At the completion of this article, the reader should have a better understanding of dry eye management with IPL, including:
- Understand the role of IPL treatment in reducing symptoms, improving tear quality and managing inflammation
associated with dry eye disease (DED) - Review the strengths and limitations of established dry eye treatment protocols, including tear supplements,
immunosuppressants and thermal heating - Recognise how IPL treatments, following the ‘Toyos Protocol’, can improve DED symptoms and signs, reduce inflammation and stimulate meibum liquefaction.
associated with dry eye disease (DED)
Dr Nicholas Young
BSc(Hons). BOptom PhD(Med)
PGCertOcTher
Optometrist, Clinic Director
Dry Eye Centre, Melbourne, VIC
With dry eye being a multifaceted ocular condition, Dr Nicholas Young says traditional theories of tear dysfunction are shifting towards inflammation and sensory factors as central causes. Intense pulsed light (IPL) therapy has now emerged as a safe and effective treatment that alleviates symptoms and enhances tear quality.
Objective signs of dry eye include loss of tear film homeostasis, loss of tear stability, hyperosmolarity, as well as ocular surface inflammation and damage. Combining less obvious features such as neurosensory abnormalities, dry eye disease (DED) is a condition of mixed aetiology.1 Subjectively, patients experience a variety of symptoms, ranging from minimal to severe.
Dry eye is also the most reported reason for seeking eyecare (other than vision correction)2 and is associated with significant morbidity, and cost to the community.3
Prevalence
Prevalence of dry eye is difficult to estimate due to inconsistencies in study design.4 Up to 57% of participants in one Australian study report at least one symptom5 but estimates of about 15%are more common.6 An increased incidence of disease associated with screen time and comorbidities such as mental health appears to have accompanied the COVID pandemic lockdowns.7
Pathophysiology
The pathophysiology of DED is multifactorial.8 The dichotomous narratives of ‘aqueous deficiency’ and ‘tear evaporation’, while foundational in their time, are now viewed as simplistic and outdated.
The relentless pursuit of meibomian gland treatments is a soft target with diminished returns and overshadows other pathology, such as tissue inflammation and neurosensory dysfunction.
The strongest clue that tear dysfunction alone is an inadequate target for therapy relies on one simple fact: the signs and symptoms of DED often do not overlap. It is common for patients whose tear metrics are indistinguishable from each other, to report different types and degrees of symptoms. This view is supported by meta-analysis, where some studies fail to demonstrate any clear association between signs and symptoms at all.9 Tear composition and stability is not a reliable determinant of comfort. Furthermore, no single metric is diagnostic of DED. This is the paradox of DED.
Inflammation and neurosensory function
The ultimate determinant of comfort is sensation. Uni and polymodal ocular surface trigeminal somatosensory nerve fibres constantly signal information about ocular surface temperature, touch and chemistry to the trigeminal nucleus and spinal cord. Corneal neuropathic pain (allodynia) is said to occur when these nerves respond in the absence of, or to normally non-painful stimuli. Whereas hyperalgesia represents an exaggerated sensation to surface conditions which would normally evoke a response.10
Complex processes involving the immune system can also affect sensory feedback. Ocular tissue inflammation and nervous system physiology are intricately balanced to provide comfort under normal conditions and physical symptoms when challenged.10 Elevated levels of inflammatory mediators, such as cytokines, MMP’s and reactive oxygen species accompany abnormal sensation in DED. Metanalyses confirm that inflammation, rather than tear dysfunction, is the core of DED.11
Rosacea
Some of the common types of inflammation found in patients with DED are eyelid inflammation (blepharitis), telangiectasis, conjunctival injection, infection (bacteria, Demodex) and MGD.12 These signs may be accompanied by facial flushing (rosacea).
Rosacea is an inflammatory skin condition characterised by classic patterns of facial erythema and telangiectasias and sometimes cystic or non-cystic acne. There are four primary subtypes: erythrotelangiectatic (vascular), papulopustular (inflammatory), phymatous and ocular. While this classification has recently been updated, ocular rosacea, which bears the clinical features described, can easily be overlooked by the inexperienced observer and is increasingly acknowledged as one of the more significant inflammatory comorbidities of DED.13
Current treatments
Tear Supplements
Most treatments for DED are tear supplements which promote improvements in one or another, or a combination of tear film components. But short retention times, or retention with blur, inclusion of preservatives and industrial chemicals, overuse, polypharmacy, tachyphylaxis and ineffectiveness or worsening of symptoms, leave many patients requiring alternative or additional care.
Tear supplements can be stratified by osmolarity. However, in my experience, this metric is subject to a high degree of variance;14 making its interpretation difficult in the clinic. Tear supplement efficacy on ocular surface inflammation is unproven and meta-analyses conclude their general effects on DED are clinically indistinguishable from each other.15 Consensus opinion favours tear supplements for transient or mild symptoms. Their use as adjunct therapy following application of more advanced treatments, might also be helpful.
