Research suggests that further lowering of IOP plays an important role in preventing progression of low tension POAG. Target IOPs are at least 30% lower than the level at which progressive damage was occurring. Therapies are those for POAG. SEE 9.1, PRIMARY OPEN ANGLE GLAUCOMA, for a more in-depth discussion of these therapies. There is evidence that initial therapy with brimonidine 0.2% b.i.d. is superior to timolol 0.5% b.i.d. in preventing visual field progression in low tension POAG.

Ischemia to the optic nerve head may play a role in the pathogenesis of low tension POAG. Modification of cardiovascular risk factors is appropriate in managing general health, but has not proven beneficial in managing glaucoma. Refer to an internist for control of blood pressure, cholesterol, and optimal management of other comorbid conditions to maximize optic nerve perfusion. If possible avoid use of antihypertensive drugs at bedtime and use preferentially in the morning.

If there are no suggestive optic nerve or visual field changes and IOP is <24 mm Hg, no treatment other than close observation is usually necessary.

Patients with an IOP >24 to 30 mm Hg but with normal examinations are candidates for IOP-lowering therapy (threshold varies per glaucoma specialist). A decision to treat a patient should be based on the patient’s choice to elect therapy and baseline risk factors such as age, CCT, initial IOP, optic nerve appearance, and family history. The results of the ocular hypertension treatment study (OHTS) showed that treatment reduced the development of visual field loss from 9.5% to 4.4% at 5 years, with a 20% average reduction of IOP. If treatment is elected, a therapeutic trial in one eye, as described for treatment of POAG, should be used. Some clinicians may elect to monitor these patients with close observation. Risk calculators have been developed to approximate the level of risk progression to glaucoma if left untreated. These may help guide clinicians and patients as to whether treatment should be initiated. SEE 9.1, PRIMARY OPEN ANGLE GLAUCOMA.

Compression gonioscopy is essential to determine if the trabecular blockage is reversible and may break an acute attack.

Topical therapy with β-blocker ([e.g., timolol 0.5%] caution with asthma or COPD), α-2 agonist (e.g., brimonidine 0.1%), prostaglandin analog (e.g., latanoprost 0.005%), and CAI (e.g., dorzolamide 2%) should be initiated immediately. In urgent cases, three rounds of these medications may be given, with each round being separated by 15 minutes.

Topical steroid (e.g., prednisolone acetate 1%) may be useful.

Systemic CAI (e.g., acetazolamide 250 to 500 mg i.v. or two 250-mg tablets p.o. in one dose if unable to give i.v.) if reduction in IOP is urgent or if IOP is refractory to topical therapy. Do not use in sulfonamide-induced angle closure.

NOTE: Prior to initiation of systemic CAIs or osmotic agents, renal function should be tested.

When acute angle closure glaucoma is the result of:

In phacomorphic glaucoma, the lens should be removed as soon as the eye is quiet and the IOP controlled, if possible. SEE 9.12.4, PHACOMORPHIC GLAUCOMA.

Address systemic problems such as pain and vomiting.

For pupillary block (all forms) or primary angle crowding: If the IOP decreases significantly, definitive treatment with laser (YAG) PI or surgical iridectomy is performed once the cornea is clear and the anterior chamber is quiet, typically 1 to 5 days after attack.

NOTE: If affected eye is too inflamed initially for laser PI, perform laser PI of the fellow eye first. An untreated fellow eye has a 40% to 80% chance of acute angle closure in 5 to 10 years. Repeated angle closure attacks with a patent PI may indicate plateau iris syndrome. SEE 9.13, PLATEAU IRIS.

Patients are discharged on a regimen of maintenance dose IOP-lowering drops and oral medications (described above). Close monitoring with IOP measurement each day is necessary immediately after an angle closure attack. Once the IOP has been reasonably reduced, follow-up frequency is guided by overall clinical response and stability.

NOTE: If IOP does not decrease after two courses of maximal medical therapy, a laser (YAG) PI should be considered if there is an adequate view of the iris. If IOP still does not decrease after more than one attempt at laser PI, then a laser iridoplasty or surgical PI is needed. If all preceding treatments are unsuccessful or refractory, a guarded filtration procedure should be considered.

For secondary angle closure: Treat the underlying problem. Consider argon laser gonioplasty to open the angle, particularly in plateau iris syndrome or nanophthalmos. Goniosynechiolysis can be performed for chronic angle closure of <6 months’ duration. Systemic steroids may be required to treat serous choroidal detachments secondary to inflammation.

Laser trabeculoplasty contraindicated in CACG prior to PI and can induce greater scarring of the angle.

If patient has angle closure with pupillary block, perform laser PI to prevent further angle closure episodes. The TM may have sustained enough damage that the IOP will still be elevated despite a patent iridotomy, necessitating continued use of medications to lower the IOP.

Laser iridoplasty may be performed (and repeated) to decrease the formation of new PAS. May not be effective, or may serve as only a temporary measure. If iridoplasty fails and other medical therapy has been maximized, the patient may need additional surgery. ECP may be attempted in cases with early glaucoma, but trabeculectomy or tube shunt is usually indicated in more advanced cases. MIGS usually contraindicated due to closed angle.