A Systematic Approach to Dry Eye using LipiFlow Treatment

2014 ◽  
Vol 07 (02) ◽  
pp. 104 ◽  
Author(s):  
Mitchell A Jackson ◽  

The complex strategy to understanding dry eye syndrome has led to a widespread change in approaching this condition as an ocular surface disease, stratified as evaporative dry eye, aqueous deficient dry eye, and ocular allergy. The diagnostic armamentarium has vastly expanded to include tear osmolarity and inflammatory markers as redefined by the new International Dry Eye WorkShop (DEWS) in 2007. The Tear Film & Ocular Surface Society (TFOS) panel on meibomian gland dysfunction (MGD) further expanded the interpretation of evaporative dry eye and its therapeutic options, including the newest US Food and Drug Administration (FDA)-approved device known as LipiFlow Thermal Pulsation System. This paper will give an overview on understanding dry eye disease, its etiology, diagnostic methods, and current therapeutic options.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ricaurte Ramiro Crespo-Treviño ◽  
Anna Karen Salinas-Sánchez ◽  
Francisco Amparo ◽  
Manuel Garza-Leon

AbstractMany recent studies have showed that morphological changes are one of the key signs of meibomian gland disease (MGD). These changes can be seen even before symptom onset, potentially underestimating the prevalence of MGD; however, until now, there is no conclusive information about the impact of meibomian gland (MG) morphology in tear film physiology and disease. This study aimed to investigate the prevalence of anatomical and morphological MG alterations between patients with evaporative dry eye disease (DED) and healthy controls. Retrospective chart review of seventy-five patients with evaporative DED and healthy individuals who had dry eye assessments included Ocular Surface Disease Index questionnaire, meibum quality, meibum expressibility, lid margin abnormality, ocular staining, non-invasive tear film break-up time, and meibography. We did not find significant differences in MG alterations in the upper lid between healthy and DED subjects. Patients with evaporative DED presented MG alterations in the lower lid more frequently than healthy subjects (54.8 vs. 30.3%; p = 0.03). The presence of shortened glands was the only MG alteration that was more prevalent in the lower lid in dry-eye patients than in healthy subjects (p < 0.05). Subjects with evaporative DED presented more alterations in the lower lid than healthy subjects.


2019 ◽  
Vol 35 (1) ◽  
Author(s):  
Sameera Irfan

Dry eyes is a common, chronic condition that has a prevalence of about 5- 50%.1 According to the Dry Eye Workshop II report (DEWS II report), published in 2017, the updated definition of Dry Eye Disease is, “a multifactorial disease of the ocular surface characterised by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyper-osmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles.” The Tear Film & Ocular Surface Society (TFOS) released their report on the international work on Meibomian Gland Dysfunction (MGD)2 in 2011, which defined MGD, classified it and considered it as the primary cause of dry eye disease worldwide. Previously dry eye disease was considered as an aqueous deficiency problem, but after this report by TFOS, there is a paradigm shift towards “not producing enough lipids to retain the tears that are being produced”. This has led to a huge impact on the treatment protocols which were previously focused on managing the sequelae and symptoms of dry eyes rather than targeting directly on the underlying cause, the MGD. It has now been accepted worldwide that dry eye occurs when the ocular surface system cannot adequately protect itself from the desiccating stress due to the lack of a healthy meibomian gland secretion. This article is mainly focussed on the Meibomian Gland Dysfunction, discussing the normal anatomy of the glands, how they are affected by disease, its implications on the ocular surface and finally, the various treatment strategies. Key words: Blepharitis, Dry eyes, Meibomian gland dysfunction, blepharospasm.


