Targeted therapy that addresses the root cause of intraocular inflammation and prevents the development of posterior and peripheral anterior synechiae is critical to successful management of uveitic glaucoma. Unlike some primary ope- angle glaucoma cases, where there can be an inherent vulnerability to IOP in the normal range, the target IOP in uveitic glaucoma does not necessarily have to be particularly low especially if there is no preexisting optic nerve disease. Use of aqueous humor suppressants first line is recommended, particularly when the uveitis is active. Latanoprost, travoprost, and bimatoprost can all rarely induce uveitis in eyes that are not necessarily predisposed to inflammation [8–10]. Nonetheless, there is data to suggest that latanoprost and bimatoprost can be effective in lowering IOP in quiescent uveitis [11, 12]. Overall, prostaglandin analogs should be avoided when uveitis is active because they are ineffective in that setting [13]. When the IOP is very high, use oral carbonic anhydrase inhibitors to improve bioavailability of medicines to the target tissue (the ciliary body). Since it is well known that pilocarpine can exacerbate synechiae formation in the anterior segment [14], it is wise to avoid cholinergic agents in uveitic glaucoma.

Strategies to protect the optic nerve and avoid surgical interventions can vary by glaucoma-prone uveitic entity. Unless glaucoma develops in FHIC, this condition has a relatively benign course and steroids should be used sparingly for fear of inducing steroid-induced glaucoma. Overall, the success rate of medical therapy in the setting of FHIC is fairly high (77 % in one series [15]) and many of these patients can avoid surgery. PSS shares some features with FHIC in that both entities can produce heterochromia and cytomegalovirus has been implicated in both conditions [16, 17]. While the IOP episodes in PSS tend to be episodic and possibly self-limiting, the IOP levels achieved can reach alarmingly high levels (60–70 mm Hg). Frequently, these episodes happen sporadically and IOP between events is entirely normal. In these instances, I give the well-informed patient a small supply of topical dorzolamide-timolol and oral acetazolamide to be used as needed for symptoms consistent with elevated IOP (halos around light and brow ache) with the understanding they will return to the office if they feel they need to use these medicines at the earliest available opportunity. On the other hand, frequent recurrent attacks are worrisome and consideration to anterior chamber tap with assessment for viral infection (PCR for HSV, HZV, and CMV) should be considered. There is one retrospective report that chronic use of valganciclovir in PSS patients with CMV positive aqueous humor aspirates had fewer glaucomacyclitic crises [18].

HKU with secondary glaucoma is one entity where early and aggressive antiviral therapy can be effective in directly addressing trabecular meshwork dysfunction. As mentioned above, one needs to be vigilant regarding this diagnostic possibility as keratitis can be conspicuously absent when glaucoma occurs [6]. All herpetic viruses are highly successful obligate intracellular parasites and depending on the competency of the immune system, recurrent HKU attacks can irreversibly damage the outflow pathway. In these instances antiviral and glaucoma therapy can fail, leading to the need for filtration surgery. In my personal experience, herpetic trabeculitis can even become contiguous with endothelial cell involvement leading to corneal decompensation requiring Descemet’s stripping endothelial keratoplasty. In the setting of HKU, one needs to use prostaglandin analogs cautiously under the cover of antiviral therapy, as these agents are known to be associated with ocular herpes viral reactivation [19–21].

Since low-grade inflammation in JIA can continue unabated for many years, it pays to aggressively lower IOP in order to protect vision long-term. This philosophy runs contrary to the view that most uveitic glaucoma patients do not necessarily need a low-target IOP. Foster and associates found topical therapy alone controls IOP only in a minority of cases and that oral carbonic anhydrase inhibitors are frequently needed to control IOP [22].

