While PEX itself is untreatable as of 2011, it is possible for doctors to minimize the damage to vision and to the optic nerves by the same medical techniques used to prevent glaucoma.

- Eyedrops. This is usually the first treatment method. Eyedrops can help reduce intraocular pressure within the eye. The medications within the eyedrops can include beta blockers (such as levobunolol or timolol) which slow the production of the aqueous humor. And other medications can increase its outflow, such as prostaglandin analogues (e.g. latanoprost). And these medicines can be used in various combinations. In most cases of glaucoma, eyedrops alone will suffice to solve the problem.

- Laser surgery. A further treatment is a type of laser therapy known as trabeculoplasty in which a high-energy laser beam is pointed at the trabecular meshwork to cause it to "remodel and open" and improve the outflows of the aqueous humor. These can be done as an outpatient procedure and take less than twenty minutes. One report suggests this procedure is usually effective.

- Eye surgery. Surgery is the treatment method of last resort if the other methods have not worked. It is usually effective at preventing glaucoma. Eye surgery on PEX patients can be subject to medical complications if the fibers which hold the lens have become weakened because of a buildup from the flakes; if the lens-holding fibers have weakened, then the lens may become loose, and complications from eye surgery may result. In such cases, it is recommended that surgeons act quickly to repair the phacodonesis before the lenses have dropped. A surgeon cuts an opening in the white portion of the eye known as the sclera, and removes a tiny area of the trabecular meshwork which enables the aqueous humor to discharge. This lowers the internal pressure within the eye and lessens the chance of future damage to the optic nerve. Cases with pseudophacodonesis and dislocated IOL have been increasing in number, according to one report. In cataract surgery, complications resulting from PEX include capsular rupture and vitreous loss.

- Drug therapy. There are speculations that if genetics plays a role in PEX, and if the specific genes involved can be identified, that possibly drugs can be developed to counteract these mutations or their effects. But such drugs have not been developed as of 2011.

Patients should continue to have regular eye examinations so that physicians can monitor pressure levels and check whether medicines are working.

Intraocular pressure can be lowered with medication, usually eye drops. Several classes of medications are used to treat glaucoma, with several medications in each class.

Each of these medicines may have local and systemic side effects. Adherence to medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate them or to communicate with the treating physician to improve the drug regimen. Initially, glaucoma drops may reasonably be started in either one or in both eyes. Wiping the eye with an absorbent pad after the administration of eye drops may result in fewer adverse effects, like the growth of eyelashes and hyperpigmentation in the eyelid.

Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. A 2003 study of patients in an HMO found half failed to fill their prescriptions the first time, and one-fourth failed to refill their prescriptions a second time. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms.

The possible neuroprotective effects of various topical and systemic medications are also being investigated.

- Prostaglandin analogs, such as latanoprost, bimatoprost and travoprost, increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow.

- Topical beta-adrenergic receptor antagonists, such as timolol, levobunolol, and betaxolol, decrease aqueous humor production by the epithelium of the ciliary body.

- Alpha2-adrenergic agonists, such as brimonidine and apraclonidine, work by a dual mechanism, decreasing aqueous humor production and increasing uveoscleral outflow.

- Less-selective alpha agonists, such as epinephrine, decrease aqueous humor production through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma. Epinephrine's mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due to further narrowing of the uveoscleral outflow (i.e. further closure of trabecular meshwork, which is responsible for absorption of aqueous humor).

- Miotic agents (parasympathomimetics), such as pilocarpine, work by contraction of the ciliary muscle, opening the trabecular meshwork and allowing increased outflow of the aqueous humour. Echothiophate, an acetylcholinesterase inhibitor, is used in chronic glaucoma.

- Carbonic anhydrase inhibitors, such as dorzolamide, brinzolamide, and acetazolamide, lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.

Risk factors such as UVB exposure and smoking can be addressed. Although no means of preventing cataracts has been scientifically proven, wearing sunglasses that counteract ultraviolet light may slow their development. While adequate intake of antioxidants (such as vitamins A, C, and E) has been thought to protect against the risk of cataracts, clinical trials have shown no benefit from supplements; though evidence is mixed, but weakly positive, for a potential protective effect of the nutrients lutein and zeaxanthin. Statin use is somewhat associated with a lower risk of nuclear sclerotic cataracts.

