Treatment Algorithm for Pars Planitis
Intermediate uveitis may be idiopathic or may occur because of systemic diseases such as sarcoidosis, multiple sclerosis, cat scratch disease, or Lyme disease. Recurrent idiopathic intermediate uveitis is called pars planitis. Our experience suggests that, at least in a tertiary referral practice, 50% of the cases with intermediate uveitis are pars planitis. Although pars planitis may remit spontaneously in approximately half of patients within five years, the potential for long-term vision-threatening complications such as cataract, glaucoma, macular edema, epiretinal membranes, cyclitic membranes, and phthisis bulbi warrants early, aggressive therapy.
Our approach to treating pars planitis follows a steroid-sparing step-ladder algorithm aimed at complete suppression of active inflammation, regardless of visual acuity. This strategy is associated with a lower risk of cataract development over the disease course and improved visual outcomes by preventing permanent macular damage, including macular edema and epiretinal membrane formation. Our step ladder algorithm for the treatment of patients with idiopathic pars planitis differs slightly from that described previously on this web site for the treatment of patients with recurrent anterior non-granulomatous uveitis.
Our approach is as follows: We do not use steroid drops instead, the first step on our therapeutic step ladder in the care of patients with idiopathic pars planitis is regional steroid injection therapy after ruling out infectious etiologies especially ocular toxoplasmosis. We prefer to inject through the pre-orbital septum Transseptal), through the lower lid, similar to the administration of the peri bulbar injection for anesthesia, the difference being that the steroid (40 mg of Kenalog) is administered through a short (1/2 inch) 27-gauge needle. Results of studies in our clinic suggest that this approach is equal in efficacy to posterior sub-Tenon’s injection technique, is associated with considerably less intraocular pressure elevation, and is much more acceptable to the patient.
If, after a series of six transeptal steroid injections separated by at least two weeks (usually every 4 weeks), the patient’s pars plana inflammation recurs or continues to recur, we add a systemic nonsteroidal anti-inflammatory drug (for example, oral naproxen, 500 mg twice a day).
The choice between systemic immunosuppressive chemotherapy, for example with low dose cyclosporin or with once-a-week Methotrexate, or pars plana vitrectomy depends greatly on the individual circumstance, based on the patient’s age, sex, presence of retinal vasculitis, other medical disease, and whether or not the patient is phakic or aphakic. If we choose an immunosuppressive chemotherapeutic agent, we will usually begin with either low dose of methotrexate once a week or systemic low dose azathioprine, based on the patients age, sex, and past medical history, including liver problems or kidney problems). In a 2010 study conducted at our clinic, pars plana vitrectomy combined with peripheral endolaser photocoagulation was found to substantially reduce the likelihood of recurrent pars plana inflammation in patients with idiopathic recurrent pars planitis. Although the mechanism of pars plana vitrectomy combined with endolaser photocoagulation is not fully understood, some have argued that the immunologic characteristics of the eye are significantly changed by producing a “unicameral” eye rather than a bicameral one; others have argued one rids the eye of long lived “memory” immunologically competent cells from the vitreous matrix, cells which are at least partially responsible for a continued or recurrent out-pouring of inflammatory cytokines. Regardless of the mechanism or explanation, we agree with others that this therapeutic technique is in fact effective, and therefore we include pars plana vitrectomy in our therapeutic armamentarium in the care of patients with recurrent pars planitis.
If the above-mentioned treatments fail, next step in stepladder approach is biologic response modifier agents; however, it is important to note that tumor necrosis α inhibitors are contraindicated in patients with multiple sclerosis. Before initiating these agents, we recommend testing for HLA-DR15, which is closely associated with multiple sclerosis, along with a brain magnetic resonance imaging (MRI).
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