It is steroid induced. One needs to monitor and shift to mild steroids with Nnapefenac Sodium. If the situation is still not in control, one may discontinue steroids and may use topical cyclosporin for its steroid sparing role to prevent corneal haze.
Can you explain the exact pathophysiology of steroid induced raised IOP? I mean what structure or function exactly steroids impair that leads to the raised IOP?
1) Steroid alters trabecular meshwork cell morphology by increasing nuclear transport of the human glucocorticoid receptor GRbeta [PMID: 10438153].
2) Corticosteroids increase expression of extracellular matrix protein fibronectin, polymerized glycosaminoglycans, and elastin. Elevated amounts of named substances thus lead to their accumulation in the trabecular meshwork, obstructing the outflow pathway [PMID: 1607235].
3) The endothelial cells of the trabecular meshwork are phagocytic and can thus remove and destroy debris entering the meshwork from the anterior chamber. Corticosteroids are known to suppress phagocytic activity, and supression of phagocytosis mayallow debris in the aqueous humor to accumulate and act as a barrier to outflow [PMID: 1110131].
4) Corticosteroids cause physical obstruction of the trabecular meshwork with pigmented, crystalline steroid particles [PMID: 18344759].