Argon laser trabeculoplasty (ALT) may be used to treat open-angle glaucoma, but this is a temporary solution, not a cure. A 50-μm argon laser spot is aimed at the trabecular meshwork to stimulate the opening of the mesh to allow more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty uses a thermal argon laser in an argon laser trabeculoplasty procedure.

A newer type of laser trabeculoplasty uses a "cold" (nonthermal) laser to stimulate drainage in the trabecular meshwork. This newer procedure, selective laser trabeculoplasty (SLT), uses a 532-nm, frequency-doubled, Q-switched , which selectively targets melanin pigment in the trabecular meshwork cells. Studies show SLT is as effective as ALT at lowering eye pressure. In addition, SLT may be repeated three to four times, whereas ALT can usually be repeated only once.

Nd:YAG laser peripheral iridotomy (LPI) may be used in patients susceptible to or affected by angle closure glaucoma or pigment dispersion syndrome. During laser iridotomy, laser energy is used to make a small, full-thickness opening in the iris to equalize the pressure between the front and back of the iris, thus correcting any abnormal bulging of the iris. In people with narrow angles, this can uncover the trabecular meshwork. In some cases of intermittent or short-term angle closure, this may lower the eye pressure. Laser iridotomy reduces the risk of developing an attack of acute angle closure. In most cases, it also reduces the risk of developing chronic angle closure or of adhesions of the iris to the trabecular meshwork.

Diode laser cycloablation lowers IOP by reducing aqueous secretion by destroying secretory ciliary epithelium.

Cryotherapy (freezing) or laser photocoagulation are occasionally used alone to wall off a small area of retinal detachment so that the detachment does not spread.

In early stages of keratoconus, glasses or soft contact lenses can suffice to correct for the mild astigmatism. As the condition progresses, these may no longer provide the person with a satisfactory degree of visual acuity, and most practitioners will move to manage the condition with rigid contact lenses, known as rigid, gas-permeable, (RGP) lenses. RGP lenses provide a good level of visual correction, but do not arrest progression of the condition.

In people with keratoconus, rigid contact lenses improve vision by means of tear fluid filling the gap between the irregular corneal surface and the smooth regular inner surface of the lens, thereby creating the effect of a smoother cornea. Many specialized types of contact lenses have been developed for keratoconus, and affected people may seek out both doctors specialized in conditions of the cornea, and contact lens fitters who have experience managing people with keratoconus. The irregular cone presents a challenge and the fitter will endeavor to produce a lens with the optimal contact, stability and steepness. Some trial-and-error fitting may prove necessary.

In general, the younger the child, the greater the urgency in removing the cataract, because of the risk of amblyopia. For optimal visual development in newborns and young infants, a visually significant unilateral congenital cataract should be detected and removed before age 6 weeks, and visually significant bilateral congenital cataracts should be removed before age 10 weeks.

Some congenital cataracts are too small to affect vision, therefore no surgery or treatment will be done. If they are superficial and small, an ophthalmologist will continue to monitor them throughout a patient's life. Commonly, a patient with small congenital cataracts that do not affect vision will eventually be affected later in life; generally this will take decades to occur.

Scleral lenses are sometimes prescribed for cases of advanced or very irregular keratoconus; these lenses cover a greater proportion of the surface of the eye and hence can offer improved stability. Easier handling can find favor with people with reduced dexterity, such as the elderly.

While surgeries do exist to correct for severe cases of floaters, there are currently no medications (including eye drops) that can correct for this vitreous deterioration. Floaters are often caused by the normal aging process and will usually disappear as the brain learns to ignore them. Looking up/down and left/right will cause the floaters to leave the direct field of vision as the vitreous humour swirls around due to the sudden movement. If floaters significantly increase in numbers and/or severely affect vision, then one of the below surgeries may be necessary.

Currently, insufficient evidence is available to compare the safety and efficacy of surgical vitrectomy with laser vitreolysis for the treatment of floaters. A 2017 Cochrane Review did not find any relevant studies that compared the two treatments.

Aggressive marketing campaigns are currently promoting the use of laser vitreolysis for the treatment of floaters. No strong evidence currently exists for the treatment of floaters with laser vitreolysis. Currently, the strongest available evidence comparing these two treatment modalities are retrospective case series.

