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The ‘other’ IPL

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Nicholas Young
BSc(Hons) BOptom PhD(Med) PGCertOcTher
Dry Eye Centre, Heathmont VIC

Product
Lumenis M22 IPL

Supplier
Lumenis Australia

 

Dry eye disease (DED) represents a diverse group of pathologies resulting in various descriptions of ocular discomfort and pain.

Prevalence of DED is difficult to estimate due to inconsistencies in definition and measurement, and between regions.1 Up to 57 per cent of participants in one Australian study report at least one symptom,2 but estimates of about 15 per cent are more common.3 Other than vision correction, DED is also the most commonly reported reason for seeking eye care4 and is associated with significant morbidity and cost to the community.5

The pathophysiology of DED is multifactorial.6 Current and emerging evidence confirms that simplistic notions of aqueous deficiency, and tear evaporation, once thought the hallmarks of the disease, are merely pieces of a more complex puzzle.7

One clue to this is the common failure of overlap between the signs and symptoms of DED; patients whose glands are dysfunctional and whose tear films are compromised can be completely non-symptomatic. Similarly, good tear stability is not always a determinant of comfort. No single metric is diagnostic of DED and some studies fail to demonstrate any clear association between signs and symptoms. This is the paradox of DED.8,9

To help us understand this, numerous important mechanisms have been proposed, two of which include ocular surface inflammation and nerve form and function. Ocular inflammatory and nervous system physiology are intricately balanced to provide a measured response to physical changes in temperature, pressure and surface chemistry. Complex cellular and neurological processes involving sensory feedback can be modified by altered conditions on the ocular surface, resulting in symptoms.10 Surgical or other trauma to corneal nerves can also result in symptoms10,11 culminating in peripheral and possibly centralised neuropathic sensitisation.12

Enter IPL

While there are novel pharmacological approaches to managing ocular surface inflammation, intense pulsed light (IPL) is a mechanical solution to the problem. The effect of light on the haemolysis of red blood cells has been known for more than 80 years.13 However, IPL refines the knowledge to selectively transmit broad spectrum pulsed light through an applicator to the skin, enabling photocoagulation of intra-vascular red blood cells, effectively sealing off the vessel and thereby reducing inflammation.

IPL was invented by Lumenis in the early 1990s, and approved by the FDA in 1995 for treating vascular lesions such as rosacea. About 85 per cent of rosacea patients also experience other inflammatory conditions of the eye such as blepharitis and MGD.14 In 2002 this link led to a finding that IPL can be used to treat DED.

Commercialisation of the technology was achieved in 2008, and studies suggest the treatment is highly effective and safe.15 Our own clinic has achieved excellent results using the Quadra 4 device originally commercialised for this treatment. We have now performed several hundred treatments using the Lumenis M22 with optimised pulse technology.

 

EQ-225-Figure -1 - Online

Figure 1. Patient prior to IPL treatment

 

EQ-225-Figure -2 - Online

Figure 2. Patient post IPL treatment

 

Unlike alternative forms of IPL used in eye care, the Lumenis M22 is approved for treating rosacea and other inflammatory skin conditions. This indication is particularly important for us, as many patients have measurable inflammation of the ocular surface and lid adnexia, often without detectable MGD or other tear dysfunction. Secondary action of warming the meibomian glands with the IPL’s heat enables easier gland access for patients requiring manual expression.

Other features of the Lumenis M22 include a cooling head to improve patient comfort, and the ability to customise procedures in response to patient feedback. The Lumenis M22 system enables optimisation of wavelength filtering, pulse duration, size, shape and depth for different skin types and treatment effects. In addition, the head produces a consistent flash which, unlike other IPL devices, does not degrade over time, and has a lifespan of several 100,000 flashes.

Care of the dry eye patient is a consuming occupation, requiring many approaches and a great deal of patience. Knowing who to treat with IPL is no less of a skill; however, the advent of IPL has changed the way we practise and assisted many of our patients to finally achieve comfort. 

 

1.  Janine AS. The epidemiology of dry eye disease: report of the epidemiological subcommittee of the international dry eye workshop. Ocul Surf 2007; 5: 2: 93-107.

2.  Chia EM, Mitchell P, Rochtchina E, et al. Prevalence and associations of dry eye syndrome in an older population: the Blue Mountains Eye Study. Clin Exp Ophthalmol 2003; 31: 3 :229-232.

3.  Moss SE, Klein R, Klein BE. Prevalence of and risk factors for dry eye syndrome. Arch Ophthalmol 2000; 118: 9: 1264-1268.

4.  Doughty MJ, Fonn D, Richter D, et al. A patient questionnaire approach to estimating the prevalence of dry eye symptoms in patients presenting to optometric practices across Canada. Optom Vis Sci 1997; 74: 8: 624-631.

5.  Pflugfelder SC. Prevalence, burden, and pharmacoeconomics of dry eye disease. Am J Manag Care 2008; 14: S102–S106.

6.  Stern ME, Beuerman RW, Fox RI, et al. A unified theory of the role of the ocular surface in dry eye. In Lacrimal Gland, Tear Film, and Dry Eye Syndromes 2. US: Springer 1998; pp 643-651.

7.  Shtein RM, Harper DE, Pallazola V, et al. Discordant Dry Eye Disease (An American Ophthalmological Society Thesis). Trans Amer Ophthalmol Soc 2016; 114.

8.  Nichols KK, Nichols JJ, Mitchell GL. The lack of association between signs and symptoms in patients with dry eye disease. Cornea 2004 ; 23: 8: 762-770.

9.  Pult H, Purslow C, Murphy PJ. The relationship between clinical signs and dry eye symptoms. Eye 2011; 25: 4: 502-510.

10.  Belmonte C, Acosta MC, Gallar J. Neural basis of sensation in intact and injured corneas. Exp Eye Research 2004; 78: 3: 513-525.

11.  Nettune GR, Pflugfelder SC. Post-LASIK tear dysfunction and dysesthesia. Ocular Surface 2010; 8: 3: 135-145.

12.  Rosenthal P, Baran I, Jacobs DS. Corneal pain without stain: is it real? Ocular Surface 2009; 7: 1: 28-40.

13.  Meyerstein W. Effect of light on red blood cells. The light sensitivity of blood from different vertebrate species. J Physiol 1941; 99: 4: 510.

14.  VisoE, Millan AC, Rodriguez-Ares MT. Rosacea-associated meibomian gland dysfunction: an epidemiological perspective. Eur Ophthalm Rev 2014; 8: 1: 13–16.

15.  Toyos R, McGill W, Briscoe D. Intense pulsed light treatment for dry eye disease due to meibomian gland dysfunction; a 3-year retrospective study. Photomed Laser Surgery 2015; 33: 1: 41-46.



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