eMedicine Specialties > Ophthalmology > Lens

Cataract, Senile

Author: Vicente Victor D Ocampo, MD, Consulting Staff, Department of Ophthalmology, Asian Hospital and Medical Center, Philippines
Coauthor(s): C Stephen Foster, MD, FACS, FACR, FAAO, Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution
Contributor Information and Disclosures

Updated: May 20, 2009

Introduction

Background

Senile cataract is a vision-impairing disease characterized by gradual, progressive thickening of the lens. It is one of the leading causes of blindness in the world today. This is unfortunate, considering that the visual morbidity brought about by age-related cataract is reversible. As such, early detection, close monitoring, and timely surgical intervention must be observed in the management of senile cataracts. The succeeding section is a general overview of senile cataract and its management.

Pathophysiology

The pathophysiology behind senile cataracts is complex and yet to be fully understood. In all probability, its pathogenesis is multifactorial involving complex interactions between various physiologic processes. As the lens ages, its weight and thickness increases while its accommodative power decreases. As the new cortical layers are added in a concentric pattern, the central nucleus is compressed and hardened in a process called nuclear sclerosis.

Multiple mechanisms contribute to the progressive loss of transparency of the lens. The lens epithelium is believed to undergo age-related changes, particularly a decrease in lens epithelial cell density and an aberrant differentiation of lens fiber cells. Although the epithelium of cataractous lenses experiences a low rate of apoptotic death, which is unlikely to cause a significant decrease in cell density, the accumulation of small scale epithelial losses may consequently result in an alteration of lens fiber formation and homeostasis, ultimately leading to loss of lens transparency. Furthermore, as the lens ages, a reduction in the rate at which water and, perhaps, water-soluble low-molecular weight metabolites can enter the cells of the lens nucleus via the epithelium and cortex occurs with a subsequent decrease in the rate of transport of water, nutrients, and antioxidants.

Consequently, progressive oxidative damage to the lens with aging takes place, leading to senile cataract development. Various studies showing an increase in products of oxidation (eg, oxidized glutathione) and a decrease in antioxidant vitamins and the enzyme superoxide dismutase underscore the important role of oxidative processes in cataractogenesis.

Another mechanism involved is the conversion of soluble low-molecular weight cytoplasmic lens proteins to soluble high molecular weight aggregates, insoluble phases, and insoluble membrane-protein matrices. The resulting protein changes cause abrupt fluctuations in the refractive index of the lens, scatter light rays, and reduce transparency. Other areas being investigated include the role of nutrition in cataract development, particularly the involvement of glucose and trace minerals and vitamins.

Senile cataract can be classified into 3 main types: nuclear cataract, cortical cataract, and posterior subcapsular cataract. Nuclear cataracts result from excessive nuclear sclerosis and yellowing, with consequent formation of a central lenticular opacity. In some instances, the nucleus can become very opaque and brown, termed a brunescent nuclear cataract. Changes in the ionic composition of the lens cortex and the eventual change in hydration of the lens fibers produce a cortical cataract. Formation of granular and plaquelike opacities in the posterior subcapsular cortex often heralds the formation of posterior subcapsular cataracts.

Frequency

United States

At least 300,000-400,000 new visually disabling cataracts occur annually in the United States, with complications of modern surgical techniques resulting in at least 7000 irreversibly blind eyes. In the Framingham Eye Study from 1973-1975, senile cataract was seen in 15.5% of the 2477 patients examined. The overall rates of senile cataract in general and of its 3 main types — nuclear, cortical, and posterior subcapsular — rapidly increased with age, so that for the oldest age group, 75 years and older, nuclear, cortical, and posterior subcapsular cataracts were found in 65.5%, 27.7%, and 19.7% of the study population, respectively. Nuclear opacities were the most commonly seen lens change.

International

Senile cataract continues to be the main cause of visual impairment and blindness in the world. At least 5-10 million new visually disabling cataracts occur yearly, with modern surgical techniques resulting in 100,000-200,000 irreversibly blind eyes. Published data estimate that 1.2% of the entire population of Africa is blind, with cataract causing 36% of this blindness. In a survey conducted in 3 districts in the Punjab plains, the overall rates of occurrence of senile cataract was 15.3% among 1269 persons examined who were aged 30 years and older and 4.3% for all ages. This increased markedly to 67% for ages 70 years and older. An analysis of blind registration forms in the west of Scotland showed senile cataract as 1 of the 4 leading causes of blindness.

