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Oedema is the accumulation of liquids of varying consistency (liquid, soft or hard) in the intercellular spaces or interstices of tissues that manifests with swelling and the feeling of tension and fullness.

Oedema is caused by increased capillary permeability, sodium chloride retention, and insufficient drainage by the lymphatic system and various additional pathophysiological mechanisms.

CORNEAL OEDEMA:
PATHOPHYSIOLOGY

Corneal oedema is a relatively common pathological condition characterized by abnormal fluid accumulation within the corneal stroma and between keratocytes.1

As previously mentioned, one of the key properties of the cornea is its transparency, which is maintained by the fluid-regulating activity of the corneal endothelium.2,3

When this endothelial layer becomes dysfunctional, due to a variety of risk factors that we will examine later, the pump mechanism responsible for maintaining stromal dehydration is impaired. As a result, fluid accumulates in the stroma, leading to a loss of corneal transparency and, consequently, a variable degree of visual impairment.2,4

It is important to note that corneal endothelial cells have no mitotic activity

When individual endothelial cells are damaged, the surrounding cells enlarge and spread to maintain the integrity of the endothelial barrier. However, if the number of damaged cells exceeds the system’s compensatory capacity, fluid leaks into the stroma, resulting in corneal oedema.3,4,5

Endothelial pump failure → impaired fluid and ion homeostasis2

Accumulation of fluid in the stroma and between keratocytes1,3

Disruption of stromal collagen organization → corneal thickening1,3

Loss of transparency → visual impairment of variable severity1,3

Irreversible endothelial damage →when the remaining cells can no longer maintain function, fluid regulation fails and corneal oedema develops1,4,5

CORNEAL OEDEMA: RISK FACTORS

 Corneal oedema becomes more common after the age of 50. It can be triggered by any condition that alters the anatomy or function of the corneal endothelium and consequently affects the structural and functional integrity of the other corneal layers.1,4,5
INCREASED OCULAR PRESSURE
CATARACT SURGERY
INCORRECT CONTACT LENS USE
FUCHS' DISEASe
Major risk factors include direct trauma, inflammatory or phlogistic damage, exposure to toxic agents, and degenerative or dystrophic diseases.
The most frequent examples, illustrated on the slide, include improper use of contact lenses, cataract surgery, elevated intraocular pressure, and Fuchs’ endothelial dystrophy.1,6
Fuchs’ dystrophy is the most common form of posterior corneal dystrophy. It is characterized by excrescences known as corneal guttata on Descemet’s membrane, which progressively thickens, leading to diffuse corneal oedema and impaired visual function.7,8
The disease is often asymptomatic in its early stages and is more prevalent in women.8

CORNEAL OEDEMA: SYMPTOMS AND COMPLICATIOnS

Corneal oedema is characterized by both objective signs and subjective symptoms.

Clinical signs include corneal thickening, loss of transparency, epithelial bullae, and folds in Descemet’s membrane1,5 which can be observed during slit-lamp examination.

Symptoms reported by patients include blurred and distorted vision, halos around light sources, and a general reduction in visual acuity. These visual disturbances significantly impair quality of life by limiting the ability to drive, particularly at night, use electronic devices, work efficiently, and engage in recreational activities9 such as reading or watching television.

In more severe cases, patients may experience ocular discomfort, photophobia, and a foreign body sensation. Pain can occur when epithelial bullae rupture or when corneal decompensation is advanced.1,5,9

BLURRED VISION DISTORSION PAIN PAIPHOTOPHOBIA HALOS AROUND LIGHTS FOREIGN BODY SENSATION REDUCED VISUAL ACUITY

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References:
1. Krachmer, J. H., Mannis, M. J., & Holland, E. J. (2011). Cornea (3rd ed.). Elsevier Mosby.

2. Bonanno, J. A. (2012). Identity and regulation of ion transport mechanisms in the corneal endothelium. Progress in Retinal and Eye Research, 31(6), 622–638.
3. Meek, K. M., & Knupp, C. (2015). Corneal structure and transparency. Progress in Retinal and Eye Research, 49, 1–16.

4. Joyce, N. C. (2012). Proliferative capacity of the corneal endothelium. Progress in Retinal and Eye Research, 31(4), 323–352.

5. Bourne, W. M. (2003). Biology of the corneal endothelium in health and disease. Eye, 17(8), 912–918.

6. Efron, N., Morgan, P. B., & Brennan, N. A. (2003). Corneal hypoxia and oedema associated with contact lens wear. Clinical & Experimental Optometry, 86(5), 267–278

7. Price, F. W., & Price, M. O. (2005). Descemet’s stripping endothelial keratoplasty in Fuchs’ dystrophy. Journal of Cataract & Refractive Surgery, 31(11), 2039–2045.

8. Waring, G. O., Bourne, W. M., Edelhauser, H. F., & Kenyon, K. R. (1982). Corneal endothelial dystrophies. Survey of Ophthalmology, 27(6), 357–396.

9. Dickinson, C., & Sheppard, J. D. (2017). Impact of corneal edema on patient-reported outcomes. Current Opinion in Ophthalmology, 28(4), 332–338.

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