Cataract removal can be performed at any stage and no longer requires ripening of the lens. Surgery is usually 'outpatient' and performed using local anesthesia. About 9 of 10 patients can achieve a corrected vision of 20/40 or better after surgery.

Several recent evaluations found that cataract surgery can meet expectations only when significant functional impairment due to cataracts exists before surgery. Visual function estimates such as VF-14 have been found to give more realistic estimates than visual acuity testing alone. In some developed countries, a trend to overuse cataract surgery has been noted, which may lead to disappointing results.

Phacoemulsification is the most widely used cataract surgery in the developed world. This procedure uses ultrasonic energy to emulsify the cataract lens. Phacoemulsification typically comprises six steps:

- Anaesthetic – The eye is numbed with either a subtenon injection around the eye (see: retrobulbar block) or topical anesthetic eye drops. The former also provides paralysis of the eye muscles.

- Corneal incision – Two cuts are made at the margin of the clear cornea to allow insertion of instruments into the eye.

- Capsulorhexis – A needle or small pair of forceps is used to create a circular hole in the capsule in which the lens sits.

- Phacoemulsification – A handheld ultrasonic probe is used to break up and emulsify the lens into liquid using the energy of ultrasound waves. The resulting 'emulsion' is sucked away.

- Irrigation and aspiration – The cortex, which is the soft outer layer of the cataract, is aspirated or sucked away. Fluid removed is continually replaced with a saline solution to prevent collapse of the structure of the anterior chamber (the front part of the eye).

- Lens insertion – A plastic, foldable lens is inserted into the capsular bag that formerly contained the natural lens. Some surgeons also inject an antibiotic into the eye to reduce the risk of infection. The final step is to inject salt water into the corneal wounds to cause the area to swell and seal the incision.

Extracapsular cataract extraction (ECCE) consists of removing the lens manually, but leaving the majority of the capsule intact. The lens is expressed through a 10- to 12-mm incision which is closed with sutures at the end of surgery. ECCE is less frequently performed than phacoemulsification, but can be useful when dealing with very hard cataracts or other situations where emulsification is problematic. Manual small incision cataract surgery (MSICS) has evolved from ECCE. In MSICS, the lens is removed through a self-sealing scleral tunnel wound in the sclera which, ideally, is watertight and does not require suturing. Although "small", the incision is still markedly larger than the portal in phacoemulsion. This surgery is increasingly popular in the developing world where access to phacoemulsification is still limited.

Intracapsular cataract extraction (ICCE) is rarely performed. The lens and surrounding capsule are removed in one piece through a large incision while pressure is applied to the vitreous membrane. The surgery has a high rate of complications.

Scleral buckle surgery is an established treatment in which the eye surgeon sews one or more silicone bands (or tyres) to the sclera (the white outer coat of the eyeball). The bands push the wall of the eye inward against the retinal hole, closing the break or reducing fluid flow through it and reducing the effect of vitreous traction thereby allowing the retina to re-attach. Cryotherapy (freezing) is applied around retinal breaks prior to placing the buckle. Often subretinal fluid is drained as part of the buckling procedure. The buckle remains in situ. The most common side effect of a scleral operation is myopic shift. That is, the operated eye will be more short sighted after the operation. Radial scleral buckle is indicated for U-shaped tears or Fishmouth tears, and posterior breaks. Circumferential scleral buckle is indicated for multiple breaks, anterior breaks and wide breaks. Encircling buckles are indicated for breaks covering more than 2 quadrants of retinal area, lattice degeneration located on more than 2 quadrant of retinal area, undetectable breaks, and proliferative vitreous retinopathy.

Enzymatic vitreolysis has been trialled to treat vitreomacular traction (VMT) and anomalous posterior vitreous detachment. Whilst the mechanism of action may have an effect on clinically significant floaters, as of March 2015 there are no clinical trials being undertaken to determine whether this may be a therapeutic alternative to either i) conservative management, or ii) vitrectomy.

Patients usually do not require treatment due to benign nature of the disease. In case cataract develops patients generally do well with cataract surgery.

Peri-ocular injection of corticosteroids (injection of corticosteroids very close but not into the eye). In resistant cases oral administration of corticosteroids, immunosuppressive drugs, and laser or cryotherapy of the involved area may be indicated.

