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Report

Super Sunday lives up to its name

07/05/2018By Lewis Williams PhD
It may have been hosted in a new venue, but OA NSW/ACT’s premier conference still possessed the detailed insights and clinical information that has made it one of the largest optometric events on the calendar. LEWIS WILLIAMS reports.

This year’s Super Sunday conference, held for the first time at the Big Top at Sydney’s Luna Park, attracted about 500 delegates, easily equalling past attendance figures.

As per previous practice, the program was run as two parallel streams with the exception of the keynote address by ophthalmologist Dr Anthony Maloof, which was delivered to all delegates at midday. The MC for the event was OA NSW/ACT CEO Mr Andrew McKinnon.

Medical emergencies in optometric practice

Returning Super Sunday presenter Dr Julie Kiel opened the Stream 1 program with a lecture on medical emergencies that might occur in routine optometric practice. Originally an optometrist and an optometry academic herself, Kiel is now an emergency medicine specialist based at both the St George Hospital and The Children’s Hospital at Westmead.

Using case reports as the vehicle for her presentation, Kiel opened with a 65-year-old overweight male with a number of common ailments – Type 1 diabetes, hypertension, and hypercholesterolaemia. After walking some 100 metres from his car to the practice, the patient arrived appearing pale and sweaty, while clutching his chest and complaining of pain.

While not pathognomonic of a heart attack, chest pains are suggestive of just that and the sexes are affected equally. Discomfort or pain in the chest, arms, neck, or back should raise suspicion of an acute myocardial infarction (AMI) – better known as a heart attack.

Kiel’s advice was to get the patient to sit down promptly and rest, and then call an ambulance. She presented a flow sheet of symptoms, body locations, and subjective feelings that are suggestive of an AMI, and presented Australian figures that showed 55,000 AMIs per year (one every 10 minutes), resulting in 9,000 deaths (about one per hour). Unfortunately, the survival rate for out-of-hospital AMIs is low.

Next, Kiel detailed the pathophysiology of a heart attack, beginning with the build-up of plaque inside a cardiac blood vessel, its rupturing subsequently, followed by a blood clot forming at the site. This then leads to local ischaemia and cardiac muscle incompetence, and it is the ischaemia that causes the pain reported. The worst-case scenario involves vessels servicing the left ventricle as it pumps the most blood.


"In cases where diabetics become less responsive or unresponsive during a consultation, the episode was unlikely to be due to hyperglycaemia as passing out is uncommon."
Dr Julie Kiel, emergency medicine specialist

Kiel then moved on to current thinking on CPR. Although mouth-to-mouth resuscitation can be performed, it is not essential. However, CPR itself is considered vital for all unresponsive/non-breathing cases and interruptions to the procedure must be minimised. Importantly, the rate of CPR compressions is now 100–120 per minute.

The fast-paced beat rate of the Bee Gees hit, Stayin Alive, is taught commonly as a guide to the CPR rate and first responders are advised to ignore any potential damage from the CPR compressions as they are far outweighed by the potential benefits. If ventilations are to be included, the recommendation is 30 compressions to two ventilations.

Coronary heart disease remains the biggest killer in Australia, followed by dementia/Alzheimer’s disease, then stroke and smoking-related diseases.

While anaphylactic responses to optometric eye drops are rare, other causes of anaphylaxis exist (especially in asthmatics) and they were the next topic Kiel addressed. Anaphylaxis is the result of an immunoglobulin E-mediated mast cell degranulation that releases inflammatory immune mediators into the blood stream. Those mediators increase vascular permeability, cause peripheral vasodilation, increased mucus production, and, the smooth muscles in the bronchi to contract, leading to airway compromises or even cardiovascular collapse.

Anaphylaxis is likely to occur 20–30 minutes after exposure to an antigen and can result in a tight or swollen throat or swollen airways, which can sometimes be fatal. In some cases, anaphylaxis is preceded by facial swelling (including lips and eyes), hives or welts, abdominal pain, or vomiting (the latter two features are suggestive of an insect allergy).

