Updated: May 20, 2009
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.
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.
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.
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.
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.
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.
Studies on the prevalence of senile cataract between males and females have yielded contrasting results.
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.
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.
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.
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.
Cataract, Traumatic
Aside from being age related and due to trauma, cataract formation in adult patients also may be due to chronic uveitis, long-term steroid use, or posterior pole pathologies (eg, intraocular tumor, long-standing retinal detachment).
Nuclear cataracts are characterized by homogeneity of the lens nucleus with loss of cellular laminations, while cortical cataracts typically manifest with hydropic swelling of the lens fibers with globules of eosinophilic material (morgagnian globules) seen in slitlike spaces between lens fibers. Finally, a posterior subcapsular cataract is associated with posterior migration of the lens epithelial cells in the posterior subcapsular area, with aberrant enlargement of the epithelial cells (Wedl or bladder cells).
Costello et al examined senile cataracts using electron microscopy to highlight differences in the cellular architecture of the various forms of age-related lens changes.10 Comparisons were made between a typical nuclear cataract with a central opacity and a transparent rim, and a more advanced or mature, completely opaque nuclear cataract. The former was described as having no obvious cell disruption, cellular debris, or changes that could readily account for the central opacity. The fiber cells had intact uniformly stained cytoplasms with well-defined plasma membrane borders and gap junctions. The mature cataract exhibited various types of cell disruption in the perimeter but not in the core of the nucleus in the form of globules, vacuoles, multilamellar membranes, and clusters of highly undulating membranes.
Clinical staging of senile cataract is based largely on the visual acuity of the patient. A patient who cannot read better than 20/200 on the visual acuity chart is said to have a mature cataract. If the patient can distinguish letters at lines better than 20/200, then the cataract is described as being immature. An incipient cataract is found in a patient who can still read at 20/20 but possesses a lens opacity as confirmed by slit lamp examination.
No time-tested and proven medical treatment exists to delay, prevent, or reverse the development of senile cataracts.
Aldose reductase inhibitors, which are believed to inhibit the conversion of glucose to sorbitol, have shown promising results in preventing sugar cataracts in animals. Other anticataract medications being investigated include sorbitol-lowering agents, aspirin, glutathione-raising agents, and antioxidant vitamins C and E.
The definitive management for senile cataract is lens extraction. Over the years, various surgical techniques have evolved from the ancient method of couching to the present-day technique of phacoemulsification. Almost parallel is the evolution of the IOLs being used, which vary in ocular location, material, and manner of implantation. Depending on the integrity of the posterior lens capsule, the 2 main types of lens surgery are the intracapsular cataract extraction (ICCE) and the extracapsular cataract extraction (ECCE). Below is a general description of the 3 commonly used surgical procedures in cataract extraction, namely ICCE, standard ECCE, and phacoemulsification. Reading books on cataract surgeries for a more in-depth discussion of the topic, particularly with regard to technique and procedure, is also recommended.
Prior to surgery, a thorough preoperative evaluation must be conducted, which would also include a thorough explanation of the procedure to be performed and its accompanying risks.
In relation to the surgery, no established dietary restrictions exist that would affect the course of the operation.
After surgery, the patient is dissuaded from performing activities that would increase the intraocular pressure, especially after undergoing ICCE or standard ECCE. These activities include lifting heavy loads, chronic vigorous coughing, and straining.
No drug is available that has been proven to prevent the progression of senile cataracts. Medical therapy is used preoperatively and postoperatively to ensure a successful operation and subsequent visual rehabilitation.
Autonomic drugs used to ensure maximal pupillary dilation preoperatively, which is essential for a successful lens extraction. Short-acting mydriatics often are used. Most commonly used mydriatics are phenylephrine hydrochloride and tropicamide.
Direct-acting adrenergic agent available in 2.5% and 10% concentrations. Acts locally as potent vasoconstrictor and mydriatic by constricting ophthalmic blood vessels and radial muscles of the iris. Favorably used by many ophthalmologists because of rapid onset and moderately prolonged action, as well as the fact that it does not produce compensatory vasodilation. Most ophthalmologists prefer 2.5% to 10% concentration because of fewer risks of severe adverse systemic effects. Onset of action is within 30-60 min lasting for 3-5 h.
1 gtt 30-60 min prior to surgery, (2.5 or 10%) on affected eye until maximal pupillary dilation achieved
2.5% solution: 1 gtt 30-60 min to affected eye prior to surgery, until maximal pupillary dilation achieved
Bretylium may potentiate action of vasopressors on adrenergic receptors, possibly resulting in arrhythmias; MAOIs may significantly enhance adrenergic effects of phenylephrine, and pressor response may be increased 2- to 3-fold; guanethidine may increase pressor response of direct-acting vasopressors, possibly resulting in severe hypertension; concomitant use of 10% ophthalmic solutions and systemic beta-blockers may cause acute hypertension and rupture of congenital cerebral aneurysm; may potentiate cardiovascular depressant effects of potent inhalation anesthetics
Documented hypersensitivity; narrow-angle glaucoma; 10% solution is contraindicated in infants; aneurysms; preexisting cardiovascular diseases; cardiovascular complications, including ventricular arrhythmias and myocardial infarctions
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Exceeding recommended dosages or applying to instrumented, traumatized, diseased, or postsurgical eye or adnexa, or patients with suppressed lacrimation, as during anesthesia, may result in absorption of sufficient drug to produce systemic vasopressor response; significant elevation in blood pressure reported following conjunctival instillation of recommended dosages (10% ophthalmic solution); caution in children of low body weight, elderly persons, and persons with insulin-dependent diabetes, hypertension, hyperthyroidism, generalized arteriosclerosis, or cardiovascular disease; closely monitor patients who develop symptoms of high blood pressure; any mydriatic is contraindicated in patients with glaucoma since it occasionally may increase intraocular pressure; during times of temporary pupillary dilation or when vasoconstriction of intrinsic vessels lower intraocular pressure, may free adhesions; rebound miosis in older persons a day after receiving may occur, but reinstillation of drug may result in reduction of mydriasis; may be of particular importance when using drops prior to cataract surgery; due to a strong action of drug on dilator muscle, older individuals may develop transient pigment floaters in aqueous humor 30-45 min following administration presenting with an appearance similar to anterior uveitis or microscopic hyphema; to prevent pain, a drop of suitable topical anesthetics may be applied prior to use
Help decrease and control inflammatory response following cataract surgery especially in the immediate postoperative period. The most commonly used ophthalmic steroid is prednisolone acetate 1%. Dexamethasone 0.1% ophthalmic solution sometimes is used as an alternative.
