The most posterior aspect of the stroma forms a thin, acellular layer (15- μ m thick) that is tightly adherent to Descemet membrane. This novel layer is called pre-Descemet layer, or Dua layer, and is important in deep anterior lamellar keratoplasty (DALK). Dua layer is strong and resists air dissection from Descemet membrane. During DALK, air is injected on the stromal side of Dua layer to create a big-bubble stromal dissection, forming a type I bubble. This bubble is sturdier and less likely to tear or burst, in contrast to an air dissection between Dua layer and Descemet membrane (a type II bubble).

Dua HS, Faraj LA, Said DG, Gray T, Lowe J. ­Human corneal anatomy redefined: a novel pre-­ Descemet’s layer (Dua’s layer). Ophthalmology. 2013;120(9):1778–1785.

Randleman JB, Dawson DG, Grossniklaus HE, McCarey BE, Edelhauser HF. Depth-­ dependent cohesive tensile strength in ­human donor corneas: implications for refractive surgery. J Refract Surg. 2008;24(1):S85–S89.

Schlötzer-­Schrehardt U, Bachmann BO, Tourtas T, et al. Ultrastructure of the posterior corneal stroma. Ophthalmology. 2015;122(4):693–699.

Sridhar M. Anatomy of the cornea and ocular surface. Indian J Ophthalmol. 2018; 66(2):​ 190–194.

Descemet membrane is the basement membrane of the corneal endothelium (see Fig 1-4). Its thickness increases with age; at birth, it is 3 µm, increasing to 10–12 µm by adulthood. It is composed of an anterior banded zone that develops in utero and a posterior amorphous, non- banded zone that is laid down throughout life. The Schwalbe line is a gonioscopic landmark that defines the end of the Descemet membrane and the beginning of the trabecular meshwork.

Corneal endothelial cells lie on the posterior surface of the cornea (see Fig 1-4), compos­ ing a monolayer of closely interdigitated cells arranged in a mosaic pattern of mostly hex­ agonal shapes. If cell loss occurs, especially as a result of trauma or surgery, the defective area is initially covered through a pro­cess of cell enlargement and spread of surrounding cells or perhaps peripheral stem cells. ­These cell findings can be observed by specular or confocal microscopy as polymegethism (variability in cell size) and polymorphism (vari­ ability in cell shape). It was previously thought that the corneal endothelial cells ­were unable to replicate. Scientists are now investigating ­whether ­these cells have some mitotic ability, particularly the cells in the corneal periphery. Migration of ­these cells may be aug­ mented by pharmacological agents such as Rho kinase inhibitors.

Cell density varies throughout the endothelial surface; the concentration is typically highest in the periphery. Central endothelial cell density decreases with age at an average rate of approximately 0.6% per year, diminishing from a count of about 3400 cells/mm² at age 15 years to about 2300 cells/mm² at age 85 years. The normal central endothelial cell count is between 2000 and 3000 cells/mm². It has been observed that eyes with an endo­ thelial cell count below 500 cells/mm² may be at risk for development of corneal edema.

As mentioned ­earlier, the corneal endothelium helps maintain corneal transpar­ ency by controlling corneal hydration and maintaining stromal deturgescence. It does so through its functions as a barrier to the aqueous humor and as a metabolic pump that moves ions, and draws ­water osmotically, from the stroma into the aqueous humor. The barrier and pump functions of the endothelium can be mea­sured clinically by fluoropho­ tometry and pachymetry. The endothelium must also be permeable to nutrients and other molecules from the aqueous humor. Increased permeability and insufficient pump sites occur with reduced endothelial cell density, although the cell density at which clinically evident edema occurs is not an absolute.

For more detailed information on the histology and physiology of the cornea, see BCSC Section 2, Fundamentals and Princi­ples of Ophthalmology, Chapter 8.

Amann J, Holley GP, Lee SB, Edelhauser HF. Increased endothelial cell density in the paracentral and peripheral regions of the ­human cornea. Am J Ophthalmol. 2003; 135(5): 584–590.

Koizumi N, Okumura N, Ueno M, Kinoshita S. New therapeutic modality for corneal endothelial disease using Rho-­associated kinase inhibitor eye drops. Cornea. 2014;33(11):S25–31.

Whikehart DR, Parikh CH, Vaughn AV, Mishler K, Edelhauser HF. Evidence suggesting the existence of stem cells for the ­human corneal endothelium. Mol Vis. 2005;11: 816–824.