Intraocular pressure variation (ocular hypertension) in diabetes mellitus

Table 1 Mechanisms of development of ocular hypertension specific to proliferative diabetic retinopathy

Intervention	Cause of IOP rise	Mechanism of OHT	Intervention1
Nil	Rubeosis iridis and neovascularization of angle	Progressive and zipping angle closure	Retinal laser photocoagulation
			Intracameral anti-VEGF injection
Retinal laser photo-coagulation	Intraocular inflammation	Acute release of cytokines in response to laser-induced tissue injury	Topical drugs: Corticosteroids, non-steroidal anti-inflammatory drugs, cycloplegics
		Ciliary body edema
Intravitreal injection	Acute rise in intraocular fluid volume after anti-VEGF injection	Vitreous pressure	Immediate anterior chamber paracentesis
		Forward movement of iris-lens diaphragm	Intravenous mannitol, oral glycerol
	Corticosteroid response	Trabecular dysfunction and aqueous outflow impedance	Topical antiglaucoma medication like aqueous suppressants
Vitreoretinal surgery	Surgical trauma	Acute inflammation	Topical drugs (as above)
		Erythroclastic response	Uveoscleral outflow stimulators
		Ciliochoroidal effusion	Topical drugs (as above), oral steroids
		Fibrinous membrane formation	Membranectomy
			Tissue plasminogen activator injection
			Laser peripheral iridotomy
	Intraocular tamponade	Silicone oil	Inferior (Ando) iridectomy
			Oil removal
		Intraocular gas expansion	Topical drugs (as above)
			Gas removal or exchange
	Corticosteroid response	As above	As above

¹Increased intraocular pressure control may be aided by antiglaucoma medication, nonpenetrating glaucoma surgery, filtering surgeries and/or placement of glaucoma drainage devices or diode laser cyclophotocoagulation as required.

VEGF: Vascular endothelial growth factor; OHT: Ocular hypertension; IOP: Increased intraocular pressure.