Table 3.

Phases of injury following a chemical burn [1]

Phase	Time (days)	Findings
Immediate	0	Mild chemical burns result in limited conjunctival and corneal epithelial defects. More severe injuries result in more extensive epithelial defects affecting the limbus, limbal ischaemia, corneal haze, raised intraocular pressure and intraocular damage (e.g. lens opacification).
Acute	0–7	Inflammation plays a critical role here, and can contribute to ocular surface melting. Rate and success of re-epithelialisation is multifactorial, being influenced by health of limbal stem cells, presence of growth factors, ocular surface dryness, etc. Rapid changes in corneal transparency occurs in the days following injury. Intraocular pressure can be affected at all stages of injury, and must be frequently monitored.
Early reparative	7–21	This is the transition period where regeneration of the ocular surface and the acute inflammatory response gives way to scarring, stromal repair and chronic inflammation. Milder injuries complete re-epithelialisation and more severe injuries can develop persistent epithelial defects.
Late reparative	>21	Mild chemical-burns display adequate healing and subsiding of inflammation. Localised limbal stem cell deficiency (LSCD) can result in sectorial conjunctivalisation (pseudopterygium) of the cornea. In more severe injuries, persistent epithelial defects can result in permanent scarring and secondary infections. Limbal stem cell deficiency and development of conjunctival cicatrisation, lid abnormalities and dry ocular surface result in conjunctivalisation and vascularisation of the cornea. Glaucoma is an often missed cause of irreversible visual loss.