20/20 isn’t everything: See why every child MUST have a comprehensive eye exam to prepare for school

17 10 2013

Dr. Richard Maharaj and Dr. Chris Schell demonstrate some common vision problems that children struggle with everyday in the classroom. A very important message on why comprehensive eye examinations (not a vision screening) must happen for each child prior to (or at the very least, as soon as possible) school age. Vision screenings are well-intentioned, but as shown in the video, may miss these subtle diagnoses and give parents a false sense of security. Their little eyes are starting a 12+ year marathon which will serve the basis of learning.  You wouldn’t run a real marathon without preparing your muscles and endurance would you?  Why do we assume newly developing eyes should be treated with less concern or preparation.  See a Doctor of Optometry for a comprehensive eye examination.

Putting Pressure on the Eyelid: Glaucomatous Lid Disease

4 01 2013

Chronic Disease – A burden that many of our patients carry.  Curing a condition isn’t nearly as common as managing it however eye physicians shouldn’t lose sight of the bigger picture.    Treating glaucoma, a common ocular chronic disease, has evolved into more then IOP measurement with a Schiotz tonometer and measuring cup/disc ratios with a direct ophthalmoscope.  We monitor visual field progression, RNFL loss, structure function maps, and even multifocal-ERG may hold a promise in managing this neuropathy.  All this even though the only factor we are able to modify is IOP.  Interestingly, in the race to reduce the medicinal load on our patients, we have inadvertently been accelerating damage to the lid surface – most specifically the line of Marx (LOM), meibomian gland orifice (MGO) and acini (MGA).

A recent study at  University G d’Annunzio of Chieti-Pescara, in  Chieti, Italy, in vivo laser scanning confocal microscopy was used to reveal morphological changes to the MG in patients being treated for glaucoma compared to a control group.  Specifically the eyelid margin epithelial cell density, mean acinar density (MAD) and area (MAA), glandular orifice area, secretion reflectivity and non-homogeneous appearance of interstice and acinar wall were observed in these groups.

Patients that were on 2 or more drugs had the greatest morphological changes to the lid surface, specifically preserved prostaglandin analogues (PGA).  There was a reduced burden on preservative-free PGA, however a measurable difference between preserved and non-preserved beta-blockers was not observed.

Glaucoma and the lid surface

The reason this small study stands out is simply the co-morbidity that exists in this clinical subset of patients.  It is widely accepted that PGA offers a more convenient delivery model to our patients which leads to increased compliance, however are we just accepting their ocular surface disease as a necessary evil?  Managing the lid surface in this group can make a significant impact on their quality of life and daily comfort which may in turn increase their compliance with chronic topical therapy.  The picture above is a glaucoma patient where the diagnostic picture of glaucoma was obvious, but when looking at the lid surface it was even more obvious why he was markedly non-compliant.  He had a deteriorating lid surface noted by an anteriorly thickened LOM and moderate MGD.  His non-compliance resulted in accelerated glaucomatous neuropathy over the course of the year.   To properly manage the lids, he underwent LipiFlow thermal pulsation OU and is now enrolled in an ocular surface disease program with specific attention to the lid surface (LOM) every 3 months (top/below picture is before and after lid management respectively).  Since then, his compliance with topical glaucoma therapy has increased and RNFL thinning and field loss is statistically reduced.

Target IOP is just one facet of managing this disease and in the race to achieve this target, the lid surface may get left behind.  I see this in my practice every day – patients frustrated  by glaucoma.  When a probing history is taken though, these patients aren’t bothered by their field loss; in fact most early to moderate cases are asymptomatic.  Their symptoms are secondary to the treatment and often times patients feel the doctor is responsible for making their eyes worse.  I routinely enroll glaucoma patients in an ocular surface program and anecdotal evidence suggests these patients are happier and stable.  With the nuances involved in being a glaucoma patient from doctor visits to cost of drops to accepting the disease itself, being happier about it can make the long road pleasant.

1. AGNIFILI L, Fasanella V, Costagliola C, Ciabattoni C, et al. In vivo 
confocal microscopy of meibomian glands in glaucoma. Br J Ophthalmol. 2012.