Conversely, next-level immunosuppressants such as cyclosporin, lifitigrast, macrolides and tetracyclines interrupt different cellular processes responsible for upregulation of proinflammatory surface cytokines. While these medications can be very effective, they can also be poorly tolerated and since macrolides and tetracyclines are classed as antibiotics, the latter capable of profound adverse effects on gut health, long-term use is not desirable.
Steroids also have well documented side effects. Findings of iatrogenic facial rosacea following fluorinated steroids use in the 1960s,16 contraindicates these for treating ocular rosacea and has led to the use of non-fluorinated steroids such as hydrocortisone for eyelids.17 However, it has been shown that even this lower-potency steroid can cause contact dermatitis and rebound telangiectasias with prolonged use.18
Thermal Heating: Warm/hot compresses
Heat, externally applied to the eyelid, is often advocated for liquefying meibomian glands. Despite some supportive level two and three data, there remain inconsistencies with this treatment. They include patient compliance, lack of a standardised heating device, and temperature, duration or frequency of treatment.
To ensure a liquid state, meibum’s usual melting temperature is 32°C, which is lower than normal eyelid (33°C) and cornea (37°C) temperatures. However, due to altered chemical composition, gland inspissation can result in phase transition temperatures of around 45°C.19 It would appear then that an external lid temperature of 45°C should be sufficient to melt meibum. However, heat loss occurs between the front and back surface of the eye lid during heating. Indeed, external lid temperatures exceeding 50°C, could be needed to melt stubborn meibum, risking aggravation of conditions such as ocular rosacea.
Furthermore, eyelid skin burns have been reported to occur after 35 minutes of continuous exposure to thermal contact of 45°C, as well as from accidental over heating of face masks20 and corneal warpage from excessive heat transfer to the cornea is also a risk.9, 22 Therefore, warming devices should not exceed 5-10 min or 45°C, in order to prevent adverse effects,7,19 but at these temperatures and durations, are most likely ineffective for inspissated glands.
IPL and dermatology
Pulsed dye lasers have been used in dermatology since the early 1980s. They have been used to treat lesions such as rosacea, port wine stains and haemangiomas. In 1987, studies of rabbit ear veins and human leg veins concluded that a 585nm laser pulsed at 0.45ms could cause thermal coagulation of blood vessels with a diameter less than 0.4mm. However, the treatments caused hyperpigmentation, hypopigmentation, purpura and scarring.21
In 1992, a chance meeting of Drs Mitchel Goldman, Richard Fitzpatrick (dermatologists) with Shimon Eckhouse (engineer), resulted in a prototype flash lamp device designed to improve the flexibility of treatment algorithms around variables such as pulse intensity, duration and frequency. Studies showed that rabbit ear veins could be thermo-coagulated without any significant skin damage , but the first human trials resulted in burning (60%) and scarring (20%). These and similar early findings did nothing to help the development of IPL. Proponents of lasers dismissed IPL as harmful, useless and labelled it the ‘photo burner’. Its further development would see strongly divisive literature published and even defamation litigation pursued in the courts among adversaries of the technology.21
The IPL breakthrough came with the understanding that skin could be protected with the use of a sapphire lightguide, a pause between successive pulses to ‘rest’ the skin, cooling gel to couple the lightguide to the skin and, in the most recent and advanced devices, the use of a refrigerated lightguide.
After its invention in the 1960s as an industrial device for, among other uses, vaporising paint off aircraft, IPL was finally registered by the FDA for skin treatments in August 1995. Its appeal rapidly spread to become arguably the safest and one of the most efficacious aesthetic devices available today.
IPL and optometry
In 2002, a fortuitous discovery by US ophthalmologist Dr Rolando Toyos occurred when it was noticed that patients with both facial rosacea and dry eye disease experienced ocular symptom relief following facial IPL treatment.22 Research continued with the light therapy company Dermamed using a device called the ‘Quadra 4 Diamond Series II’ IPL. This led to the commercialisation of IPL for DED in 2008.
The Dry Eye Centre in Melbourne subsequently acquired this device and became the first clinic in Australia to treat DED with an IPL device developed specifically for dry eye disease.
How does IPL work?
The principle of IPL involves passing a broad spectrum of incoherent light through a sapphire lightguide to the skin via a wavelength cut off filter. The filter excludes ultraviolet light and facilitates wavelength optimisation for targeting chromophores such as red blood cells. IPL devices typically emit light in the wavelength range of 500nm to 1400nm.23
Pulsed light generates multiple instances of light, each being separated by a rest phase. The latter protects the skin epidermis, while the former targets the chromophore of interest. The target chromophore for DED is red blood cells, while heat is also absorbed by meibomian glands. Important features of IPL include wavelength optimisation filtering, pulse duration, size, shape and depth for different skin types and treatment effects. In addition, the lightguide should produce a consistent non-degrading flash with integrated cooling.23
If these conditions are met, IPL is a highly standardised, reproducible and measurable procedure. The treatment is performed with calibrated equipment, known and documented metrics, in a controlled space by a suitably qualified practitioner.