Mortality/Morbidity

Most morbidity associated with senile cataracts occurs postoperatively and is discussed in further detail later. Failure to treat a developing cataract surgically may lead to devastating consequences, such as lens swelling and intumescence, secondary glaucoma, and, eventually, blindness.

  • While the risk of dying as a result of cataract extraction is almost negligible, studies have shown an increased risk of mortality in patients who underwent surgery. In a comparison of 167 patients aged 50 years or older who underwent cataract extraction at the New England Medical Center in a period of 1 year to 824 patients who elected 1 of 6 other surgical procedures, it was found that the former had almost twice the mortality of the latter. Further analysis showed no significant correlation between diabetes and increased mortality. In a similar 5-year mortality analysis, patients with cataracts who were younger than 75 years had significantly higher age-specific rates of mortality than would be expected from US life tables.
  • These data imply an association between senile cataracts and increased mortality. Meddings et al suggest that senile cataract may be a marker of generalized tissue aging.1 Hirsch and Schwartz who proposed the concept that senile cataracts reflect systemic phenomena rather than only a localized ocular disease share this view.2

Race

Although race has been suggested as a possible risk factor for senile cataract, scarce literature exists to prove this theory. However, it has been observed that unoperated cataracts account for a higher percentage of blindness among blacks compared to whites.

Sex

Studies on the prevalence of senile cataract between males and females have yielded contrasting results.

  • In the Framingham Eye Study from 1973-75, females had a higher prevalence than males in both lens changes (63% vs 54.1%) and senile cataract (17.1% vs 13.2%).
  • Sperduto and Hiller noted that each of the 3 types of senile lens opacities was found more often in women than in men.3 In a separate investigation by Nishikori and Yamomoto, the male-to-female ratio was 1:8 with a female predominance in patients older than 65 years who were operated on for senile cataract.4
  • In a hospital-based, case-control study of senile cataract conducted in Japan, it was observed that an increased risk of cataract was found in males who were presently spending 7 hours or more outdoors and in females with 4 or fewer remaining teeth. However, in another analysis by Martinez et al, no sexual difference was noted in the prevalence of senile cataract.5

Age

Age is an important risk factor for senile cataract. As a person ages, the chance of developing a senile cataract increases. In the Framingham Eye Study from 1973-1975, the number of total and new cases of senile cataract rose dramatically from 23.0 cases per 100,000 and 3.5 cases per 100,000, respectively, in persons aged 45-64 years to 492.2 cases per 100,000 and 40.8 cases per 100,000 in persons aged 85 years and older.

Clinical

History

Careful history taking is essential in determining the progression and functional impairment in vision resulting from the cataract and in identifying other possible causes for the lens opacity. A patient with senile cataract often presents with a history of gradual progressive deterioration and disturbance in vision. Such visual aberrations are varied depending on the type of cataract present in the patient.

  • Decreased visual acuity  
    • Decreased visual acuity is the most common complaint of patients with senile cataract. The cataract is considered clinically relevant if visual acuity is affected significantly. Furthermore, different types of cataracts produce different effects on visual acuity.
    • For example, a mild degree of posterior subcapsular cataract can produce a severe reduction in visual acuity with near acuity affected more than distance vision, presumably as a result of accommodative miosis. However, nuclear sclerotic cataracts often are associated with decreased distance acuity and good near vision.
    • A cortical cataract generally is not clinically relevant until late in its progression when cortical spokes compromise the visual axis. However, instances exist when a solitary cortical spoke occasionally results in significant involvement of the visual axis.
  • Glare
    • Increased glare is another common complaint of patients with senile cataracts. This complaint may include an entire spectrum from a decrease in contrast sensitivity in brightly lit environments or disabling glare during the day to glare with oncoming headlights at night.
    • Such visual disturbances are prominent particularly with posterior subcapsular cataracts and, to a lesser degree, with cortical cataracts. It is associated less frequently with nuclear sclerosis. Many patients may tolerate moderate levels of glare without much difficulty, and, as such, glare by itself does not require surgical management.
  • Myopic shift
    • The progression of cataracts may frequently increase the diopteric power of the lens resulting in a mild-to-moderate degree of myopia or myopic shift. Consequently, presbyopic patients report an increase in their near vision and less need for reading glasses as they experience the so-called second sight. However, such occurrence is temporary, and, as the optical quality of the lens deteriorates, the second sight is eventually lost.
    • Typically, myopic shift and second sight are not seen in cortical and posterior subcapsular cataracts. Furthermore, asymmetric development of the lens-induced myopia may result in significant symptomatic anisometropia that may require surgical management.
  • Monocular diplopia
    • At times, the nuclear changes are concentrated in the inner layers of the lens, resulting in a refractile area in the center of the lens, which often is seen best within the red reflex by retinoscopy or direct ophthalmoscopy.
    • Such a phenomenon may lead to monocular diplopia that is not corrected with spectacles, prisms, or contact lenses.

