Cataract and Refractive Surgery Comanagement

22 CATARACT AND REFRACTIVE SURGERY COMANAGEMENT


Cataract Surgery Management


Jim Owen and Brian Chou


CATARACTS


ICD-9: 366.0—INFANTILE, JUVENILE, AND PRESENILE CATARACT


ICD-9: 366.1—SENILE CATARACT


ICD-9: 366.2—TRAUMATIC CATARACT


ICD-9: 366.3—CATARACT SECONDARY TO OCULAR DISORDERS


ICD-9: 366.4—CATARACT ASSOCIATED WITH OTHER DISORDERS


ICD-9: 366.8—OTHER CATARACT


ICD-9: 366.9—UNSPECIFIED CATARACT


ICD-9: 743.3—CONGENITAL CATARACT AND LENS ANOMALIES


image     THE DISEASE


Cataracts are a clouding of the crystalline lens. They are the leading cause of blindness in the world according to the World Health Organization. Depending on the location of clouding in the crystalline lens, cataracts are categorized as capsular, cortical, or nuclear.


Etiology


Although cataracts can be congenital, the most common cause of cataracts is because of natural aging. Other cataracts are associated with ocular inflammation, systemic disease (e.g., diabetes, Wilson’s disease), radiation exposure, trauma, and the prolonged use of corticosteroids and other medicines (e.g., phenothiazines).


The Patient


Clinical Symptoms


Patients with cataract may complain of reduced vision, glare while driving into oncoming headlights and sunlight, a dulling of colors, and double images.


Clinical Signs



  • Reduced best spectacle-corrected visual acuity with variable refraction.
  • Crystalline lens opacity noted with biomicroscopy. Dilated examination of the lens using an optic section and retroillumination assists in visualizing the affected portion of the crystalline lens.
  • The practitioner’s view of the posterior pole with fundoscopy is degraded proportionate to the density of the cataract.

Ancillary Tests


When a dense cataract obscures the practitioner’s view of the posterior pole during fundoscopy, the following measurements are useful:



  • Retinal acuity meter—This device provides an estimate of the patient’s achievable visual acuity following cataract surgery. A patient looks through pinhole glasses at a backlight visual acuity chart. Since the patient can alter head position and gaze, he or she is able to view around dense opacities.
  • B-scan ultrasound—When a dense cataract or vitreous hemorrhage obscure the direct view of the fundus, a B-scan can image the internal eye anatomy and determine whether the retina is intact.

The traditional indication for cataract surgery has been a best spectacle-corrected visual acuity worse than 20/40. However, functional disability can occur even with acuity in the 20/25 to 20/30 range. When case history describes functional disability, cataract surgery can also be justified when the following measurements show visual reduction:



  • 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


Currently, there are IOL’s that correct more than spherical distance vision (Fig. 22-1). Toric IOLs can correct corneal astigmatism, diffractive lenses provide vision at far and near, and there is a flexible plate haptic lens that provides vision at distance and up to intermediate distances.


image

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

Although there is no universal postoperative schedule, the following represents the author’s usual schedule and measurements performed at each:



  • 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


image     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


Treatment is based on the suspected cause of postoperative uveitis. For infectious endophthalmitis, refer to the section “Infectious Endophthalmitis” of this chapter. For phacoanaphylaxis, refer to Chapter 10, section “Anterior Uveitis”. If case history indicates patient nonadherence in using the corticosteroid drops or an abrupt taper, the use of the drops should be reinstituted, emphasizing the importance of compliance to the patient. For preexisting uveitis, refer to Chapter 10, section “Anterior Uveitis”. For epithelial down growth, the patient should undergo argon laser treatment of the affected areas. In the case of prostaglandin-analog–induced uveitis, switch the patient to another class of ocular hypotensive. With UGH syndrome, the patient should have the IOL explanted or reanchored to prevent further iris chafing. For vitreous to the wound or iris prolapse, the patient should be referred promptly to the cataract surgeon for surgical management.


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


image     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


Medical therapy primarily involves topical hyperosmotics, including 2% and 5% NaCl drops and ointment. Topical hyperosmotics draw out excess fluid from the cornea. Hyperosmotic ointment is usually used at bedtime, while the drops are used three to five times daily in the morning. In some cases, ocular hypotensives can also minimize the degree of corneal edema.


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


image     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


When prescribing topical ocular hypotensives postoperatively, β-blockers are the drugs of choice. Avoid prostaglandin analogs and epinephrine derivatives. Prostaglandin analogs can exacerbate intraocular inflammation, while epinephrine can lead to cystoid macular edema (CME). Intraocular pressure may also be quickly reduced by “burping” the paracentesis site to release aqueous.


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.


