Uveal effusion syndrome is defined by an idiopathic ciliochoroidal effusion, which may be accompanied by concomitant serous retinal detachment (Figure 29.1).¹

This typically occurs in otherwise healthy middle-aged males.¹

The pathophysiology suggested is a compromise of posterior segment drainage due to decreased scleral permeability and scleropathy; studies have shown an accumulation of glycosaminoglycan-like deposits and scleral thickening in patients with uveal effusion.²,³

It is divided into three types³:

Important to exclude secondary causes of serous choroidal detachment, such as uveitis, hypotony, hypertension, elevated uveal venous pressure (eg, Sturge-Weber, arteriovenous fistula), and neoplasm.

Treatment consists of scleral thinning procedures such as quadrantic partial thickness sclerectomy and sclerostomy to drain suprachoroidal fluid as well as to treat the underlying scleropathy (Figure 29.2).⁴ Some surgeons also combine pars plana vitrectomy with external drainage for cases with concomitant rhegmatogenous retinal detachment. Systemic steroid use is controversial; a recent
case series of type 3 uveal effusion syndrome showed improved visual acuity for patients treated with corticosteroids compared to observation.¹,⁵ The evidence remains weak, however, supporting the routine use of steroids for the management of uveal effusion syndrome.