Corneal endothelial decompensation occurs when the single layer of endothelial cells lining the back of the cornea falls below the density needed to keep the stroma properly dehydrated, and because these cells do not regenerate after birth, decompensation is a one-way process that management can only slow or, ultimately, surgically bypass rather than reverse.
Why the Endothelium Cannot Repair Itself
Human corneal endothelial cells are arrested in the G1 phase of the cell cycle after birth and do not proliferate to replace cells lost to injury, disease, or normal aging; instead, remaining cells enlarge and spread to cover the gap, a process called polymegathism and pleomorphism that can be seen on specular microscopy long before symptoms develop (see specular microscopy).
Once cell density falls below a critical threshold, generally cited in the range of 500 to 800 cells per square millimeter depending on the individual cornea’s baseline function, the remaining cells can no longer pump fluid out of the stroma fast enough to counteract its tendency to imbibe water, and the cornea begins to swell.
Causes
- Fuchs endothelial corneal dystrophy, a primary, often bilateral, genetically influenced endothelial disease and one of the most common causes (see Fuchs endothelial dystrophy)
- Pseudophakic and aphakic bullous keratopathy, from surgical trauma to the endothelium during cataract surgery, historically more common with older intracapsular and extracapsular techniques and less common with modern phacoemulsification
- Prior intraocular surgery or trauma causing acute endothelial cell loss
- Chronic angle closure or other causes of markedly elevated intraocular pressure
- Herpetic endotheliitis and other inflammatory endothelial insults
- Graft failure after a previous corneal transplant
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From Choroida — the team behind this siteClinical Progression
- Early, subclinical disease: reduced endothelial cell density detectable on specular microscopy without visible corneal edema or symptoms
- Stromal edema: corneal thickening visible on examination, with blurred vision, often worse on waking because of reduced tear evaporation overnight allowing the cornea to swell further
- Epithelial edema and bullae: fluid tracks into the epithelium, forming microcystic edema and eventually painful bullae that can rupture, causing significant discomfort
- Subepithelial fibrosis and scarring: a late finding in chronic, longstanding bullous keratopathy, which can persist and limit vision even after successful endothelial replacement
Evaluation
- Slit-lamp examination for stromal thickening, folds in Descemet membrane, and epithelial or subepithelial changes
- Specular or confocal microscopy to assess endothelial cell density and morphology
- Corneal pachymetry to quantify and track stromal thickness over time
- Assessment for a treatable contributing cause, such as elevated intraocular pressure or active inflammation
Management
Medical Therapy
Hypertonic saline drops or ointment can draw fluid osmotically out of the cornea and provide symptomatic improvement in early or mild disease, though the effect is temporary and does not slow the underlying endothelial cell loss.
A hair dryer held at arm’s length, blown across the open eye briefly in the morning, is a low-cost adjunct some patients find helpful for early morning blur, working on a similar evaporative principle.
Bandage contact lenses relieve pain from ruptured bullae by protecting exposed corneal nerves, and lowering intraocular pressure when elevated reduces the fluid gradient driving edema.
Surgical Treatment
Once vision or comfort is significantly affected, endothelial keratoplasty is the standard treatment, replacing only the diseased endothelial layer rather than the full corneal thickness.
- Descemet membrane endothelial keratoplasty (DMEK) transplants an ultrathin layer of donor Descemet membrane and endothelium, giving the fastest and most complete visual recovery among current endothelial techniques
- Descemet stripping endothelial keratoplasty (DSEK) transplants a thin layer of donor stroma along with Descemet membrane and endothelium, technically somewhat easier to perform and handle than DMEK
- Full-thickness penetrating keratoplasty is reserved for cases with additional anterior corneal pathology, such as significant scarring, that endothelial keratoplasty alone would not address (see DSEK/DMEK)
Palliative Options
For eyes with poor visual potential from other coexisting disease, where a corneal transplant would not meaningfully improve vision, a Gundersen conjunctival flap or other palliative surgery can be used purely for comfort, covering the painful, exposed corneal surface without aiming to restore transparency.
Prognosis
Endothelial keratoplasty offers excellent visual outcomes in appropriately selected patients, with DMEK generally providing the fastest and most complete visual recovery of current techniques.
Long-term graft survival depends on the underlying cause of the original decompensation and on ongoing endothelial cell loss from the graft itself over time, since transplanted endothelium is also non-regenerating and subject to the same gradual attrition.
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From Choroida — the team behind this siteReferences
- Waring GO 3rd, Bourne WM, Edelhauser HF, Kenyon KR. The corneal endothelium: normal and pathologic structure and function. Ophthalmology. 1982;89:531-590.
- Price MO, Price FW Jr. Descemet’s stripping endothelial keratoplasty. Curr Opin Ophthalmol. 2007;18:290-294.
- Melles GR, Ong TS, Ververs B, van der Wees J. Descemet membrane endothelial keratoplasty (DMEK). Cornea. 2006;25:987-990.
- Bourne WM. Biology of the corneal endothelium in health and disease. Eye (Lond). 2003;17:912-918.
