6.1.4 identify and manage external pathology Flashcards
What is the DEWS II (Dry Eye Workshop II) definition of dry eye disease?
“Dry eye is a multifactorial disease of the ocular surface characterised by a loss of homeostasis of the tear film, and accompanied by ocular sx, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles”
How does hyperosmolarity of the tears occur and affect the eye?
Loss of homeostasis of the tears and excessive evaporation leads to hyperosmolarity (saltier) tears. This causes direct damage to the ocular surface and indirect damage through the consequent inflammatory cascade (including corneal, conjunctival and goblet cell apoptosis)
How can hyperosmolarity be measured and what is the diagnostic limit?
Equipment such as the Tearlab or i-Pen
Current diagnostic cut off is 308 mOsm/Lb
Why do neurosensory abnormalities occur in dry eye disease?
Repeated physiological stimulation and noxious stimuli- which would be dry eye hyperosmolarity and inflammation, sensitise the corneal nociceptors- the exact role of it in dry eye disease is yet to be explained
What are the classifications of Dry Eye Disease and what is more popular?
- Aqueous-deficient dry eye (ADDE)
- Evaporative dry eye (EDE)
- Mixed type
- Majority is primarily EDE
What is the impact of DED on quality of life (QOL)?
- Pain and irritation
- lower general and ocular well-being
- poorer visual performance
- limits and degrades performance of vision-related activities such as driving- transient blur is experience
- it’s on par with angina
- px with dry eye are 3x more likely to report problems with common activities like using computer
What is the impact on DED on visual performance and infection?
- Marked drop in visual acuity and contrast sensitivity
- High order aberrations
- Increased risk of infection is not quantified in literature but they do rub eyes more so that can increase risk of infection as biotic burden increases in the eye
What is consistent research evidence?
At least one well conducted study that has been published in a peer reviewed journal, along with the existence of a plausible biological rationale and corroborating basic research or clinical data
What is probable/suggestive research evidence?
From inconclusive information from peer reviewed publications or inconclusive or limited information to support the association, but either not published or published somewhere other than in a peer-reviewed journal
What is inconclusive research evidence?
Implies either directly conflicting information in peer-reviewed publications or inconclusive information but with some basis for a biological rationale
What are modifiable risk factors?
They can be changed by making adjustments to lifestyle
What are non-modifiable, consistent/probable/inconclusive risk factors for DED?
What are modifiable, consistent/probable DED risk factors?
What are sx of DED and how accurate are they?
- itching, burning, photophobia or a gritty sensation
- occasionally blurred or smeary vision that clears with a blink
- Aggravated by prolonged visual tasks especially that require concentration
- Local environments also aggravate sx- dusty/smoky/dry environments
- sx improve during rainy or foggy days or high-humidity environments like the shower
- sx are reliable and repeatable measures of DED
What different questionnaires are there for investigating sx of DED and what are they for?
Screening-McMonnies Questionnaire
Monitoring- Ocular Surface Disease Index (OSDI)
Reporting habitual sx- Dry Eye Questionnaire (DEQ)
Screening in contact lens wear- Contact Lens Dry Eye Questionnaire (CLDEQ)
Current DEWS II recommends that OSDI (12 questions with grading on a scale) or DEQ-5 (5 questions, >5 score suggests DED) is used to diagnose and monitor DED
What key questions would you ask someone if suspecting DED?
Medication, lifestyle, smoking, environment
Exclude Sjogren’s syndrome
How does Sjogren’s syndrome affect DED and the body?
It is an aqueous deficiency of tear film
- true dry eye
- autoimmune disease- associated with joint problems and dry mouth, salivary problems
- exocrine glands in body affected
How can the McMonnies Questionnaire be used in practice?
14 questions, but only 3 questions can give accurate diagnosis of dry eye and has same use as of the whole questionnaire
- How often do your eyes have sx of dryness?
- How often do your eyes have sx of scratchiness?
- Are your eyes uncomfortable in a smoky atmosphere?
Answer: Never, sometimes, often, constantly
What are the current DEWSII recommendations in using tools to monitor and diagnose DED?
OSDI or DEQ-5
How can the DEQ-5 be used in practice and how does it suggest dry eye?
It has a short length and discriminative ability. It is 5 questions and a score of 6 or above suggests DED
What are px signs of dry eye and how do you check?
Blink rate- full/partial, should be 12 per min
Ocular adnexa- check skin tone to signs of acne or ocular manifestations of rosacea (can be associated with MGD)- consider co-management with dermatologist or GP
Eyelids and lashes- check for trichiasis/entropian/ectropian/epiblepharon, MGD is found in over 65% of people with dry eye known to have lipid layer abnormalities. Check for crusting, thickened lid margin (tylosis), lid margin redness (erythema), dilated veins on lid margin (telangiectasia), lid notching, foamy tears and gland orifice obstruction
What clinical tests can you do to check for dry eye?