Dr. Richard Maharaj OD FAAO


twitter: @eyelabsinc

Is ‘Standard’ of care enough? AMD through the lens of Fundus Autofluorescence

6 11 2012

In optometric practice, the AMD demographic is rising as the baby-boomers balloon the aging population. AMD being the complex condition it is requires a comprehensive evaluation of all factors involved from the patient’s family and medical history all the way to the metabolic functioning of the basal layer of RPE cells. Ophthalmological evaluation in addition to visual functioning has been the gold standard of care until the emergence of in vivo dissection techniques offered by optical coherence tomography. OCT has opened the doorway to allowing primary care providers with the ability to decipher the need for tertiary intervention. In the vast majority of AMD patients that fall into the dry category, management of these patients can be scrutinized down to a metabolic level. Current understanding of the disease as an inflammatory condition has opened a new realm of pharmaceutical development that targets inflammatory precursors to prevent further degradation. The ENVISION CLARITY trial, for example, involves a vision cycle modulator (VCM) called acu-4429 which inhibits the disproportionate accumulation of A2-E in the post-mitotic RPE .  In pursuit of new therapies for diseases like AMD, the landscape of eye care is changing below our feet.

A 'normal' digital fundus image

A ‘normal’ digital fundus image

Fundus Autofluorescence of the same eye

Fundus Autofluorescence of the same eye revealing moderate AMD

… when the common denominator dictates what practitioners should and should not do, this actually reduces the standard of care to, arguably, a lower calibre of care

Dry AMD or non-exudative AMD has been reported to make up some 85-90% of AMD, the remainder being comprised of the exudative form. In recent years, research has pointed to disregulation of local inflammatory factors as the main contributor to AMD. AMD is known as a polygenic disease giving each individual multiple sequences to increase the risk of developing the condition.

Considering the inflammatory role of the disease, the metabolism of the RPE becomes an important indicator of local tissue health; specifically the accumulation of lipofuscin as a by-product of the RPE. Fundus autoflurescence (FAF) can therefore demonstrate the concentration and distribution of associated lipofuscin which correlates to the condition of the RPE in AMD patients . A dark area or hypofluoresced area demarks atrophic RPE as the major fluorophore is absent in this area. Hypo areas may also be a result of overlying haemorrhagic changes, increased melanotic tissue and the presence of subretinal fluid.

Hypo and hyperfluoresced areas in FAF can migrate from one to the next, depending on the local state of the tissue. Pigment epithelial and neurosensory detachment and areas with extracellular fluid accumulation associated with exudative lesions can be observed in FAF as increased or decreased signal. Fluid accumulation under pigment epithelium detachment, extracellular deposition of material under the RPE (drusen), and fluid originated from CNV can occur with increased, normal or decreased FAF intensity . It is always important to rely on multiple modalities of imaging to correlate FAF findings.

Once the advanced state of the disease is confirmed, a risk assessment results in the need for intervention. AREDS, a widely accepted study, looked at the natural history of AMD and also studied the modified risk of a specific pharmacological dose of nutritional supplements on the progression to advanced forms of AMD. The findings suggested that a combination dose of zinc, copper, Vitamin C, E and beta-carotene resulted in a risk reduction of 25% of disease progression and a 19% risk reduction of moderate vision loss (defined by ETDRS) over 5 years.

AREDS 2, which will be completed by 2013 was undertaken to extend the risk reduction protocol to include omega 3 (DHA and EPA) in addition to lutein and zeathanthin . Also, the question of whether beta-carotene should be included is being assessed as studies have shown that beta-carotene used with vitamin E in smokers has statistically significant risk of developing lung cancer. Although results haven’t been released, pharmaceutical companies have released versions of these supplements consistent with AREDS 2 to include both the omega-3 and lutein and zeathanthin (10mg lutein/2mg zeaxanthin and 350mg DHA/650mg EPA).

The availability of technologies like FAF will make them integral components of primary eye care. New therapeutics will only be as effective as the technology quantifying its efficacy by means of measuring the metabolic state of the retina.  Current discussions in all clinical practices revolve around standards of care and how clinicians can rise to that standard. One question that arises:  is a standard enough?  Is common ground the best way to drive health care decisions? Establishing a standard requires common agreement of the majority of a spectrum of clinicians based on current evidence and available tools. However in this scenario when the common denominator dictates what practitioners should and should not do, this actually reduces the standard of care to, arguably, a lower calibre of care. Individual standards give the practitioner the opportunity to think outside the box and truly reach a higher calibre of care.

Dr. Richard Maharaj OD, FAAO