Bullous keratopathy is a disorder associated with progressing loss of endothelial cells of different origin.
This leads to chronic edema in all corneal layers, appearance of bullae in the epithelium (and pain when they rupture), local metabolic disorders, persisting opacities and vision loss up to blindness due to secondary glaucoma or infection. In select cases, the eye cannot be salvaged.
Bullous keratopathy usually develops after ocular surgery (cataract extraction with or without intraocular lens implantation, repeat glaucoma surgery, vitrectomy, etc.). Other less common triggers include injury, burns, multiple recurrences of herpes simplex keratouveitis. A family history of bullous keratopathy is not uncommon.
Damage to the endothelium (the innermost layer of the cornea facing the iris) results in progressing corneal edema. The endothelium is a defensive barrier that prevents fluid from entering the cornea. When the endothelium is compromised and can no longer function properly, fluid flows into the cornea and makes it opaque (edema). Patients experience blurry vision and vision loss up to blindness.
As the disease progresses, the aqueous humor begins detaching the epithelium (the superficial layer of the cornea) by forming bullae – bubbles of various sizes which produce foreign body sensation or gritty eyes.
Sometime after, the disease reaches its peak with patients complaining of excruciating pain (as though they are stabbed by a dagger or hit by a lightning bolt). The onset of pain is sudden. It causes excessive tearing and photophobia. This is due to bubbles bursting and leaving erosions in their place. Wound healing in these patients is very ineffective, and persisting erosions pose a threat of secondary infection which often translates into purulent inflammation, corneal melting and endophthalmitis. In select cases, the eye cannot be salvaged.
Full-scale surgeries like corneal grafting or other interventions often pose a challenge due to lack of corneal grafts, serious comorbidities, contraindications to lengthy general anesthesia, etc. At the same time, the pain causes great suffering.
To address this issue, we developed and patented excimer laser phototherapeutic keratectomy (PTK) [A.A. Kasparov, E.A. Kasparova, 1999]. The technique can be performed on an out-patient basis in an operating room for laser surgeries. It does not require general anesthesia (eye drops can be used) and only takes 8 minutes.
PTK effectively removes the abnormal swollen epithelium together with bullae and creates a laser-induced membrane that prevents the aqueous humor from entering the cornea. In all patients with bullous keratopathy who had undergone PTK, the following changes were noted: paused progression of bullous keratopathy, alleviation of pain, substantial decrease in edema and improved visual acuity.
A female patient with bullous keratopathy prior to PTK. Large bullae in the epithelium; sharp pain; vision loss (to 20⁄500). The same eye 1 month after surgery. No pain; visual acuity improved (from 20⁄500 to 20⁄100); her condition is stable. The patient has been followed up since 2000.
Earlier stages (up to 6 months postop) of the disease when the epithelium has been damaged as a result of cataract surgery, vitrectomy, etc. can be managed with another technique of ours – intracameral LEACKT. The method halts the progression of the disease and allows the cornea to recover and regain transparency (E.A. Kasparova, 2008).
A male patient with bullous herpes keratouveitis in his left eye. Prior to intracameral LEACKT (BCVA=UCVA= 20⁄250 OS).
The same eye after 3 sessions of intracameral LEACKT (UCVA= 20⁄20 OS).