Search tips
Search criteria 


Logo of brjopthalBritish Journal of OphthalmologyVisit this articleSubmit a manuscriptReceive email alertsContact usBMJ
Br J Ophthalmol. 2007 September; 91(9): 1253–1254.
PMCID: PMC1954928

Pressure dependent stromal oedema following deep anterior lamellar keratoplasty

A 53 year old man with keratoconus and a steroid related intraocular pressure response developed acute hydrops and underwent deep anterior lamellar keratoplasty after poor spontaneous recovery of vision. Intraocular pressure rose to 40 mm Hg on postoperative administration of topical prednisolone 0.5%, resulting in a well localised area of stromal oedema. Resolution of the oedema followed reduction of intraocular pressure, but recurrence ensued if the pressure rose above 30 mm Hg. Following acute hydrops, the regenerative process involves endothelial proliferation across the break in Descemet's membrane. This localised functional deficit is demonstrated after only a moderate intraocular pressure rise.

Case report

A 53 year old man was referred with acute hydrops in the left eye. He had a history of asthma, severe atopic keratoconjunctivitis, keratoconus, primary open angle glaucoma controlled on latanoprost eye drops, and a steroid related rise in intraocular pressure. A penetrating keratoplasty had been carried out on the right eye eight years earlier, after which the patient achieved 6/9 best‐corrected visual acuity (BCVA). Over the next two months the hydrops resolved, leaving apical scarring and a large visible break in Descemet's membrane. His BCVA improved from counting fingers to 6/60. He was contact lens intolerant, and therefore underwent a left deep anterior lamellar keratoplasty (by the Melles technique1). Postoperatively he was given 0.5% prednisolone eye drops three time daily and on review four weeks postoperatively his intraocular pressure had risen to 40 mm Hg. There was localised stromal oedema and mild epithelial oedema overlying the area of the previous break in Descemet's membrane. His intraocular pressure was lowered to 14 mm Hg with acetazolamide, and the stromal oedema cleared. Topical latanaprost was stopped to help control an exacerbation of asthma and his intraocular pressure subsequently rose to 32 mm Hg. Once again there was a localised area of stromal oedema overlying the previous break in Descemet's membrane, which cleared as the intraocular pressure was lowered to 20 mm Hg by topical dorzolamide. At three months postoperatively his topical steroid was discontinued and his intraocular pressure remained at 10 mm Hg. Three years later his corneal stroma is clear and he achieves 6/9 BCVA with a spectacle correction following suture removal.


Clarity of the normal cornea is achieved by maintaining the corneal stroma in a relatively dehydrated state. The intraocular pressure and stromal imbibition pressure promote the accumulation of fluid in the stroma. These forces are balanced by the osmotic gradient generated by active solute transport across the corneal membranes, particularly the endothelium. It has been shown that if the endothelial function is normal, then increased intraocular pressure does not cause stromal oedema.2

In advanced keratoconus, hydrops results from rupture of Descemet's membrane. Histological studies have shown that the endothelium then spreads across the break in Descemet's membrane and secretes basement membrane, restoring the normal anatomy over three to four months. This correlates with the resolution of the stromal oedema, suggesting that there is functional as well as anatomical recovery of the endothelial layer.3 The case presented here, however, provides evidence that the function of the regenerated endothelium and basement membrane remains impaired.

The endothelium in the region of the break in Descemet's membrane was able to maintain the clarity of the overlying corneal stroma when the intraocular pressure was normal. However, when the intraocular pressure was raised, the cornea became oedematous. We could find no earlier documentation of this effect, presumably because such cases have previously undergone penetrating keratoplasty, removing the area of re‐endothelialised stroma.

In summary, this case highlights the residual functional impairment of the regenerated endothelium and basement membrane at the site of a break in Descemet's membrane. Localised stromal oedema occurred overlying this region with only a moderate increase in intraocular pressure.


1. Melles G R J, Lander F, Rietveld F J R. et al A new surgical technique for deep anterior lamellar keratoplasty. Br J Ophthalmol 1999. 83327–333.333 [PMC free article] [PubMed]
2. Melamed S, Ben‐Sira I, Ben‐Shaul Y. Corneal endothelial changes under induced intraocular pressure elevation: a scanning and transmission electron microscopic study in rabbits. Br J Ophthalmol 1980. 64164–169.169 [PMC free article] [PubMed]
3. Stone D L, Kenyon K R, Stark W J. Ultrastructure of keratoconus with healed hydrops. Am J Ophthalmol 1976. 82450–458.458 [PubMed]

Articles from The British Journal of Ophthalmology are provided here courtesy of BMJ Publishing Group