CATARACT

Cataracts are characterized as lens opacity or cloudiness in the eye. Key causes include aging, injury, endocrine disorders, and inherited factors. Understanding the disease mechanism starts with the lens's anatomical structure.

The lens is transparent, composed of 65% water and 35% protein, primarily crystallins. Crystallins maintain transparency, refractive properties, and prevent light scattering, crucial for clear vision. The lens is avascular, relying on aqueous humor for nutrients and waste removal. It's rich in antioxidants like glutathione and vitamin C, which protect against oxidative stress, a factor that damages proteins, leading to cloudiness.

Aging leads to constant exposure to oxidative stress from free radicals (metabolism byproducts), UV radiation, and environmental toxins. This decreases antioxidants, resulting in protein oxidation and denaturation of crystallins. Damaged crystallins aggregate, causing the lens to harden and become opaque, forming cataracts.

Diabetes mellitus causes sorbitol buildup in the lens, attracting water, making the lens swell and cloudy. Excess sugar also attaches to lens proteins, stiffening them and causing aggregation, blocking light. Hypothyroidism impairs lens metabolism, decreasing sodium and potassium, leading to electrolyte imbalance and oxidative stress. Hyperparathyroidism increases calcium deposition in the lens, disrupting epithelial cells and reducing clarity.

Blunt trauma causes shock waves that damage lens fibers and capsule integrity, leading to rosette-shaped cataracts. Penetrating injuries from sharp objects directly disrupt lens fibers and rupture the capsule, causing rapid cataract formation due to aqueous humor leakage. Chemical burns lead to pH imbalances and protein denaturation. Radiation exposure (UV, X-rays) generates free radicals, causing oxidative stress and protein aggregation.

Cataracts present as gradual, painless blurring or loss of vision, often bilateral. Photophobia occurs due to light scattering. Other signs include opaque or cloudy white pupils, decreased visual acuity, and progressive nearsightedness due to lens thickening and hardening. Diagnosis involves a slit lamp exam (using pupil dilators to view the front eye) and an ophthalmoscopic examination (to view the fundus/retina).

Pharmacological agents are primarily used for diagnostic procedures, not treatment. Midriatics (e.g., epinephrine, phenylephrine) dilate pupils; applying pressure to the inner canthus prevents systemic effects. Cycloplegics (e.g., atropine, scopolamine) dilate pupils and paralyze the ciliary body to reduce aqueous humor production. Acetazolamide and mannitol are given to decrease aqueous humor for better visualization.

Surgical options include intracapsular (removal of entire lens and capsule, now rare due to invasiveness) and extracapsular (removal of the lens, leaving the capsule intact, still requires a large incision). Phacoemulsification is the most common modern technique, using a small incision to emulsify and suction out the cloudy lens before implanting an intraocular lens (IOL).

Various intraocular lenses (IOLs) are used after cataract removal. Aphakic eyeglasses (thick lenses for those without natural lenses), contact lenses (hard, soft, gas permeable), and artificial IOLs are available. Hard lenses are durable but require larger incisions; soft lenses are foldable for small incisions but can be expensive and unsuitable for certain conditions (e.g., diabetic retinopathy). Gas permeable lenses are contact lenses for surface use, not typically IOLs.

Pre-operatively, nurses assess vision in affected and unaffected eyes and administer premedications like midriatics. Post-operatively, instructions are crucial to prevent increased intraocular pressure (IOP), such as avoiding coughing, sneezing, lifting heavy objects, and bending at the waist. Patients should maintain a semi-Fowler's position and wear a patch or protective shield on the affected eye to prevent infection and injury.