2021 ◽  
Vol 10 (19) ◽  
pp. 1382-1386
Author(s):  
Swapneel Mathurkar ◽  
Sachin Daigavane ◽  
Madhumita Prasad ◽  
Kervi Mehta

BACKGROUND Meibomian gland dysfunction (MGD) is one of the causes of evaporative dry eye disease. It is the terminal duct obstruction of the Meibomian gland and is associated with glandular secretion changes. These changes lead to decreased amount of lipids secretion which accounts for instability of tear film leading to evaporative dry eye disease. Chronic smoking also causes irritative, burning eyes along with unstable tear film. We wanted to study the corelation of chronic smoking with Meibomian gland dysfunction. METHODS This is a hospital based observational cross-sectional study that enrolled a total of 100 subjects having Meibomian gland disease (MGD), out of whom 61 were smokers and 39 were non-smokers. All enrolled subjects underwent tear film breakup time (TBUT), Schirmer I test (SIT) and slit-lamp microscope examination of lid margin abnormalities, Meibomian gland expression as well as meibum. RESULTS Our study found that the patients with Meibomian gland dysfunction with the history of chronic smoking had a remarkably decreased value of tear film break up time (TBUT), Schirmer’s 1 Test which explains the dry eye symptoms as compared to MGD patients without smoking. No significant differences were seen in lid margin irregularity and meibum secretion. Meibomitis is found in 29 smokers with MGD and 5 non-smokers with MGD which is not significant. CONCLUSIONS Chronic smoking is associated with MGD. KEY WORDS Cigarette Smoking, Meibomian Gland Dysfunction, Tear Film Tests


2018 ◽  
Vol 103 (1) ◽  
pp. 119-124 ◽  
Author(s):  
Erlend Christoffer Sommer Landsend ◽  
Hilde Røgeberg Pedersen ◽  
Øygunn Aass Utheim ◽  
Jiaxin Xiao ◽  
Muhammed Yasin Adil ◽  
...  

AimsTo investigate the aetiology and characteristics of dry eye disease (DED) in a Nordic cohort of patients with congenital aniridia.MethodsThirty-four Norwegian and one Danish subject with congenital aniridia and 21 healthy controls were examined. All subjects underwent an extensive dry eye examination, including evaluation of meibomian glands (MGs) by meibography, measurement of tear production and tear film osmolarity and grading of vital staining of the ocular surface. Moreover, slit-lamp biomicroscopy was undertaken, including grading of aniridia-associated keratopathy (AAK).ResultsMean tear film osmolarity was significantly higher (314±11 mOsmol/L) in patients with aniridia compared with the healthy control group (303±11 mOsmol/L, p=0.002). Vital staining score was higher in the aniridia group (4.3±3.0) compared with healthy controls (2.4±1.6, p=0.02). The degree of staining correlated positively with the stage of AAK (r=0.44, p=0.008) and negatively with corneal sensitivity (r=−0.45, p=0.012). Number of expressible MGs was lower in aniridia subjects (2.9±1.6) than in controls (4.0±1.3, p=0.007). MG loss, staged from 0 to 3, was higher in the aniridia group than in the control group, both in upper eyelid (0.86±0.89 vs 0.10±0.31, p=0.001) and lower eyelid (0.94±0.73 vs 0.30±0.47, p=0.003). Computerised analyses showed thinning (p=0.004) and lower density (p<0.001) of the MGs compared with the healthy population.ConclusionsPatients with congenital aniridia demonstrate increased tear film osmolarity, ocular surface staining, loss of MGs and lower MG expressibility. We conclude that meibomian gland dysfunction and keratopathy are related to development of DED in aniridia.


