A. Overview

1. Opacity or cloudiness of crystalline lens which may prevent transmission of clear image
2. Usually manifests as gradual, painless, unilateral visual loss
3. Pupil may appear white ("leukocoria")
4. Congenital or acquired
5. Risks for Acquired
   1. Aging - probably most important risk factor [1,3]
   2. Smoking
   3. Trauma
   4. Radiation Exposure - may include total sun exposure (without protection)
   5. Metabolic Disturbances - diabetes, galactosemia, Wilson's Disease
   6. Prolonged intraocular inflammation
   7. Glucocorticoids - systemic as well as inhaled agents increase risk fo cataracts [4]
   8. Lower educational status
6. Congenital
   1. 1/3 inherited trait (often autosomal dominant)
   2. 1/3 due to other syndromes
   3. 1/3 idiopathic
7. Over 16 million persons with cataracts worldwide

B. Senile Cataracts [3]

1. Opacification of the lens due to simple aging
2. Occurs from "Sclerosis" of crystalline lens
   1. First have compaction of fibers
   2. Then have increased density of lens
   3. Increases in cortical thickness of lens leads to myopia
   4. Yellowing of lens occurs as well due to chemical modification of proteins
3. Most senile cataracts are Nuclear Sclerotic Cataracts
4. Statins are associated with reduced nuclear cataract risk [7]

C. Naming of Cataracts
[Figure] "Schematic of the Lens"

1. According to position of opacification
2. Subcapsular - directly under outer lens capsule
3. Anterior Subcapsular Cataract - may not affect vision considerably
4. Posterior Subcapsular Cataract
   1. Interfere with vision more severely than anterior due to glare and axial position
   2. Frequent in diabetics, with chronic glucocorticoids, after radiation exposure
   3. Similar to frost on a cold mug
5. Cortical Cataracts
   1. Within cortical material between capsule and nucleus
   2. Often appears as white wheel spokes at periphery

D. Progression of Visual Changes

1. Patient begins with normal vision and changes progress at variable rates and may include:
2. Glare with halo effect around lights
3. Generalized blurriness with loss of best corrected visual acuity
4. Induced myopic shift leadaing to "second sight" with improved near vision
5. May have monocular diplopia (as opposed to diplopia from motility disturbances)
6. Total Blindness will eventually occur

E. Cataract Surgery [3,5]

1. Usuall performed on outpatient basis under topical and/or intraocular anesthesia
2. Types
   1. Intracapsular Extraction: complete removal of lens, rarely indicated in modern practice
   2. Extracapsular Extraction: (see below)
   3. Condition of eye without a lens is called aphakia
3. Correction of vision following removal of normal lens
   1. Contact lenses - excellent for vision; tolerance often difficult
   2. Cataract glasses - peripheral vision reduced, objects magnified, rarely in USA today
   3. Intraocular lenses - anterior chamber, iris supported, posterior chamber; pseudoaphakia
4. Spectacles required in most cases after surgery
   1. No accomodation of new lens for near versus far vision
   2. Bifocal lenses often prescribed
   3. Avoidance of spectacles through monovision concept in which one eye is corrected for distance vision, the other for near vision by proper selection of intraocular lens power
5. Extracapsular Extraction
   1. Removal of small section anterior capsule, cortex and nucleus
   2. This leaves posterior capsule in place
   3. Allows placement of posterior chamber lens implant behind iris in remaining capsule bag
   4. Preferred method is phacoemulsification
   5. ~60% of such extractions with implants will require subsequent posterior capsulectomy
   6. This proceedure uses YAG laser
6. Indications for Surgery
   1. Based on patient reporting specific vision induced impairment of activities
   2. Generally not based on morphologic appearance of lens
   3. On occasion, an advanced cataractous lens is removed due to induced glaucoma
7. Routine preoperative evaluation does not affect outcomes of cataract surgery [6]
8. About 5000 surgeries per million people per year in USA [1]

References

1. Asbell PA, Dualan I, Mindel J, et al. 2005. Lancet. 365(9459):599
2. Shingleton BJ and O'Donoghue MW. 2000. NEJM. 343(8):556
3. Solomon R and Donnenfeld ED. 2003. JAMA. 290(2):248
4. Cumming RG, Mitchell P, Leeder SR. 1997. NEJM. 337(1):8
5. Obstbaum SA. 1996. JAMA. 275(21):1675 (Case Discussion)
6. Schein OD, Katz J, Bass EB, et al. 2000. NEJM. 342(3):168
7. Klein BE, Klein R, Lee KE, Grady LM. 2006. JAMA. 295(23):2752