Physical

After a thorough history is taken, careful physical examination must be performed. The entire body habitus is checked for abnormalities that may point out systemic illnesses that affect the eye and cataract development.

  • A complete ocular examination must be performed beginning with visual acuity for both near and far distances. When the patient complains of glare, visual acuity should be tested in a brightly lit room. Contrast sensitivity also must be checked, especially if the history points to a possible problem.
  • Examination of the ocular adnexa and intraocular structures may provide clues to the patient's disease and eventual visual prognosis.  
    • A very important test is the swinging flashlight test which detects for a Marcus Gunn pupil or a relative afferent pupillary defect (RAPD) indicative of optic nerve lesions or diffuse macular involvement. A patient with RAPD and a cataract is expected to have a very guarded visual prognosis after cataract extraction.
    • A patient with long-standing ptosis since childhood may have occlusion amblyopia, which may account more for the decreased visual acuity rather than the cataract. Similarly, checking for problems in ocular motility at all directions of gaze is important to rule out any other causes for the patient's visual symptoms.
  • Slit lamp examination should not only concentrate on evaluating the lens opacity but the other ocular structures as well (eg, conjunctiva, cornea, iris, anterior chamber).  
    • Corneal thickness and the presence of corneal opacities, such as corneal guttata, must be checked carefully.
    • Appearance of the lens must be noted meticulously before and after pupillary dilation.
    • The visual significance of oil droplet nuclear cataracts and small posterior subcapsular cataracts is evaluated best with a normal-sized pupil to determine if the visual axis is obscured. However, exfoliation syndrome is appreciated with the pupil dilated, revealing exfoliative material on the anterior lens capsule.
    • After dilation, nuclear size and brunescence as indicators of cataract density can be determined prior to phacoemulsification surgery. The lens position and integrity of the zonular fibers also should be checked because lens subluxation may indicate previous eye trauma, metabolic disorders, or hypermature cataracts.
  • The importance of direct and indirect ophthalmoscopy in evaluating the integrity of the posterior pole must be underscored. Optic nerve and retinal problems may account for the visual disturbance experienced by the patient. Furthermore, the prognosis after lens extraction is affected significantly by detection of pathologies in the posterior pole preoperatively (eg, macular edema, age-related macular degeneration).

Causes

Numerous studies have been conducted to identify risk factors for development of senile cataracts. Various culprits have been implicated, including environmental conditions, systemic diseases, diet, and age.

West and Valmadrid stated that age-related cataract is a multifactorial disease with different risk factors associated to the different cataract types.6 In addition, they stated that cortical and posterior subcapsular cataracts were related closely to environmental stresses, such as ultraviolet (UV) exposure, diabetes, and drug ingestion. However, nuclear cataracts seem to have a correlation with smoking. Alcohol has been associated with all cataract types.

A similar analysis was completed by Miglior et al.7 They found that cortical cataracts were associated with the presence of diabetes for more than 5 years and increased serum potassium and sodium levels. A history of surgery under general anesthesia and the use of sedative drugs were associated with reduced risks of senile cortical cataracts. Posterior subcapsular cataracts were associated with steroid use and diabetes, while nuclear cataracts had significant correlations with calcitonin and milk intake. Mixed cataracts were linked with a history of surgery under general anesthesia.

