Meibomian glands are large sebaceous glands that are located as separate gland strands in parallel arrangement within the tarsal plates of the eyelids. Their oily product, meibum, is secreted via a holocrine mechanism during which meibocytes are transformed into the meibum. Following production in the gland acini, meibum is transported through the ductal system via the connecting duct and the central duct towards the orifice at the free eyelid margin close to the inner eyelid border. Meibum is a complex mixture of various lipids and minor protein components as well as other components of the meibocytes, which form a clear liquid at body temperature. It is transported within the gland by the force of secretory pressure from continuous secretion and by muscular action of the orbicularis muscle and Riolans muscles during blinking. After it is delivered onto the posterior eyelid margin, meibum moves from the posterior eyelid margin reservoir onto the tear meniscus and is pulled as a thin layer onto the pre-ocular tear film every time the eyelid opens. During closure of the eyelid, it is compressed and a small part is continuously renewed. Meibum also has a barrier function against the spillage of tears over the inner border of the eyelid and against the entry of skin lipids (sebum) from the free eyelid margin (Knop and Knop, 2009a; Knop et al, 2009).
Obstructive meibomian gland dysfunction (MGD) is a common source of complaint among patients with dry eye syndrome and its prevalence increases with age. The principal clinical consequence of obstructive MGD is evaporative dry eye syndrome. Moreover, chronic obstruction of the meibomian glands may also result in degeneration of the secretory gland tissue that can lead to a secondary hypo-secretion even if the primary obstruction is later resolved by therapeutic approaches. Risk factors in the pathogenesis of obstructive MGD include age, hormonal disturbances and environmental influences (e.g., contact lenses). Furthermore, qualitative alterations in the composition of the meibum may lead to hyper-keratinization of the ductal epithelium and increased viscosity of the meibum. This can result in obstruction of the duct and orifice leading to a lack of meibum on the eyelid margin and tear film with downstream hyper-evaporative dry eye syndrome. At the same time, obstruction leads to a stasis of meibum inside the meibomian gland with increased pressure and resulting dilatation of the ducts and in atrophy of the acini with rarefaction of the secretory meibocytes and gland dropout. Stasis can also increase the growth of commensal bacteria, their production of oil degrading enzymes and release of toxic mediators. These factors can act as self-enforcing feedback loops that aggravate the primary hyper-keratinization and compositional disturbance of meibum and can hence lead to a progressive MGD (Knop and Knop, 2009b).
Conventional treatments of obstructive MGD entail eyelid hygiene (e.g., lid washing and use of preservative-free artificial tears), omega-3 dietary supplementation (e.g., eicosapentaenoic acid and docosahexaenoic acid), topical antibiotics (e.g., bacitracin and erythromycin), topical corticosteroids, topical cyclosporine, oral antibiotics (e.g., doxycycline, minocycline, and tetracycline), oral omega-6 fatty acids (e.g., linoleic acid and gamma-linolenic acid), as well as unclogging of glands that are blocked, which can be achieved by applying warm compresses to the eyelid or gentle lid massaging (Olson et al, 2003; Romero et al, 2004; Yoo et al, 2005; Perry et al, 2006; Pinna et al, 2007; Souchier et al, 2008; and Foster et al, 2009). Moreover, eyelid-warming devices have also been employed in the treatment of patients with MGD. However, the effectiveness of these devices has not been established
In a prospective, non-comparative, interventional case series, Goto et al (2002) assessed the short term safety and effectiveness of an infra-red warm compression device as treatment for non-inflamed MGD. In a total of 37 cases, subjective symptom scores and subjective face scores improved significantly, from 12.3 to 8.4, and from 7.0 to 5.3. The results for tear evaporation rates during forced blinking, fluorescein staining, rose bengal staining, tear film break up time (BUT), and meibomian gland orifice obstruction score had also improved significantly at the end of the 2-week period of infra-red thermotherapy. The authors concluded that the infra-red warm compression device was safe and effective for the treatment of MGD. Moreover, they noted that while the results were promising, the small sample size and lack of comparison group limit the generalizability of the findings.