The ‘Toyos Protocol’
The accepted treatment standard is the ‘Toyos Protocol’.22 It consists of a triple six-millisecond pulse, interspaced with two 50ms rest phases. Treatment takes place directly beneath the lower eyelid lash line, proceeding from tragus to tragus and includes the lateral walls and dorsum of the nose.
Depending on face width, up to 17 flashes across the face may be delivered from right to left. Facial contouring imposed by the cheek bone, also necessitates horizontal placement of the sapphire lightguide below the primary treatment zone. Depending on the device in use, direct treatment of the upper eyelids might also be possible.
The Fitzpatrick skin grading scale is used to determine pulse intensity. Treatment may be followed with or without meibomian gland expression, although a recent study suggests that post-IPL gland expression is preferable.23 Anecdotally, spot treatments can be used to treat active chalazia. At the Dry Eye Centre, we receive many referrals for this purpose and have achieved excellent results on both isolated and recurring lesions across the lids.
For DED, approximately four treatments are done usually in three to four-week intervals, depending on the patient and the device. However, this is only a guide and additional treatments might be needed as part of the initial treatment cycle. Improvement should not be promised, as some patients do not respond to IPL. Treatments are usually also combined with other care routines, the combination of which can remain effective for many months or longer.22 Future maintenance treatments might also be needed depending on the presenting condition.
Patient education
Treatments are performed with no down time and generally no side effects. However, there are contra-indications for IPL, and practitioners should check with their device supplier for a list of these, and develop a patient informed consent form, before proceeding.
The treatment plan including what to expect before, during and after IPL, as well as success rates and alternatives to IPL, should also be discussed with the patient. Practitioners who use devices with degrading flash units, should also inform their patients of this, as treatment efficacy may vary with the lifecycle of the flash cartridge.
Practitioners should also obtain a preceptorship on the use of their device from their device company, education provider or suitably qualified mentor. Injury to patients is possible and IPL should not be used without such training.
Mechanisms
Thrombosis
Haemoglobin readily absorbs light energy and coagulates red blood cells. Vessel thrombosis follows coagulation.24 Vessel closure is important, not just for cosmesis, but to also reduce tissue damage from an overactive immune system. The concentration of ocular surface inflammatory mediators is reduced following IPL, and it is hypothesised that these reductions interfere with the vicious cycle of inflammation.25
Meibum liquification
Heat from IPL is thought to pass directly into the meibomian gland, facilitating phase transition to a liquid.25 Anecdotally, evidence of this is often seen at the slit lamp immediately following treatment. One of the other characteristics of MGD is the presence of bacteria which contribute to the inspissation of meibum. It is thought that IPL simultaneously eliminates these bacteria.26 The same treatment algorithm also destroys demodex.27
Skin turnover
Rosacea increases tissue inflammation and epithelial cell turn over. Ocular rosacea affects lid margin and gland duct epithelium. Dead epithelial skin cells create debris which can block meibomian gland orifices. It is hypothesised that IPL reduces tissue inflammation, epithelial cell debris and therefore meibomian gland obstruction.25
Elastin and collagen synthesis
Lid strength is required to pump meibum from their glands to the ocular surface. Age-related extracellular collagen and elastin decline leads to tissue weakening which can affect eyelid apposition reducing the effect of blinking. IPL stimulates collagen and elastin and is thought to play a role in eyelid firming, and blink function, which may help to maintain meibomian gland health. One of the proposed mechanisms of this activity is cellular photo modulation.25
Efficacy
IPL is both a safe and effective dry eye treatment. Several meta-analyses have now reported positive IPL outcomes. Collectively, they conclude improvements in subjective assessments such as SPEED (symptoms), OSDI (effect on lifestyle) scores and reduction of tear supplement usage.
Objective assessments favour reduced corneal fluorescein staining, improved lipid layer quality and improved tear break up times compared to baseline and in comparison with other conventional therapies.28-32
These analyses include randomised controlled and other study designs with patient numbers ranging from 539 (nine studies)31 to 1,842 (11 studies).28-32 Individual studies report improvements in visible signs of ocular inflammation, such as lid margin telangiectasias.22
Conclusion
IPL represents a paradigm shift in the treatment of DED. Many studies have demonstrated its positive effects on ocular rosacea and tear function. However, it is not a first line treatment, is not a cure, and successfully treated patients generally require maintenance treatment. Additionally, practitioners should understand that dry eye is a disease of mixed aetiology.
Duty of care requires a thorough history, knowledge of the presenting condition, investigations and possibly co-management of relevant co-morbidities and a sound understanding of the principles and implementation of treatment options. If these conditions are met, the use of IPL in a dry eye clinic can form part of a very rewarding experience for both patient and practitioner.
More reading
Dr Rolando Toyos – Challenging dry eye dogma
Dry eye disease and nutrition: are we what we eat?
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