The authors discuss pathophysiology, aetiology and current management strategies of UGH syndrome. The clinical features of UGH are different than initial descriptions. UGH today is most often associated with posterior chamber IOLs that are not placed within the capsular bag (i.e., sulcus positioned or fixated to the sclera or iris). Furthermore, there has been a surge in IOL dislocations in which the IOL is within the intact capsular bag, the incidence of which is 2% without pseudoexfoliation (PXF) and 6% with PXF. There is no evidence to support one surgical procedure with dealing with IOL dislocation over another. The mechanism of UGH comes from intraocular implant contact with uveal tissue, leading to the induction of inflammatory mediators, blood ocular barrier breakdown and erosive effects on the microvasculature. Cystoid macular oedema (CMO) occurs in 10% of these cases. The most cases of UGH-based IOP elevation are due to blood ocular barrier breakdown caused by IOL implants that are not positioned within the intact capsular bag or other anatomic alterations that lead to higher protein content in the anterior chamber, which chronically affect the trabecular function. Topical therapy (including cycloplegics) is the commonest and most successful for acute UGH exacerbations. OCT-guided treatment of CMO is important for visual recovery. Once UGH manifestations occur, they may be surgically reversible, but one can address the sequelae. A published study on 71 eyes documented surgery in 60 eyes, which were 14 IOL exchanges and 46 IOL repositioning with / without fixation or haptic amputation.