In a prospective, controlled, observer masked, single intervention trial, Mitra et al (2005) measured changes in tear film lipid layer thickness (LLT) and ocular comfort in normal subjects after 10 mins use of a novel device, which delivers meibomian therapy with latent heat. A total of 24 normal subjects were randomized into three groups: Group I underwent 10 mins treatment with the activated device, Group II used the inactivated device for the same duration of time, and Group III had no intervention. The LLT of each subject was measured with a Keeler Tearscope prior and subsequent to the 10-min period. Subjective alteration in ocular comfort was also assessed. Seven of 8 subjects (87.5 %) in Group I exhibited an increase in LLT. The mean LLT in this group showed a statistically significant increase compared to Groups II and III. Six of 8 subjects (75 %) using the activated device experienced subjective improvement in ocular comfort.
In a prospective, interventional clinical trial, Matsumoto et al (2006) evaluated the safety and effectiveness of an original warm moist air device on tear functions and ocular surface of patients with simple MGD. A total of 15 patients with simple MGD and 20 healthy volunteers were enrolled in this study. The device was applied to the eyes of the subjects for 10 mins. Temperatures of the eyelids and corneas were measured with an infra-red thermometer. Symptoms of ocular fatigue were scored using visual analog scales (VAS). Schirmer test, tear film BUT, DR-1 tear film lipid layer interferometry, fluorescein staining, and rose bengal staining were also performed before and after the application of the eye steamer. After the initial study, another 2-week, prospective, clinical trial was carried out in 10 patients with MGD who received the warm moist air treatment. Ten other patients were also recruited and received warm compress treatment with hot towels for 2 weeks to evaluate the long-term effects of the warm moist air device and the warm compresses on tear film LLT and ocular surface health. The warm moist air device and the warm compresses were applied for 10 mins twice-daily. The changes in VAS scores for symptoms, tear film BUT values, fluorescein, and rose bengal staining scores were examined before and after each treatment during the second trial. VAS scores of ocular fatigue improved significantly with short- and long-term applications of the warm moist air device in both studies. The mean corneal surface and eyelid temperatures showed significant elevation within safe limits 10 mins after the moist air application. The mean tear film BUT prolonged significantly in patients receiving warm moist air applications but did not change significantly in those treated with warm compresses. DR-1 tear film lipid layer interference showed evidence of lipid expression in the patients and controls, with thickening of the tear film lipid layer after 10 mins of warm moist air device use. In the 2-week trial, tear film LLT increased in both warm moist air device and warm compress groups, with a greater extent of increase in the warm moist air device group. The authors concluded that the use of warm moist air device provided symptomatic relief of ocular fatigue and improvement of tear stability in patients with MGD. The new warm moist air device appears to be a safe and promising alternative in the treatment of MGD.
Korb and Blackie (2011) determined (i) the pressure needed to express the first non-liquid material from non-functional lower lid meibomian glands, (ii) the pressure required to evacuate all of the expressible material from the glands (simulating the authors' methodology for therapeutic meibomian gland expression), and (iii) the level of pain associated with these procedures. All patients (n = 28) were recruited from those presenting for ocular examinations at a single practice. Custom instrumentation exerting pressures from 1.0 to 150.0 psi was developed to quantify the pressure applied during expression. The instrument was applied to the inner surface of the lower lid. The lid was then compressed between the thumb and the contact surface of the instrument. The applied pressure was displayed on a digital meter. The first procedure evaluated the pressure required to obtain the first non-liquid material from non-functional glands. The second evaluated the pressure needed for evacuating all expressible gland contents. The pain response was monitored throughout the procedure. The pressure to obtain the first non-liquid material ranged from 5 to 40 psi (mean of 16.1 +/- 8.2 psi) and for the evacuation of expressible contents, from 10 to 40 psi (mean of 25.6 +/- 11.4 psi). Only 7 % of the patients could tolerate the pressure necessary to administer complete therapeutic expression along the entire lower eyelid. The authors concluded that forces of significant magnitude are needed for therapeutic expression. Pain is the limiting factor for the conduct of this treatment.
In summary, there is currently insufficient evidence to support the use of devices for evacuating meibomian glands by means of heat and intermittent pressure for the treatment of MGD.