Steroid implants have been explored as a treatment option for individuals with non-infectious uveitis. Research comparing fluocinolone acetonide intravitreal implants to standard-of-care treatments (prednisolone with immunosuppressive agents) found that while the steroid implant treatment possibly prevents the recurrence of uveitis, there may be adverse safety outcomes, such as the increased risk for needing cataract surgery and surgery to lower intraocular pressure.

Non-surgical treatments of FCED may be used to treat symptoms of early disease. Medical management includes topical hypertonic saline, the use of a hairdryer to dehydrate the precorneal tear film, and therapeutic soft contact lenses. Hypertonic saline draws water out of the cornea through osmosis. When using a hairdryer, the patient is instructed to hold it at an arm's length or directed across the face on a cold setting, to dry out the epithelial blisters. This can be done two or three times a day. Definitive treatment, however, (especially with increased corneal edema) is surgical in the form of corneal transplantation. The most common types of surgery for FCED are Descemet's stripping automated endothelial keratoplasty (DSAEK) and Descemet's membrane endothelial keratoplasty (DMEK), which account for over half of corneal transplants in the United States.

More speculative future directions in the treatment of FED include in-vitro expansion of human corneal endothelial cells for transplantation, artificial corneas (keratoprosthesis) and genetic modification. Surgery where the central diseased endothelium is stripped off but not replaced with donor tissue, with subsequent Rho-Associated Kinase (ROCK) inhibition of endothelial cell division may offer a viable medical treatment.

A greater understanding of FED pathophysiology may assist in the future with the development of treatments to prevent progression of disease. Although much progress has been made in the research and treatment of FED, many questions remain to be answered. The exact causes of illness, the prediction of disease progression and delivery of an accurate prognosis, methods of prevention and effective nonsurgical treatment are all the subject of inquiries that necessitate an answer.

Increased attention must be given to research that can address the most basic questions of how the disease develops: what are the biomolecular pathways implicated in disease, and what genetic or environmental factors contribute to its progression? In addition to shaping our understanding of FED, identification of these factors would be essential for the prevention and management of this condition.

Galactosemic infants present clinical symptoms just days after the onset of a galactose diet. They include difficulty feeding, diarrhea, lethargy, hypotonia, jaundice, cataract, and hepatomegaly (enlarged liver). If not treated immediately, and many times even with treatment, severe mental retardation, verbal dyspraxia (difficulty), motor abnormalities, and reproductive complications may ensue. The most effective treatment for many of the initial symptoms is complete removal of galactose from the diet. Breast milk and cow's milk should be replaced with soy alternatives. Infant formula based on casein hydrolysates and dextrin maltose as a carbohydrate source can also be used for initial management, but are still high in galactose. The reason for long-term complications despite a discontinuation of the galactose diet is vaguely understood. However, it has been suggested that endogenous (internal) production of galactose may be the cause.

The treatment for galactosemic cataract is no different from general galactosemia treatment. In fact, galactosemic cataract is one of the few symptoms that is actually reversible. Infants should be immediately removed from a galactose diet when symptoms present, and the cataract should disappear and visibility should return to normal. Aldose reductase inhibitors, such as sorbinil, have also proven promising in preventing and reversing galactosemic cataracts. AR inhibitors hinder aldose reductase from synthesizing galactitol in the lens, and thus restricts the osmotic swelling of the lens fibers. Other AR inhibitors include the acetic acid compounds zopolrestat, tolrestat, alrestatin, and epalrestat. Many of these compounds have not been successful in clinical trials due to adverse pharmokinetic properties, inadequate efficacy and efficiency, and toxic side effects. Testing on such drug-treatments continues in order to determine potential long-term complications, and for a more detailed mechanism of how AR inhibitors prevent and reverse the galactosemic cataract.

Several options exist for the treatment of BRVO. These treatments aim for the two of the most significant complications of BRVO, namely macular edema and neovascularization.

- Systemic treatment with oral Aspirin, subcutaneous Heparin, or intravenous thrombolysis have not been shown to be effective treatments for CRVO and for BRVO no reliable clinical trial has been published.

- Laser treatment of the macular area to reduce macular edema is indicated in patients who have 20/40 or worse vision and did not spontaneously improve for at least 3 months (to permit the maximum spontaneous resolution) after the development of the vein occlusion. It is typically administered with the argon laser and is focused on edematous retina within the arcades drained by the obstructed vein and avoiding the foveal avascular zone. Leaking microvascular abnormalities may be treated directly, but prominent collateral vessels should be avoided.