  • Systemic diseases and senile cataract  
    • Senile cataracts have been associated with a lot of systemic illnesses, to include the following: cholelithiasis, allergy, pneumonia, coronary disease and heart insufficiency, hypotension, hypertension, mental retardation, and diabetes.
    • Systemic hypertension was found to significantly increase the risk for posterior subcapsular cataracts. In a related study by Jahn et al, hypertriglyceridemia, hyperglycemia, and obesity was found to favor the formation of posterior subcapsular cataracts at an early age.8
    • A possible pathway for the role of hypertension and glaucoma in senile cataract formation was proposed with induced changes in the protein conformational structures in the lens capsules, subsequently causing alterations in membrane transport and permeability of ions, and, finally, increasing intraocular pressure resulting in the exacerbation of cataract formation.
  • UV light and senile cataract  
    • The association of UV light and development of senile cataract has generated much interest. One hypothesis implies that senile cataracts, particularly cortical opacities, may be the result of thermal damage to the lens.
    • An animal model by Al-Ghadyan and Cotlier documented an increase in the temperature of the posterior chamber and lens of rabbits after exposure to sunlight due to an ambient temperature effect through the cornea and to increased body temperature.9
    • In related studies, people living in areas with greater UV exposure were more likely to develop senile cataracts and to develop them earlier than people residing in places with less UV exposure.
  • Other risk factors  
    • Significant associations with senile cataract were noted with increasing age, female sex, social class, and myopia. Consistent evidence from the study of West and Valmadrid suggested that the prevalence of all cataract types was lower among those with higher education.6 Workers exposed to infrared radiation also were found to have a higher incidence of senile cataract development.
    • Although myopia has been implicated as a risk factor, it was shown that persons with myopia who had worn eyeglasses for at least 20 years underwent cataract extraction at a significantly older age than emmetropes, implying a protective effect of the eyeglasses to solar UV radiation.
    • The role of nutritional deficiencies in senile cataract has not been proven or established. However, a high intake of the 18-carbon polyunsaturated fatty acids linoleic acid and linolenic acid reportedly may result in an increased risk of developing age-related nuclear opacity.

More on Cataract, Senile

Overview: Cataract, Senile
Differential Diagnoses & Workup: Cataract, Senile
Treatment & Medication: Cataract, Senile
Follow-up: Cataract, Senile
References
[ CLOSE WINDOW ]

References

  1. Meddings DR, Marion SA, Barer ML, Evans RG, Green B, Hertzman C, et al. Mortality rates after cataract extraction. Epidemiology. May 1999;10(3):288-93. [Medline].

  2. Hirsch RP, Schwartz B. Increased mortality among elderly patients undergoing cataract extraction. Arch Ophthalmol. Jul 1983;101(7):1034-7. [Medline].

  3. Sperduto RD, Hiller R. The prevalence of nuclear, cortical, and posterior subcapsular lens opacities in a general population sample. Ophthalmology. Jul 1984;91(7):815-8. [Medline].

  4. Nishikiori T, Yamamoto K. Epidemiology of cataracts. Dev Ophthalmol. 1987;15:24-7. [Medline].

  5. Martinez GS, Campbell AJ, Reinken J, Allan BC. Prevalence of ocular disease in a population study of subjects 65 years old and older. Am J Ophthalmol. Aug 1982;94(2):181-9. [Medline].

  6. West SK, Valmadrid CT. Epidemiology of risk factors for age-related cataract. Surv Ophthalmol. Jan-Feb 1995;39(4):323-34. [Medline].

  7. Miglior S, Marighi PE, Musicco M, Balestreri C, Nicolosi A, Orzalesi N. Risk factors for cortical, nuclear, posterior subcapsular and mixed cataract: a case-control study. Ophthalmic Epidemiol. Jun 1994;1(2):93-105. [Medline].

  8. Johns KJ, Feder RS, Rosenfeld SI, et al. Lens and cataract. In: American Academy of Ophthalmology Basic and Clinical Science Course. Vol. 11. 1999-2000.

  9. Al-Ghadyan AA, Cotlier E. Rise in lens temperature on exposure to sunlight or high ambient temperature. Br J Ophthalmol. Jun 1986;70(6):421-6. [Medline].

  10. Costello MJ, Oliver TN, Cobo LM. Cellular architecture in age-related human nuclear cataracts. Invest Ophthalmol Vis Sci. Oct 1992;33(11):3209-27. [Medline].