Topical anti-inflammatory agent for ophthalmic use. A good glucocorticoid that, on the basis of weight, has 3-5 times anti-inflammatory potency of hydrocortisone. Glucocorticoids inhibit edema, fibrin deposition, capillary dilation, and phagocytic migration of acute inflammatory response as well as capillary proliferation, deposition of collagen, and scar formation. Indicated for treatment of steroid-responsive inflammation of palpebral and bulbar conjunctiva, cornea, and anterior segment of the globe.
During initial 24-48 h postoperative period may be used frequently even up to q1h, followed by tapered dosing to bid/qid
Not established
None reported
Documented hypersensitivity; viral, fungal, mycobacterial, or tubercular infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not discontinue therapy prematurely; administration beyond 20 mL should be made by physician with aid of magnification, such as slit-lamp biomicroscopy, and where appropriate, fluorescein staining; if signs and symptoms fail to improve after 2 d, reevaluate patient; prolonged use may result in glaucoma with damage to optic nerve, defects in visual acuity, and fields of vision, and in posterior subcapsular cataract formation; if drops are used for 10 d or longer, monitor intraocular pressure periodically; prolonged use may suppress host immune response and, thus, increase hazard of secondary ocular infection; fungal infections of cornea are prone to develop coincidentally with long-term use; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use; obtain fungal cultures when appropriate
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
2 gtt into conjunctival sac q1h while awake and q2h at night; gradually reduce to q3-4h, then to tid/qid
Not established
None reported
Documented hypersensitivity; viral, fungal, mycobacterial, or tubercular infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Prolonged use may increase hazard of secondary ocular infection; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use; obtain fungal cultures when appropriate
Broad-spectrum antibiotic ophthalmic solutions often are used prophylactically in immediate postoperative period. A number of topical antibiotics are used depending on surgeon's preference, but, generally, medications are active against both gram-positive and gram-negative organisms.
Active against a broad spectrum of gram-positive and gram-negative organisms. Bactericidal action results from interference with enzyme DNA gyrase needed for bacterial DNA synthesis. In vitro and clinical studies have shown it to be active against following organisms: gram-positive (ie, Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus viridans) and gram-negative (ie, Haemophilus influenzae, Pseudomonas aeruginosa, Serratia marcescens). Other organisms have been found to be susceptible in vitro but have yet to be established firmly by clinical studies.
1-2 gtt in the eye(s) tid/qid for 1-2 wk as postoperative prophylaxis following cataract extraction
<18 years: Not recommended
>18 years: Administer as in adults
Specific drug interaction studies not conducted with ophthalmic ciprofloxacin; systemic administration of some quinolones has been shown to elevate plasma concentrations of theophylline; interfere with metabolism of caffeine; enhance effects of anticoagulant warfarin and derivatives; associated with transient elevations in serum creatinine in patients receiving cyclosporine concomitantly
Documented hypersensitivity; viral, mycobacterial, and fungal eye infections; avoid coadministration with steroid combinations after uncomplicated removal of a foreign body from cornea
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
A white crystalline precipitate located in superficial portion of corneal defect may occur (onset starts in 1-7 d); precipitate usually is cleared within 2 wk and does not adversely affect clinical course or outcome; do not use in ocular infections that may become systemic; superinfections may occur with prolonged or repeated antibiotic therapy
Indicated for infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections.
Apply 0.5-inch (1.25 cm) ribbon 2-8 times/d depending on severity of infection
Apply as in adults
None reported
Documented hypersensitivity; viral, mycobacterial, or fungal infections of eye; patients using steroid combinations after uncomplicated removal of a foreign body from cornea also should avoid using this product
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Do not use topical antibiotics to treat ocular infections that may become systemic; prolonged or repeated antibiotic therapy may result in bacterial or fungal overgrowth of nonsusceptible organisms and may lead to a secondary infection; take appropriate measures if superinfection occurs
Used for pain and inflammation associated with cataract surgery.
Nonsteroidal anti-inflammatory prodrug for ophthalmic use. Following administration, converted by ocular tissue hydrolases to amfenac, an NSAID. Inhibits prostaglandin H synthase (cyclooxygenase), an enzyme required for prostaglandin production. Indicated for treatment of pain and inflammation associated with cataract surgery.
Shake well before use
Apply 1 gtt to affected eye(s) tid; initiate 1 d prior to cataract surgery and continue on day of surgery and for 2 wk postsurgery
Not established
Concomitant use with topical corticosteroids may increase potential for healing problems
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May slow or delay healing; may cause keratitis; long-term use may cause epithelial breakdown, corneal thinning, corneal erosion, and corneal ulceration or perforation, which may threaten vision; frequent adverse effects (5-10%) include capsular opacity, decreased visual acuity, foreign body sensation, increased intraocular pressure, and a sticky sensation
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senile cataract, age-related cataract, vision loss, visual deficit, blindness
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.
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.
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.
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.
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.
Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.
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.
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