One needs to be vigilant for the development of steroid-induced glaucoma in the uveitis patient. One should resist making this diagnosis in the setting of active uveitis because mechanisms other than steroid-induced trabecular meshwork change could be operative in producing elevated IOP. In the setting of quiescent uveitis when steroids have been used and the angle is open, it is reasonable to entertain the diagnosis of steroid-induced glaucoma, especially since elevated IOP in one large series of eyes with uveitis was more likely to be related steroid-induced ocular hypertension than from other causes [23]. Withdrawing steroids should be considered but this maneuver alone may not necessarily lead to lowering of IOP. A typical pitfall to avoid is the situation where the patient cycles between a quiet eye with elevated IOP on steroids and an inflamed eye but acceptable IOP when steroids are withdrawn. If the uveitis is steroid dependent, then anti-inflammatory therapy should be maintained and alternative approaches to lower IOP need to be entertained. Of course steroid sparing anti-inflammatory therapy should be considered as deemed appropriate.

Because the trabeculum can be primarily or secondarily inflamed, there is probably little place for laser trabeculoplasty (LTP) in uveitic glaucoma. LTP can be effective in steroid-induced ocular hypertension outside the setting of uveitis despite very high preoperative IOPs [24, 25], but it is unknown whether LTP lowers IOP for steroid-induced glaucoma that occurs in uveitic glaucoma.

When it is critical to address pathological relative pupillary block it is best to adopt an efficient technique for creating a patent iridotomy. I advocate a dual laser technique where argon laser is used to seal any dilated iris vessels, thin the iris stroma and put the uveal tissue on stretch. An argon laser bed of peripheral iris tissue is treated with a series of low energy (200 mW), long duration (200 ms) burns with a relatively large spot size (200 μm). This base is thinned further using the argon laser employing short duration (100 ms) and small spot size (50 μm) burns with escalating power from 200 to 1000 mW. If power is escalated too rapidly, gas bubbles that obscure the base of the iridotomy will appear. The argon laser treatment is followed by YAG laser treatment, typically using a double pulse of 6 mJ (treatment parameters can vary depending on the response to the initial argon laser applications). In this setting, the YAG laser acts as a “hole-puncher” to create an iridotomy while minimizing bleeding and further dispersal of pigment and inflammatory debris.

In any situation where the uveal tract is actively inflamed, the disruption of the blood aqueous barrier laser treatment can contribute to rapid sealing of a patent iridotomy. When a laser peripheral iridotomy promptly closes in uveitic glaucoma associated with pupillary block consider performing a surgical iridectomy. The typical setting where one may encounter a laser iridotomy that promptly closes is in Behçet’s disease. A clear corneal approach is recommended when performing a surgical iridectomy so that the conjunctiva is preserved should filtration surgery be required a later date.

It is important to recognize scenarios where LPI is not appropriate even though the angle is closed such as occurs in secondary angle closure glaucoma due to diffuse uveal tract inflammation that leads to forward rotation of the iris lens diaphragm. In this scenario, cycloplegia and appropriate anti-inflammatory therapy, and not laser iridotomy, may be appropriate treatment to facilitate deepening of the anterior chamber.

There is probably no place for minimally invasive glaucoma surgery in uveitic glaucoma patients. There is a role for either trabeculectomy (TRX) with antimetabolite or glaucoma drainage device (GDD) implantation in medically uncontrolled uveitic glaucoma. A suggested approach is to consult with a uveitis expert regarding peri-operative management of inflammation when glaucoma filtration surgery is needed. If possible, defer surgery until the uveitis is quiescent. At times, both the uveitis and IOP are uncontrolled, and there may be no choice but to perform emergency glaucoma filtration surgery in order to protect the optic nerve. In this setting I favor emergency TRX with mitomcyin C, supplementing with postoperative subconjunctival 5-fluorouracil subconjunctival injections if the patient is phakic. In pseudophakic patients a GDD might be best. Overall, there is no evidence that GDD implantation is superior to TRX in uveitic glaucoma. Also, there is no evidence one type of GDD is better than another in uveitic glaucoma. Trans-scleral cyclophotocoagulation (TSCPC) can be tried if TRX or GDD fails and can achieve modest results in this setting [26].