  11. Bell CM, Hatch WV, Fischer HD, Cernat G, Paterson M, Gruneir A, et al. Association between tamsulosin and serious ophthalmic adverse events in older men following cataract surgery. JAMA. May 20 2009;301(19):1991-6. [Full Text].

  12. Asano S, Miyake K, Ota I, Sugita G, Kimura W, Sakka Y, et al. Reducing angiographic cystoid macular edema and blood-aqueous barrier disruption after small-incision phacoemulsification and foldable intraocular lens implantation: multicenter prospective randomized comparison of topical diclofenac 0.1% and betamethasone 0.1%. J Cataract Refract Surg. Jan 2008;34(1):57-63. [Medline].

  13. Szijarto Z, Schvoller M, Poto L, Kuhn F, Kovacs B. Pseudophakic retinal detachment after phacoemulsification. Ann Ophthalmol (Skokie). Jun 2007;39(2):134-9. [Medline].

  14. Cao X, Liu A, Zhang J, Li Y, Jie Y, Liu W, et al. Clinical analysis of endophthalmitis after phacoemulsification. Can J Ophthalmol. Dec 2007;42(6):844-8. [Medline].

  15. Rabin SM. Medicolegal concerns of cataract surgeons. In: Management and Care of the Cataract Patient. 1992:331-8.

  16. Belkin M, Jacobs DR, Jackson SM, Zwick H. Senile cataracts and myopia. Ann Ophthalmol. Jan 1982;14(1):49-50. [Medline].

  17. Bellows JG, Bellows RT. Crosslinkage theory of senile cataracts. Ann Ophthalmol. Feb 1976;8(2):129-35. [Medline].

  18. Bilge AH, Aykan U, Akin T, Unsal U. Review of sterile, postoperative, anterior segment inflammation following cataract extraction and intraocular lens implantation. Eur J Ophthalmol. Mar-Apr 2005;15(2):224-7. [Medline].

  19. Bunce GE, Kinoshita J, Horwitz J. Nutritional factors in cataract. Annu Rev Nutr. 1990;10:233-54. [Medline].

  20. Burgess CA, Sowers M. Systemic hypertension and senile cataracts: an epidemiologic study. Optom Vis Sci. Apr 1992;69(4):320-4. [Medline].

  21. Charakidas A, Kalogeraki A, Tsilimbaris M, Koukoulomatis P, Brouzas D, Delides G. Lens epithelial apoptosis and cell proliferation in human age-related cortical cataract. Eur J Ophthalmol. Mar-Apr 2005;15(2):213-20. [Medline].

  22. Chatterjee A, Milton RC, Thyle S. Prevalence and aetiology of cataract in Punjab. Br J Ophthalmol. Jan 1982;66(1):35-42. [Medline].

  23. Chylack LT Jr. Mechanisms of senile cataract formation. Ophthalmology. Jun 1984;91(6):596-602. [Medline].

  24. Eckerskorn U, Hockwin O, Muller-Breitenkamp R, Chen TT, Knowles W, Dobbs RE. Evaluation of cataract-related risk factors using detailed classification systems and multivariate statistical methods. Dev Ophthalmol. 1987;15:82-91. [Medline].

  25. Emery JM, Wilhelmus KA, Rosenberg S. Complications of phacoemulsification. Ophthalmology. Feb 1978;85(2):141-50. [Medline].

  26. Fujiwara H, Takigawa Y, Suzuki T, Nakata K. Superoxide dismutase activity in cataractous lenses. Jpn J Ophthalmol. 1992;36(3):273-80. [Medline].

  27. Ghafour IM, Allan D, Foulds WS. Common causes of blindness and visual handicap in the west of Scotland. Br J Ophthalmol. Apr 1983;67(4):209-13. [Medline].

  28. Gibson JM, Rosenthal AR, Lavery J. A study of the prevalence of eye disease in the elderly in an English community. Trans Ophthalmol Soc U K. 1985;104 (Pt 2):196-203. [Medline].

  29. Gibson JM, Shaw DE, Rosenthal AR. Senile cataract and senile macular degeneration: an investigation into possible risk factors. Trans Ophthalmol Soc U K. 1986;105 (Pt 4):463-8. [Medline].

  30. Hirneiss C, Neubauer AS, Kampik A, Schönfeld CL. Comparison of prednisolone 1%, rimexolone 1% and ketorolac tromethamine 0.5% after cataract extraction: a prospective, randomized, double-masked study. Graefes Arch Clin Exp Ophthalmol. Aug 2005;243(8):768-73. [Medline].

