Mechanisms of corneal trauma in response to rubbing and other intraocular pressure elevating activities in keratoconus

ABSTRACT

Introduction

The potential for eye rubbing to contribute to keratoconus development and progression is well established, but the mechanisms of that association have not been fully elucidated.

Areas covered

This review examines mechanisms for rubbing-related corneal trauma from both anterior and posterior surface responses to elevated intraocular pressure. Apart from rubbing-related intraocular pressure elevation, consideration is given to other sources of elevation which may contribute to corneal bulging and cone formation. Mechanisms whereby intraocular pressure-related increased posterior corneal surface distending stress and stromal hydrostatic pressure may alter keratocyte functions and increase susceptibility to such stress are examined.

Expert opinion

Elevated intraocular pressure (IOP) that is associated with a chronic habit of abnormal rubbing (CHAR) can be a major contributor of keratoconus (KC) development and progression. Anterior corneal surface protection during rubbing due to Bell’s reflex in most patients, at least for the central and para-central cornea, increases the likelihood that IOP distending stress can be an important source of KC pathogenesis, perhaps even in patients who do not have abnormal rubbing habits. That the earliest pathological changes in KC occur at the posterior corneal surface is consistent with the significance of an IOP-related distending force mechanism for KC pathogenesis.

KEYWORDS:

• Keratoconus
• cornea
• eye rubbing
• intraocular pressure

View addendum:

Under pressure: keratoconus and intraocular pressure elevation evidence

The pathogenesis of KERATOCONUS

Article highlights

• Any episode of IOP elevation and associated increased distending forces on the cornea appears likely to increase the risk of bulging in susceptible corneas.

• Elevated IOP also results in increased corneal hydrostatic pressure and the associated possibility of adverse tissue/cellular changes which may contribute to increased corneal susceptibility for bulging responses to elevated IOP.

• For example, increased hydrostatic pressure in corneal stroma may damage keratocytes and reduce their collagen maintenance functions with the associated possibility of reduced resistance to IOP distending forces and increased susceptibility for bulging responses during episodes of IOP elevation.

• Any area of corneal thinning, or other form of reduced capacity to withstand IOP distending forces, is at greater risk of corneal bulging in ectatic diseases such as keratoconus.

• Because eye rubbing, massaging, and touching have the consequences of high or very high IOP and hydrostatic pressure elevation, as well as the risk of significant inflammatory responses, avoidance of such activities may have significant prognostic value for patients with or at risk for developing KC.

• However, apart from rubbing, massaging and touching, Table 1 indicates other activities which are known to elevate IOP with associated risk of contributing to diseases such as KC.

• The potential for IOP elevation to contribute to KC development and progression may also be relevant in other baropathic diseases such as corneal responses in keratectasia other than KC, optic nerve head changes in glaucoma and axial length increases in myopia.

Declaration of interest

The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Data availability statement

A copy of a rubbing avoidance counselling handout for patients to take home is freely available on request from the author at [email protected].

Additional information

Funding

This paper was not funded.