- The second indication of laser treatment is in case of neovascularization. Retinal photocoagulation is applied to the involved retina to cover the entire involved segment, extending from the arcade out to the periphery. Ischemia alone is not an indication for treatment provided that follow-up could be maintained.

- Preservative-free, nondispersive Triamcinolone acetonide in 1 or 4 mg dosage may be injected into the vitreous to treat macular edema but has complications including elevated intraocular pressure and development of cataract. Triamcinolone injection is shown to have similar effect on visual acuity when compared with standard care (Laser therapy), However, the rates of elevated intraocular pressure and cataract formation is much higher with the triamcinolone injection, especially the higher dosage. Intravitreal injection of Dexamethasone implant (Ozurdex; 700,350 μg) is being studied, its effect may last for 180 days. The injection may be repeated however with less pronounced effect. Although the implant was designed to cause less complications, pressure rise and cataract formation is noted with this treatment too.

- Anti-VEGF drugs such as Bevacizumab (Avastin; 1.25 -2.5 mg in 0.05ml) and Ranibizumab (lucentis) injections are being used and investigated. Intravitreal anti-VEGFs have a low incidence of adverse side effects compared with intravitreal corticosteroids, but are currently short acting requiring frequent injections. Anti-VEGF injection may be used for macular edema or neovascularization. The mechanism of action and duration of anti-VEGF effect on macular edema is currently unknown. The intraocular levels of VEGF are increased in eyes with macular edema secondary to BRVO and the elevated VEGF levels are correlated to the degree and severity of the areas of capillary nonperfusion and macular edema.

- Surgery is employed occasionally for longstanding vitreous hemorrhage and other serious complications such as epiretinal membrane and retinal detachment.

- Arteriovenous sheathotomy has been reported in small, uncontrolled series of patients with BRVO. BRVO typically occurs at arteriovenous crossings, where the artery and vein share a common adventitial sheath. In arteriovenous sheathotomy an incision is made in the adventitial sheath adjacent to the arteriovenous crossing and is extended along the membrane that holds the blood vessels in position to the point where they cross, the overlying artery is then separated from the vein.

A Cochrane Review sought to evaluate the effects of perioperative antibiotic prophylaxis for endophthalmitis following cataract surgery. The review showed high-certainty evidence that antibiotic injections in the eye with cefuroxime at the end of surgery lowers the chance of endophthalmitis. Also, the review showed moderate evidence that antibiotic eye drops (levofloxacin or chloramphenicol) with antibiotic injections (cefuroxime or penicillin) probably lowers the chance of endophthalmitis compared with injections or eye drops alone. Separate studies from the research showed that a periocular injection of penicillin with chloramphenicol-suphadimidine eye drops, and an intracameral cefuroxime injection with topical levofloxacin resulted in a risk reduction of developing endophthalmitis following cataract surgery for subjects.

In the case of intravitreal injections, however, antibiotics are not effective. Studies have demonstrated no difference between rates of infection with and without antibiotics when intravitreal injections are performed. The only consistent method of antibioprophylaxis in this instance is a solution of povidone-iodine applied pre-injection.

The patient needs urgent examination by an ophthalmologist, preferably a vitreoretinal specialist who will usually decide for urgent intervention to provide intravitreal injection of potent antibiotics. Injections of vancomycin (to kill Gram-positive bacteria) and ceftazidime (to kill Gram-negative bacteria) are routine. Even though antibiotics can have negative impacts on the retina in high concentrations, the facts that visual acuity worsens in 65% of endophthalmitis patients and prognosis gets poorer the longer an infection goes untreated make immediate intervention necessary. Endophthalmitis patients may also require an urgent surgery (pars plana vitrectomy), and evisceration may be necessary to remove a severe and intractable infection which could result in a blind and painful eye.

Steroids may be injected intravitreally if the cause is allergic.

In patients with acute endophthalmitis, combined steroid treatment with antibiotics have been found to improve visual outcomes, versus patients only treated with antibiotics, but any improvements on the resolution acute endophthalmitis is unknown.

