Title: Keeping Step with DEWS2: Clinical Applications Lecturer: Scott G. Hauswirth, OD

Transcription

1 Title: Keeping Step with DEWS2: Clinical Applications Lecturer: Scott G. Hauswirth, OD Course Description: The Dry Eye Workshop 2 was an assemblage of experts in dry eye disease from around the world, and gives the most comprehensive overview of our current knowledge of dry eye disease. This lecture attempts to distill the key features of this publication, highlighting new areas of knowledge relevant to the practicing clinician. Course Objectives: 1) To review the clinically relevant adjustments of the DEWS2 committee findings from previous findings 2) To apply the basic clinical flow algorithm to today s optometric practice 3) To review the implications of this new information on treatment methods for dry eye patients Outline I. Dry Eye Workshop II: The publication a. Structure i. Definition/classification ii. Sex, gender, and hormones iii. Epidemiology iv. Tear film v. Pain and sensation vi. Pathophysiology vii. Iatrogenic viii. Diagnostic methodology ix. Management and therapy x. Clinical trial design b. Significant input from optometry i. Over ten ODs listed as contributors and committee members; many more nominated c. Definition i. 2007: Dry eye is a multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface. ii. 2017: Dry eye is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles. iii. Revised Classification Scheme

2 1. Description of schematic 2. Flow pathways 3. Other issues not mentioned d. Pathophysiology i. Key elements in understanding pathophysiology 1. Homeostasis as central concept 2. Compensatory mechanisms a. Basal tear secretions b. Blink mechanism c. Reflexive secretions d. Activation of resident immune cells i. Leads to multiple secondary effects, especially with increased chronicity ii. Critical piece to understanding conversion from acute response to chronic response e. Neural upregulation i. May also be tied to immune upregulation 3. Disruptive influences a. Evaporative stress i. Primary driving factor ii. Caused by: 1. Inadequate mechanics (blink, exposure) 2. Harsh environment (wind, low humidity) 3. Alteration of meibum a. Dietary influences b. Neuronal influences c. Hormonal influences d. Alteration of temperature/blood flow e. unknown b. Hyperosmolarity i. Cannot occur without some level of evaporation ii. Cell membrane receptors detect increased osmo and instigate c. Engagement of immune system i. May occur as one of primary driving mechanisms(ai disease) ii. Beginning in corneal epithelium iii. Leads to damage of cells and loss of integrity 1. Decreased glycocalyx 2. Decreased epithelial barrier 3. Decreased concentration of goblet cells 4. Decreased secretory function (lacrimal) 5. Damage to neurosensory unit

3 d. Disruption of neurosensory network i. Cornea most richly innervated tissue in body ii. No Schwann cell support in epithelium 1. Role is taken up by epithelial cells 2. Underscores importance of maintaining epithelial health iii. Is likely the crux of disconnect signs- symptoms iv. Is also primary regulatory mechanism in secretion e. Testing i. Testing done in order from least to most invasive ii. Relevant tests in clinical practice 1. Questionnaire quantification of symtpoms 2. Eyelids a. Anterior blepharitis b. Posterior LWE i. Instillation of lissamine ii. Grading scale c. Meibography d. MGYLS e. Blink/closure analysis 3. Conjunctiva a. Integrity staining b. Hyperemia c. Alterations of normal structure i. Pinguecula ii. Lid parallel conjunctival folds iii. Conjunctivochalasis d. Impression cytology e. Confocal imaging 4. Cornea a. Integrity staining b. Sensitivity esthesiometry c. Alterations of normal structure i. ABMD ii. Salzmann s nodules iii. Scarring iv. Other d. Confocal microscopy 5. Tear Film Aspects a. TBUT stability (+/- NaFl) b. Osmolarity c. Lipid layer thickness d. Volume i. Basal tear secretion

4 ii. Reflex tear secretion iii. Meniscus height e. Thermography f. Tear ferning g. Other compositional assays i. MMP- 9 ii. T- lymphocytes 6. Summary Test Battery a. DEQ- 5 b. TBUT/Osmo/Stain c. Subtype classification d. Grading based on subtype II. Treatment a. Tears and Tear substitutes i. Artificial tears the good, bad, and ugly ii. Serum tears autologous vs. allogenic iii. Umbilical cord serum iv. Platelet- rich plasma (PRP) b. Punctal occlusion c. Moisture chamber d. Tear stimulation i. Secretogogues ii. Neurostimulation e. Anterior blepharitis - eyelid hygiene f. MGD i. Lubricants ii. Warm compress iii. Lid margin debridement iv. Manual expression v. LipiFlow vi. IPL vii. Intraductal probing g. Blinking mechanics h. Contact lens therapies i. Pharmaceutical treatments i. Antiinflammatories 1. Corticosteroids 2. Cyclosporine A 3. Lifitigrast 4. Tetracyclines 5. Macrolides ii. Biologics j. Other therapies

5 III. How does this change our approach? a. Streamlines testing, in algorithmic approach b. Underscores the importance of inflammatory control c. Allows us to engage patients earlier, in more standardized way d. Minimal tools needed