2021 ◽  
Vol 22 (1) ◽  
pp. 422
Author(s):  
Ming-Tse Kuo ◽  
Po-Chiung Fang ◽  
Shu-Fang Kuo ◽  
Alexander Chen ◽  
Yu-Ting Huang

Most studies about dry eye disease (DED) chose unilateral eye for investigation and drew conclusions based on monocular results, whereas most studies involving tear proteomics were based on the results of pooling tears from a group of DED patients. Patients with DED were consecutively enrolled for binocular clinical tests, tear biochemical markers of DED, and tear proteome. We found that bilateral eyes of DED patients may have similar but different ocular surface performance and tear proteome. Most ocular surface homeostatic markers and tear biomarkers were not significantly different in the bilateral eyes of DED subjects, and most clinical parameters and tear biomarkers were correlated significantly between bilateral eyes. However, discrepant binocular presentation in the markers of ocular surface homeostasis and the associations with tear proteins suggested that one eye’s performance cannot represent that of the other eye or both eyes. Therefore, in studies for elucidating tear film homeostasis of DED, we may lose some important messages hidden in the fellow eye if we collected clinical and proteomic data only from a unilateral eye. For mechanistic studies, it is recommended that researchers collect tear samples from the eye with more severe DED under sensitive criteria for identifying the more severe eye and evaluating the tear biochemical and proteomic markers with binocular concordance drawn in prior binocular studies.


Author(s):  
Vidya K. Sudarshan ◽  
Joel E. W. Koh ◽  
U. Rajendra Acharya ◽  
Jen Hong Tan ◽  
Muthu Rama Krishnan Mookiah ◽  
...  

2019 ◽  
Vol 103 (10) ◽  
pp. 1475-1480 ◽  
Author(s):  
Marc Labetoulle ◽  
Tristan Bourcier ◽  
Serge Doan

Background/aimsDry eye disease (DED) is categorised by pathophysiology as aqueous deficient dry eye (ADDE), evaporative dry eye (EDE) or mixed. Treatment should be tailored to DED pathophysiology, but this is challenging to determine. This Delphi consultation aimed to categorise and weight signs and symptoms to help identify the evaporative or aqueous deficient DED origin.MethodsA panel of French DED experts created an initial list of 77 DED signs and symptoms. In a Delphi consultation, experts categorised items by DED pathophysiology. Likert scoring was used to indicate whether items were strongly or moderately indicative of ADDE or EDE. Items could also be judged non-applicable to DED, with the opportunity to suggest alternative diagnoses.ResultsExperts attributed 19 items (of which 11 were strongly indicative) to a pathophysiology of EDE and 12 items (of which four were strongly indicative) to ADDE. Items scored strongly indicative with agreement >90% for EDE were previous chalazia, rosacea/rhinophyma, telangiectasias of eyelid margin and thick non-expressible meibomian gland secretions, and for ADDE were Sjögren syndrome or associated disease, and Schirmer <5 mm after 5 min (without anaesthesia). Seventeen items indicated neither pathophysiology and 18 items were found to be suggestive of alternative diagnoses.ConclusionsThis Delphi consultation categorised signs and symptoms, using an innovative weighting system to identify DED pathophysiology. An algorithm integrating the weighting of each sign and symptom of an individual patient would be valuable to help general ophthalmologists to classify the DED subtype and tailor treatment to DED underlying mechanism.


2019 ◽  
Vol 17 ◽  
pp. 205873921881868
Author(s):  
Limei Liu ◽  
Dongdong Wei ◽  
Hongkun Xu ◽  
Changhui Liu

To study the effects of apigenin on dry eye disease (DED) in rats. Rats were divided into six groups: (I) normal control group, (II) DED control group, (III) vehicle control group, (IV) DED + apigenin 10 mg/kg, (V) DED + apigenin 20 mg/kg, and (VI) DED + apigenin 50 mg/kg. Schirmer test, tear film break-up time (BUT), and corneal fluorescein staining were used to evaluate the effects of apigenin on the ocular surface. The related inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Histopathological examination and inflammatory index were also performed. The results showed that administration of apigenin was shown a significant effect on the recovery of ocular surface function. Compared to the control group, apigenin treatment in DED rats significantly decreased the level of the tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6); however, the interleukin-10 (IL-10) level was increased. Histopathological examination further verified the anti-inflammatory effects of apigenin on DED rats. The results demonstrated that apigenin could protect DED rats via inhibition of inflammation, suggesting that it may have potential as a therapy for DED.


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