  31. Hollows F, Moran D. Cataract--the ultraviolet risk factor. Lancet. Dec 5 1981;2(8258):1249-50. [Medline].

  32. Hu TS, Lao YX. An epidemiologic survey of senile cataract in China. Dev Ophthalmol. 1987;15:42-51. [Medline].

  33. Imbach P, Odavic R, Bleher EA, Bucher U, Deubelbeiss KA, Wagner HP. [Autologous bone marrow reimplantation in children with advanced tumor. First experiences of feasibility]. Schweiz Med Wochenschr. Feb 24 1979;109(8):283-7. [Medline].

  34. Jacques PF, Chylack LT Jr, McGandy RB, Hartz SC. Antioxidant status in persons with and without senile cataract. Arch Ophthalmol. Mar 1988;106(3):337-40. [Medline].

  35. Javitt JC, Taylor HR. Cataract and latitude. Doc Ophthalmol. 1994-1995;88(3-4):307-25. [Medline].

  36. Kador PF. Overview of the current attempts toward the medical treatment of cataract. Ophthalmology. Apr 1983;90(4):352-64. [Medline].

  37. Kahn HA, Leibowitz HM, Ganley JP, Kini MM, Colton T, Nickerson RS, et al. The Framingham Eye Study. I. Outline and major prevalence findings. Am J Epidemiol. Jul 1977;106(1):17-32. [Medline].

  38. Kamei A. Characterization of water-insoluble proteins in normal and cataractous human lens. Jpn J Ophthalmol. 1990;34(2):216-24. [Medline].

  39. Kamei A. Glutathione levels of the human crystalline lens in aging and its antioxidant effect against the oxidation of lens proteins. Biol Pharm Bull. Sep 1993;16(9):870-5. [Medline].

  40. Katoh N, Sasaki K, Shibata T, Obazawa H, Fujiwara T, Kogure F, et al. Case-control study of senile cataract in Japan: a preliminary report. Jpn J Ophthalmol. 1993;37(4):467-77. [Medline].

  41. Ke Y, Jiang J, Chen P, Weng Y, Yang Y. Phacoemulsification and posterior chamber intraocular lens implantation. Zhonghua Yan Ke Za Zhi. Mar 1996;32(2):85-91. [Medline].

  42. Kini MM, Leibowitz HM, Colton T, Nickerson RJ, Ganley J, Dawber TR. Prevalence of senile cataract, diabetic retinopathy, senile macular degeneration, and open-angle glaucoma in the Framingham eye study. Am J Ophthalmol. Jan 1978;85(1):28-34. [Medline].

  43. Knekt P, Heliövaara M, Rissanen A, Aromaa A, Aaran RK. Serum antioxidant vitamins and risk of cataract. BMJ. Dec 5 1992;305(6866):1392-4. [Medline].

  44. Lee SM, Lin SY, Li MJ, Liang RC. Possible mechanism of exacerbating cataract formation in cataractous human lens capsules induced by systemic hypertension or glaucoma. Ophthalmic Res. 1997;29(2):83-90. [Medline].

  45. Lu M, Taylor A, Chylack LT Jr, Rogers G, Hankinson SE, Willett WC, et al. Dietary fat intake and early age-related lens opacities. Am J Clin Nutr. Apr 2005;81(4):773-9. [Medline].

  46. Lydahl E. Infrared radiation and cataract. Acta Ophthalmol Suppl. 1984;166:1-63. [Medline].

  47. Moffat BA, Landman KA, Truscott RJ, Sweeney MH, Pope JM. Age-related changes in the kinetics of water transport in normal human lenses. Exp Eye Res. Dec 1999;69(6):663-9. [Medline].

  48. Mozaffarieh M, Heinzl H, Sacu S, Wedrich A. Clinical outcomes of phacoemulsification cataract surgery in diabetes patients: visual function (VF-14), visual acuity and patient satisfaction. Acta Ophthalmol Scand. Apr 2005;83(2):176-83. [Medline].

  49. Packer M, Fishkind WJ, Fine IH, Seibel BS, Hoffman RS. The physics of phaco: a review. J Cataract Refract Surg. Feb 2005;31(2):424-31. [Medline].

