• alkaline injury;
  • canine cornea;
  • chemical burn;
  • endothelial cell damage;
  • ocular surface



To describe presentation, treatment, and follow-up after unilateral alkaline injuries to the eye in four dogs.

Material and method

The case notes of four patients that suffered from alkaline injuries to the eye were included in this series.


Acute clinical signs included blepharospasm and edema of the eyelids, chemosis and conjunctival hyperemia, conjunctival ischemia, destruction of the corneal epithelium, a whitish haze of the corneal stroma, mild corneal edema, and uveitis. Two patients showed depigmentation of the eyelids. Presumed endothelial cell damage resulted in severe corneal edema in two dogs. Long-term complications included phthisis bulbi, scarring of the eyelids and damage to the meibomian glands, symblepharon formation, conjunctivalization of the cornea, corneal vascularization, pigmentation, and fibrosis. Persisting corneal edema was seen in the dogs with presumed endothelial cell damage. One dog developed a mild bullous keratopathy with superficial corneal ulcerations 4½ years after the injury and had a reduced anterior chamber depth on ultrasound.


The damage to the ocular structures described here mainly affects the ocular surface. One patient presumably suffered an injury to the ciliary body epithelium resulting in a phthisical globe. Chronic corneal edema, conjunctivalization, and scarring can result in permanent visual impairment. Healing of the ocular surface can take weeks and is associated with a dramatic vascular response. However, a severely vascularized cornea has the potential to clear and allow a good visual outcome long term. Ongoing discomfort was only seen in one case with persistent corneal edema and a secondary bullous keratopathy.