For the treatment of malignant glaucoma, see Chapter 18.


image     INFECTIOUS ENDOPHTHALMITIS


ICD-9: 360.01


image     THE DISEASE


Infectious endophthalmitis is perhaps the most feared complication following cataract surgery. Despite an incidence of less than 0.1%, the condition can quickly and irreversibly devastate vision. Infectious endophthalmitis can present within the first few days after surgery or have a delayed onset, weeks to even years later.


Etiology


Several different microorganisms may cause infectious endophthalmitis. Acute infectious endophthalmitis is most commonly caused by Staphylococcus epidermidis. Delayed onset infectious endophthalmitis may be because of fungi (including Aspergillus and Candida) and Propionibacterium acnes.


The Patient


Clinical Symptoms


Worsening redness, pain, photosensitivity, and decreasing vision.


Clinical Signs


Unusually severe intraocular inflammation postoperatively, which may include granulomatous keratic precipitates and hypopyon. Signs include lid edema, conjunctival injection, pronounced cell and flare in the anterior chamber, and vitritis.


Ancillary Tests


Lab testing for postoperative infectious endophthalmitis is given in Chapters 1 and 3.


The Treatment


Bacterial endophthalmitis is an ocular emergency that requires prompt treatment to minimize vision loss. Patients should receive intravitreal antibiotics (e.g., vancomycin 1.0 mg/0.1 mL for Gram-positive coverage and ceftazidime 2.25 mg/0.1 mL for Gram-negative coverage) at the time of vitreal biopsy. Also prescribe topical fluoroquinolone (e.g., moxifloxacin 0.5% q1h), corticosteroid (e.g., prednisolone acetate 1.0% q1h), and a cycloplegic (e.g., homatropine 5% b.i.d.). Monitor the clinical outcome carefully every 4 to 8 hours until improvement is noted.


Although bacterial endophthalmitis was previously treated with systemic antibiotics, the results of the Endophthalmitis Vitrectomy Study (EVS) found no difference in final visual acuity or media clarity whether or not systemic antibiotics were employed. The EVS also found that patients presenting with hand-motion vision or better do not require an immediate pars plana vitrectomy, but patients presenting with only light perception have the best visual outcome when they undergo an immediate vitrectomy.


With fungal endophthalmitis, administer intravitreal amphotericin B (5 to 10 μg) at the time of vitreal biopsy. Therapeutic vitrectomy can be considered as well. Broad-spectrum antifungal therapy includes natamycin 5% suspension q1h, flucytosine 37.5 mg/kg p.o. q6h, and amphotericin B 0.25 to 0.3 mg/kg/d intravenously initially and then increased to 0.75 to 1.0 mg/kg/d in divided doses.


CYSTOID MACULAR EDEMA


ICD-9: 362.53


image     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


image     THE DISEASE


PCO is the most common complication following cataract surgery. A 1998 meta-analysis found that the rate of PCO after extracapsular cataract surgery with IOL implantation was 11.8% after 1 year, 20.7% after 3 years, and 28.4% after 5 years.


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


image     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.


(For Etiology, Clinical Symptoms, Clinical Signs, Ancillary Tests, The Treatment, see Chapter 18.)


WOUND LEAK


ICD-9: 360.3


image     THE DISEASE


Ocular hypotony refers to an abnormally low IOP, generally 5 mm Hg or less. One possible cause of postoperative hypotony is wound leak.


Etiology


Wound leak occurs when aqueous leaks from the anterior chamber to the globe’s exterior.


The Patient


Clinical Symptoms


The patient may be asymptomatic or complain of eye pain and reduced vision.


Clinical Signs


Low IOP, positive Seidel’s test, shallow anterior chamber, corneal folds.


Ancillary Tests


B-scan ultrasound is useful if the fundus is not easily viewed because of media opacity. In these cases, the B-scan can rule out causes of hypotony besides wound leak, including cyclodialysis and choroidal detachment.


The Treatment


In small leaks where the anterior chamber is still formed, place a bandage contact lens (e.g., lotrafilcon A), and prescribe a broad-spectrum antibiotic (e.g., moxifloxacin 0.5% q.i.d.) for prophylaxis. Recheck in 24 hours, as the wound can seal spontaneously. In larger wounds, consider applying cyanoacrylate with a bandage contact lens on top. Large wounds require suturing.


Lasik Management


Jim Owen and Brian Chou


image     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.


In 2003, the FDA approved the first femtosecond laser for use on the cornea (Fig. 22-2). This is a photodisruptive laser that creates very small cavitation bubbles within the cornea. These “bubbles” can be placed very precisely within the cornea to allow for specific and accurate dissection of the cornea.


image

Figure 22-2. A femtosecond laser for use on the cornea.

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Oct 2, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Cataract and Refractive Surgery Comanagement

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