Contact lenses have transformed the lives of millions of people. Their complications are familiar to every ophthalmologist: dry eye, allergic conjunctivitis, corneal neovascularization, microbial keratitis and, occasionally, much more serious disease. But one adverse effect is easily overlooked because it develops slowly, causes no pain and may not become apparent until many years after contact lens wear began: blepharoptosis.

The association between contact lens wear and acquired ptosis has been recognized for decades. Yet even today, a history of contact lens use is not always specifically sought when a relatively young patient presents with an apparently aponeurotic ptosis. Moreover, although the phenomenon is often thought of as a complication of rigid lenses, there is increasing evidence that soft contact lenses can also be associated with acquired blepharoptosis.

When the upper lid slowly descends

The clinical observation is deceptively simple. A patient who has worn contact lenses for many years develops unilateral or bilateral upper eyelid ptosis. Levator function remains good and the overall appearance resembles ordinary involutional aponeurotic ptosis – except that the patient may be far too young for age alone to provide a convincing explanation.

An early report by Epstein and Putterman in 1981 described acquired blepharoptosis in contact lens wearers (1). However, a particularly important step in establishing the phenomenon came from Rotterdam in 1992, when Wim van den Bosch and Hans Lemij published their study ‘Blepharoptosis induced by prolonged hard contact lens wear’ in Ophthalmology (2).

Their investigation consisted of two parts. First, 17 patients who had developed ptosis while wearing hard contact lenses were compared with patients with involutional ptosis. Clinically, the two conditions appeared remarkably similar. Second, 46 individuals who had worn hard contact lenses for at least ten years were compared with 50 matched individuals who had never worn contact lenses. The contact lens wearers had upper eyelids positioned approximately 0.5 mm lower, and there were substantially more ptotic eyelids in the lens-wearing group. The authors concluded that prolonged hard contact lens wear could eventually produce ptosis through levator aponeurosis disinsertion.

That concept has stood up remarkably well.

Why should a contact lens affect the levator?

At first glance, the association may seem surprising. The contact lens rests on the ocular surface, while the levator aponeurosis is situated much further anteriorly within the upper eyelid.

The likely culprit is not simply the presence of the lens, but what happens to the eyelid over thousands of episodes of insertion and removal.

Hard contact lenses traditionally require considerable manipulation of the upper eyelid. The lid may be pulled firmly, stretched or repeatedly displaced while inserting or removing the lens. Over decades, such recurrent mechanical traction may accelerate the same changes that occur naturally with aging: attenuation, stretching or partial dehiscence of the levator aponeurosis.

Histopathological work has subsequently strengthened the concept that long-term rigid lens wear is accompanied by structural changes within the upper eyelid. Watanabe and colleagues, for example, demonstrated pathological changes including fibrosis involving Müller’s muscle in patients with hard contact lens-associated ptosis (3).

This probably explains why the clinical phenotype is predominantly aponeurotic rather than myogenic. Levator excursion is generally preserved; what has changed is the effectiveness with which that levator force is transmitted to the eyelid.

But surely soft lenses are different?

For many years that was the intuitive assumption.

A soft contact lens is flexible, relatively easy to remove and produces substantially less direct mechanical interaction with the upper eyelid than a rigid PMMA or gas-permeable lens. Consequently, contact lens-associated ptosis became almost synonymous with hard contact lens-associated ptosis.

But clinical observations increasingly suggested that this distinction might be too absolute.

In 2011, Bleyen and colleagues examined contact lens use among patients aged 18–50 years presenting with ptosis (4). Their paper deliberately posed the question in its title: "Not only hard contact lens wear but also soft contact lens wear may be associated with blepharoptosis." Their findings supported an association not only for hard lenses, but also for prolonged soft contact lens wear.

That finding matters. Soft lenses are vastly more common than traditional hard lenses. Even if the effect of an individual soft lens is much smaller, repeated manipulation of the eyelid every morning and evening over 10, 20, or 30 years represents a considerable cumulative mechanical exposure.

One does not have to imagine dramatic trauma. The biological effect may instead resemble metal fatigue: small stresses, repeated thousands of times.

Further evidence from Rotterdam

We returned to this question in a report published in Acta Ophthalmologica in 2019 (5). Verhoekx and colleagues specifically examined the association between soft contact lens wear and blepharoptosis. The resulting letter, "Soft contact lens induced blepharoptosis," added further evidence that the association is real and should not simply be dismissed as an extrapolation from rigid lenses.