Non-invasive TBUT first: keratometer (3mm mires where it is placed-not great as tbut tends to be inferior quadrant)/topographer/tearscope/slit lamp view of tear film using white light (specular reflection)
Invasive TBUT- Sodium Fluorescein and lissamine green exam
Tear quality check- debris, foaming, lipid pattern- the more colourful the thicker the lipid layer (open/closed meshwork, wave (flow), amorphous, colour fringes, globular), meniscus height, mucous strands
Ocular surface friction- Lid parallel conjunctival folds (LIPCOF) seen with 20 mag slit lamp and white light, more temporal- grade it 0=none, 1= 1 permanent and clear parallel fold, 2=2 permanent and clear parallel folds (normally <0.2mm) 3=more than 2 permanent and clear parallel folds (normally 0.2mm). Lid Wiper Epitheliopathy (LWE) reveals trauma to the lid wiper from a thinned or unstable tear film- lissamine green stains the lid wiper horizontally- 80% of cl wearers with dryness sx will show staining- grade it horizontal length of staining: 0= <2mm, 1= 2-4mm, 2= 5-9mm, 3= >10mm, saggital length of staining: 0= <25% of the lid wiper, 1= 25-50% of the lid wiper, 2= 50-<75% of the lid wiper, 3= >=75% of the lid wiper
Redness- bulbar and palpebral (inflammatory action in process in irritated eye)
Tear film osmolarity- specialist equipment like tear lab that takes 0.5 microl sample from meniscus to analyse
How well does tear film correlate with dry eye sx and what does correlate well, what future things might better predict?
sx do not correlate well with signs of tear film
Best predictors to date are sx and corneal staining for normal and for cl wearers: tear film stability and signs of friction
osmolarity is good but not practical in practice, tear film pH (more acidic in dry eye),
Future:
Tear protein tests (inflammatory markers from lacrimal gland and ocular surface- lactoferrin and lysozyme)
Cytokine tests (measures inflammatory response)
Tear ferning- ‘dried- out’ tear samples to show electrolyte crystals
Interferometry- sophisticated enhancement of tearscope
What is the DEWS II diagnostic methodology to sift out conditions that mimic DED?
If DED suspected- the px should be given OSDI or DEQ-5 questionnaire- if this suggests DED, a detailed clinical exam should be conducted to detect a loss of homeostasis (as DEWS II report states:
- non invasive test or BUT or if unavailable with fluorescein
- if possible osmolarity should be checked and any elevation (>= 308 Osm/L or marked intraocular difference (>8mOsm/L suggests DED
- surface staining checked with fluorescein and Lissamine Green >5 corneal punctate spots >9 conjunctival spots and lid wiper staining >=2mm length and 25% of the sagittal width are diagnostic
- DED should be sub-classified along ADDE/EDE spectrumby examining lids for MGD and expressing meibum (and/or use meibography and lipid interferometry
- tear meniscus height hints at tear volume- normal is 0.3mm
How does the tear film relate to the eye, what are the layers and what glands secrete them, how does the DEWS II challenge this?
mucous layer- conjunctival goblet cells
aqueous layer- lacrimal gland
lipid layer- meibomian gland
DEWS II says the tear film might be a complex blended 2 layer structure of mucoaqueous and an outer lipid layer
What is the pathology of dry eye and the cause?
Hyperosmolarity causes the cells on the surface of the eye to be damaged=inflammation and loss of goblet cells and microvilli
What is the purpose of microvilli with regards to the tear film?
microvilli are microscopic protrusions of the cells on the ocular surface, these act as a support for the glycocalyx which is a matrix of large molecules (glycoproteins- mucins) that helps to retain fluid across the surface of the eye and prevent infection
What is the vicious cycle of DED?
What are the steps to managing dry eye in practice, once a problem with tear film is identified?
- Address the cause: if medication related-liase with GP although unlikely to change unless severe DED. Contact lens induced dry eye can be resolved by changing wear schedule, different cleaning and disinfection or changing lens material/type
- Restore the tear volume: use supplementary eye lubricants/punctal plugs
- Soothe the ocular surface: eye drops with properties to encourage the cells to regenerate and reduce any ocular surface staining
- Restore the osmolarity: therapeutic measures
- Soothe the sx: artificial tears: eye drops, gels and ointments
- Diet and lifestyle advice: change habits to avoid situations where the eye may become exposed to a dry atmosphere, modify their diet to facilitate a better quality
What causes MGD?
terminal duct obstruction due to hyperkeratinisation of the ductal epithelium, keratinised cell debris and increased meibum viscosity
Why does warmth improve MGD?