  50. Papamatheakis DG, Demers P, Vachon A, Jaimes LB, Lapointe Y, Harasymowycz PJ. Thrombocytopenia and the risks of intraocular surgery. Ophthalmic Surg Lasers Imaging. Mar-Apr 2005;36(2):103-7. [Medline].

  51. Recchia FM, Busbee BG, Pearlman RB, Carvalho-Recchia CA, Ho AC. Changing trends in the microbiologic aspects of postcataract endophthalmitis. Arch Ophthalmol. Mar 2005;123(3):341-6. [Medline].

  52. Robertson JM, Donner AP, Trevithick JR. A possible role for vitamins C and E in cataract prevention. Am J Clin Nutr. Jan 1991;53(1 Suppl):346S-351S. [Medline].

  53. Sack R, Cohen J. Comparative diets of a idiopathic senile cataract and normal population: dietary risk factors in cataractogenesis. Metab Pediatr Syst Ophthalmol. 1987;10(1):9-13. [Medline].

  54. Shaikh MR, Janjua MZ. Morphological and morphometrical study of human lens in senile cataract. J Pak Med Assoc. May 1997;47(5):141-4. [Medline].

  55. Sharma YR, Vajpayee RB, Honavar SG. Sunlight and cortical cataract. Arch Environ Health. Sep-Oct 1994;49(5):414-7. [Medline].

  56. Sommer A. Cataracts as an epidemiologic problem. Am J Ophthalmol. Mar 1977;83(3):334-9. [Medline].

  57. Sommer A, Tielsch JM, Katz J, Quigley HA, Gottsch JD, Javitt JC, et al. Racial differences in the cause-specific prevalence of blindness in east Baltimore. N Engl J Med. Nov 14 1991;325(20):1412-7. [Medline].

  58. Steinkuller PG. Cataract: the leading cause of blindness and vision loss in Africa. Soc Sci Med. 1983;17(22):1693-702. [Medline].

  59. Street DA, Javitt JC. National five-year mortality after inpatient cataract extraction. Am J Ophthalmol. Mar 15 1992;113(3):263-8. [Medline].

  60. Tseng SH, Tang MJ. Na,K-ATPase in lens epithelia from patients with senile cataracts. J Formos Med Assoc. Sep 1999;98(9):627-32. [Medline].

  61. Tseng SH, Yen JS, Chien HL. Lens epithelium in senile cataract. J Formos Med Assoc. Feb 1994;93(2):93-8. [Medline].

  62. Worgul BV, Merriam GR Jr, Medvedovsky C. Cortical cataract development--an expression of primary damage to the lens epithelium. Lens Eye Toxic Res. 1989;6(4):559-71. [Medline].

  63. Wu TT, Amini L, Leffler CT, Schwartz SG. Cataracts and cataract surgery in mentally retarded adults. Eye Contact Lens. Mar 2005;31(2):50-3. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

senile cataract, age-related cataract, vision loss, visual deficit, blindness

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Vicente Victor D Ocampo, MD, Consulting Staff, Department of Ophthalmology, Asian Hospital and Medical Center, Philippines
Vicente Victor D Ocampo, MD is a member of the following medical societies: American Academy of Ophthalmology, Philippine Academy of Ophthalmology, and Philippine Ocular Inflammation Society
Disclosure: Nothing to disclose.

Coauthor(s)

C Stephen Foster, MD, FACS, FACR, FAAO, Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution
C Stephen Foster, MD, FACS, FACR, FAAO is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Association of Immunologists, American College of Rheumatology, American College of Surgeons, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, American Uveitis Society, Association for Research in Vision and Ophthalmology, Massachusetts Medical Society, Royal Society of Medicine, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Richard W Allinson, MD, Associate Professor, Department of Surgery, Texas A&M University Health Science Center; Senior Staff Ophthalmologist, Scott and White Clinic
Richard W Allinson, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

J James Rowsey, MD, Former Director of Corneal Services, St Luke's Cataract and Laser Institute, Florida
J James Rowsey, MD is a member of the following medical societies: American Academy of Ophthalmology, American Association for the Advancement of Science, American Medical Association, Association for Research in Vision and Ophthalmology, Florida Medical Association, Pan-American Association of Ophthalmology, Sigma Xi, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.