The significance of these observations is not that every soft contact lens wearer is destined to develop ptosis – clearly they are not. Nor do observational studies prove that a soft lens directly damages the levator in every affected patient.

Rather, the accumulated evidence suggests that prolonged soft contact lens wear should be regarded as one of several acquired risk factors that may accelerate aponeurotic change in susceptible individuals.

A meta-analysis published in 2015 likewise found contact lens wear to be associated with an increased risk of acquired blepharoptosis (6), although the evidence base for soft lenses remained considerably smaller than that for rigid lenses.

The history matters

The practical implication is extremely simple.

When examining a patient with acquired ptosis, ask: ‘Do you wear contact lenses – or did you wear them in the past?’

The second half of that question is important.

A patient may have stopped wearing lenses years earlier and may not volunteer the information. Someone presenting at the age of 50 might have worn lenses daily between the ages of 18 and 45 and regard that period as irrelevant to their present eyelid problem.

I would be particularly interested in contact lens history when the patient is unusually young for involutional ptosis; has good levator function and an otherwise aponeurotic appearance; has no history of intraocular surgery or significant trauma that explains the ptosis; has asymmetrical ptosis associated with asymmetrical lens handling; or reports decades of rigid or soft contact lens use.

Obviously, association does not eliminate the need for a proper ptosis assessment. Horner syndrome, third nerve palsy, myasthenia, myogenic disease, orbital disease and other causes must still be considered where appropriate.

But contact lens history deserves a place alongside the more familiar questions about previous ocular surgery, trauma and age.

Can ptosis be prevented?

This is a more difficult question.

We do not currently have evidence demonstrating that a particular insertion or removal technique prevents ptosis. Nevertheless, if repeated upper-eyelid traction contributes to aponeurotic stretching, minimizing unnecessary force seems sensible.

Contact lens wearers could potentially be encouraged to avoid pulling vigorously on the upper lid during removal where an alternative technique is possible. Modern daily disposable lenses and improved lens materials may also alter cumulative exposure compared with older contact lens practices, although whether this reduces ptosis risk remains unknown.

There is another reason not to be alarmist. The absolute risk of clinically significant blepharoptosis in soft contact lens wearers has not been accurately quantified. Existing studies tell us considerably more about association than about the probability that an individual lens wearer will ultimately require ptosis surgery.

So this is not a reason to discourage otherwise successful contact lens use.

But it is a reason to recognize a potential long-term consequence.

And if surgery is required?

Once established, contact lens-associated ptosis behaves clinically much like other forms of acquired aponeurotic ptosis. Surgical treatment is therefore based on the same principles: restoration of upper eyelid height and contour by addressing the levator complex, with the precise technique dictated by examination findings and surgeon preference.

One practical issue deserves consideration: if the patient continues to wear contact lenses after surgery, the mechanical behavior that may have contributed to the original problem continues as well. Patients should therefore be encouraged to handle their lenses with as little eyelid traction as possible.

Whether continued contact lens use meaningfully increases the risk of postoperative recurrence is not yet well quantified.

A small diagnosis with a large lesson

Contact lens-associated ptosis is interesting because it illustrates something broader about ophthalmic disease.

We readily recognize complications that occur suddenly. A painful red eye after contact lens wear immediately raises concern about microbial keratitis. Slow mechanical effects are different. When an anatomical change develops by fractions of a millimeter over decades, the connection between cause and effect is far easier to miss.

Yet the story of contact lens-induced ptosis now spans more than four decades.

Early case observations suggested an association. Studies of prolonged hard contact lens wear demonstrated a measurable lowering of the upper eyelid and an aponeurotic phenotype. Histopathological studies supplied biological plausibility. Later epidemiological work extended the association from hard lenses to soft lenses. And subsequent observations have reinforced the message.

The evidence for soft lenses is not as extensive as that for rigid lenses, and we should be appropriately cautious about causality and absolute risk.

But the clinical message is straightforward: soft contact lens-induced blepharoptosis exists – or, at the very least, prolonged soft contact lens wear is a credible and documented risk factor for acquired aponeurotic ptosis.

Sometimes the most revealing question in a ptosis consultation is not about neurological symptoms, previous surgery or trauma.

It is simply asking the patient: "How long have you worn contact lenses?"