperopia either with or without astigmatism. During the procedure, the surgeon creates a hinged corneal flap, which is reflected back. The exposed stromal bed is then ablated with an excimer laser. The corneal flap is repositioned over the stromal bed, where the flap assumes a new curvature from the underlying ablation and then adheres without the need for sutures. Visual recovery is rapid, with most patients achieving functional vision by the next day.

Since the first LASIK procedure in 1991, the technique has evolved with improvements in microkeratectomy and the excimer laser ablation. An increasing number of surgeons are embracing femtosecond lasers in place of traditional blade technology to create the corneal tissue flap. In addition, most excimer platforms are FDA approved in an attempt to limit the induction of higher order wavefront aberrations including coma, trefoil, secondary astigmatism, spherical aberration, and quadrafoil. This is accomplished by using wavefront aberrometry, (usually Hartmann-Shack) to create the treatment plan for the patient. The continuing refinements in LASIK technology should further improve safety and visual outcomes.