Obstructive MGD melting point of lipid increases from 32 to 35 degrees Celsius. Heat increases blood flow and melts waxy meibum so the flow of the secretion from the gland increases
How can MGD be managed?
Warm compress- 45 degrees for a minimum 6 mins- poor compliance
Warm goggles- worn for 10 mins (Blephasteam by Thea Pharmaceuticals)
Lid hygiene- wipes and solutions for lid hygiene and may be more compliant that diluted baby shampoo but College of Optometrists says there is insufficient evidens of comparitive efficacy of various lid hygiene regimes
What ingredients/products are good to improve DED?
Hospitals often give Hypromellose which is for mild dry eye and initially needs to be instilled every hour for sx relief and then at a reduced frequency
Carbomers and polyvinyl alcohol are highly viscous and application can be reduced to up to 4 times a day
Preservative free preferred in cases of frequent and chronic application to minimise preservative induced toxicity
Ocular lubricants with sodium hyaluronate, hydroxypropyl guar or carmellose sodium are for moderate to severe dry eye (can be used following a 6-8 week treatment for mild dry eye)
Eye ointments with paraffin can be used additionally to lubricate especially where there are recurrent epithelial erosions- best suited before sleep- not with cl wear
Theratears- hypotonic solution to restore electrolyte balance
Optrex actimist- lyposomal sprays where lipid migrates to lid margin after spray to restore lipid layer and reduce evaporation
Celluvisc/Rohto drops-mimis mucin layer
Systane-preservative free (inflamed eye may be provoked with preservatives), adds volume and stability
Liquifilm- Benzalkonium Chloride plus EDTA
What diet and life advice can be given for px with DED?
- omega 3 and 6 should be low (1:2.3)
- omega 3 supplements
- antioxidants improve signs but not sx of dry eye (e.g. vitamin A/C/E with zinc and selenium)
- improving hydration to improve sx doesn’t have enough research to assess efficacy and safety
How does omega 3 improve DED?
omega 3 blocks expression of pro-inflammatory proteins so decreases cell death in the lacrimal gland and ocular surface and also useful in treating blepharitis
meibomian glands appear to use omega 3 fatty acids in their physiology
people on blood thinners like Heperin/Warfarin and anyone with cardiovascular condition/diabetes/risk of stroke should consult with GP before modifying diet
What is paradoxical dry eye?
Dry eye with sx burning and irritation but eyes are very watery (epiphora)- tears that drain too quickly or are too aqueous= wrong environment for ocular surface=irritation and inflammation
evert top lid
check nasolacrimal obstruction
check apposition of lower eyelid to globe (ectropian)
punctum plug in the past
trauma? nasal surger? lumps/bumps?
paradoxical reflex tearing from dry eye
How to asess the lacrimal drainage system?
Palpate lacrimal sac to see if enlarged: pain suggest dacryocystitis, check for pus
Fluorescein Dye Disappearance Test (FDDT): Instil equal amounts of NaFl, wait 5 mins, compare tear meniscus ht and degree of overspill, should disappear in 2 minutes for most people- should be symmetrical response for both eyes
Primary Jones test- instil 1 drop of NaFl, put a cotton bud soaked in anaesthetic in inferior meatus (up the nose), positive result means open to some degree
What is the anatomy of the lacrimal drainage system?
Give a rough summary of dry eye assessment routine?
- Assess sx
- Check VA stability- before and after blink (consider contrast sensitivity)
- Grade bulbal redness and LIPCOF
- Grade lid margins, MGD and blepharitis
- Examine the punctae and tear prism (plus examine tear film production)
- Examine tear quality and stability
- Fluorescein staining of the cornea
- Fluorscein TBUT
- Lissamine green staining of the conjunctiva ( apply a lot- 2 drops and wait 60secs and examine with moderate, white light)
- Examine lid wiper (Lissamine green) for signs of friction
- Decide on management
Give a rough summary of dry eye assessment routine?
- Assess sx
- Check VA stability- before and after blink (consider contrast sensitivity)
- Grade bulbal redness and LIPCOF
- Grade lid margins, MGD and blepharitis
- Examine the punctae and tear prism (plus examine tear film production)
- Examine tear quality and stability
- Fluorescein staining of the cornea
- Fluorscein TBUT
- Lissamine green staining of the conjunctiva ( apply a lot- 2 drops and wait 60secs and examine with moderate, white light)
- Examine lid wiper (Lissamine green) for signs of friction
- Decide on management