There are good results from multiple doses of intravitreal injections of anti-VEGF drugs such as bevacizumab. A 2017 systematic review update found moderate evidence that aflibercept may have advantages in improving visual outcomes over bevacizumab and ranibizumab, after one year. Present recommended treatment for diabetic macular edema is Modified Grid laser photocoagulation combined with multiple injections of anti-VEGF drugs.

Triamcinolone is a long acting steroid preparation. When injected in the vitreous cavity, it decreases the macular edema (thickening of the retina at the macula) caused due to diabetic maculopathy, and results in an increase in visual acuity. The effect of triamcinolone is transient, lasting up to three months, which necessitates repeated injections for maintaining the beneficial effect. Best results of intravitreal Triamcinolone have been found in eyes that have already undergone cataract surgery. Complications of intravitreal injection of triamcinolone include cataract, steroid-induced glaucoma and endophthalmitis. A systematic review found evidence that eyes treated with the intravitreal injection of triamcinolone had better visual acuity outcomes compared to eyes treated with macular laser grid photocoagulation, or sham injections.

With posterior lens luxation, the lens falls back into the vitreous humour and lies on the floor of the eye. This type causes fewer problems than anterior lens luxation, although glaucoma or ocular inflammation may occur. Surgery is used to treat dogs with significant symptoms. Removal of the lens before it moves to the anterior chamber may prevent secondary glaucoma.

Irvine–Gass syndrome, pseudophakic cystoid macular edema or postcataract CME is one of the most common causes of visual loss after cataract surgery. The syndrome is named in honor of S. Rodman Irvine and J. Donald M. Gass.

The incidence is more common in older types of cataract surgery, where postcataract CME could occur in 20–60% of patients, but with modern cataract surgery, incidence of Irvine–Gass syndrome have reduced significantly.

Replacement of the lens as treatment for cataract can cause pseudophakic macular edema. (‘pseudophakia’ means ‘replacement lens’) this could occur as the surgery involved sometimes irritates the retina (and other parts of the eye) causing the capillaries in the retina to dilate and leak fluid into the retina. This is less common today with modern lens replacement techniques

Intraoperative floppy iris syndrome (IFIS) is a complication that may occur during cataract extraction in certain patients. This syndrome is characterized by a flaccid iris which billows in response to ordinary intraocular fluid currents, a propensity for this floppy iris to prolapse towards the area of cataract extraction during surgery, and progressive intraoperative pupil constriction despite standard procedures to prevent this.

IFIS has been associated with tamsulosin (e.g., Flomax), a medication widely prescribed for urinary symptoms associated with benign prostatic hyperplasia (BPH). Tamsulosin is a selective alpha blocker that works by relaxing the bladder and prostatic smooth muscle. As such, it also relaxes the iris dilator muscle by binding to its postsynaptic nerve endings. Even if a patient has only taken tamsulosin once in their life, that dose is enough to cause IFIS during cataract extraction indefinitely. Various alpha-blockers are associated with IFIS, but tamsulosin has a stronger association than the others.

A joint statement of two ophthalmologic societies states that "the other major class of drugs to treat BPH — 5-alpha reductase inhibitors — do not appear to cause IFIS to any significant degree." 5-ARIs include finasteride, a medication typically used as first line therapy for BPH and androgenic alopecia. The medication is also associated with cataract formation.

IFIS may also be associated with other causes of small pupil like synechiae, pseudoexfoliation and other medications (used for conditions such as glaucoma, diabetes and high blood pressure). IFIS does not usually cause significant changes in postoperative outcomes. Patients may experience more pain, a longer recovery period, and less improvement in visual acuity than a patient with an uncomplicated cataract removal.

The severity of the condition is not linked to the duration of tamsulosin intake.

Lens subluxation is also seen in dogs and is characterized by a partial displacement of the lens. It can be recognized by trembling of the iris (iridodonesis) or lens (phacodonesis) and the presence of an aphakic crescent (an area of the pupil where the lens is absent). Other signs of lens subluxation include mild conjunctival redness, vitreous humour degeneration, prolapse of the vitreous into the anterior chamber, and an increase or decrease of anterior chamber depth. Removal of the lens before it completely luxates into the anterior chamber may prevent secondary glaucoma. A nonsurgical alternative involves the use of a miotic to constrict the pupil and prevent the lens from luxating into the anterior chamber.