Kiel then moved to seizures and what to do if confronted by a case. Best practice suggests that the patient be either seated comfortably or rolled onto their side if possible (in case they vomit). There should be no restraining or placing of things, including fingers, in the mouth, despite the fact that preventing unintentional patient self-harm has to be considered.

The episode should be timed and is usually self-limiting at 60–90 seconds, with a maximum of five minutes. While waiting for the signs to subside, call an ambulance and protect the airways as necessary. Splashing cold water on the patient’s face might also encourage them to ‘wake-up’.

Once the patient is more aware, the placement of something hard in their mouth might prevent further seizures or swallowing of the tongue, which can otherwise be fatal. While a brain tumour is an unlikely possibility, a seizure can also be caused by a fever, or withdrawal following cessation of long-term alcohol consumption. The signs are due to rapid but random brain activity.

Contrastingly, if a patient faints (syncope), the advice was simply to elevate the patient’s legs and let the condition self-resolve.

Kiel said in cases where diabetics become less responsive or unresponsive during a consultation, the episode was unlikely to be due to hyperglycaemia as passing out is uncommon. Instead, it is more likely to be due to hypoglycaemia – especially in Type 1 diabetes.

If unresponsive, no sugary remediation should be attempted, but if responsive enough, jellybeans or a sugary drink can be offered. Hypoglycaemic episodes in Type 2 diabetics can be a result of an infection or a medication mistake.

Kiel finished her presentation on the topic of dangerous ingestions by children, especially the very young. Surprisingly, if swallowed by a toddler, eucalyptus, tea tree, and other essential oils can be fatal. Other fatal entities common enough in many households include amphetamines, endone, and diabetes medications (one tablet can kill a two-year-old). In a consulting room, atropine and homatropine are present and are even more dangerous.

A special 24-hour kids and poisons hotline, which is part of the NSW Poisons Information Centre, is available on 13 11 26 and can be accessed from anywhere in Australia.

Kiel’s parting comment was probably as important as the foregoing – the general community considers optometrists to be ‘medically trained’ and, therefore, a good knowledge of practical first-aid is essential.

Ocular imposters

Brisbane optometrist, Mr David Foresto, reviewed many conditions that can either compound existing diseases or mimic other diseases, leading to confusion when a diagnosis is sought. While glaucoma is the focus of much of our attention when ocular neuropathies are involved, other conditions can also mimic properties of optic neuropathies, such as arcuate visual field defects or other visual field losses.

Mimics include both active or resolved optic neuritis (as RNFL thinning can continue after ‘resolution’), ischaemic optic neuropathies, drusen at the optic disc, and optic atrophy, each of which require different management plans.

Although some of the more recent MRI machines have magnetic fields of seven Tesla, offering a resolution of around 1.5 mm, OCT devices offer much greater resolution and reveal more without exposing patients to extreme magnetic fields. OCT is also playing an increasing role in multiple sclerosis diagnosis, as 20% of those diagnosed had or have optic neuritis as the first sign of MS, specifically RNFL and RGC complex thinning.

Although still evolving, OCT is now considered an easy, non-invasive tool for monitoring MS progression at much lower cost. However, not all optic neuritis cases can be imaged via the eye, as some cases are retrobulbar and not visible using conventional ophthalmic imaging techniques.

When trying to differentiate optic neuritis from ischaemic optic neuropathy, history taking can be key, e.g. reports of transient ischaemic attacks (TIAs) masquerading as transient vision loss, which are more likely in those over 50 years of age with cardiovascular disease. Such cases require urgent referral to assess the possibility of the case being one of giant cell arteritis, whose symptoms can include headaches, jaw pain, vision loss, fever, and fatigue.

Foresto then moved to two cases of corneal pseudo-dendrites that showed atypical staining patterns and did not respond to the usual antibiotics deployed. One feature noted was the lack of characteristic terminal ‘bulbs’ on each dendrite.

One case, a 10-year-old child, was found to have a blood tyrosine level almost 10x higher than normal. This led to a diagnosis of hereditary tyrosinaemia, an autosomal recessive genetic disorder that results in an inability to metabolise the protein tyrosine, found in meat, cheese, and high-protein plant foods.

As other organs are also affected (kidney and liver damage, bone deformity), early treatment is important. Treatments include a low protein and low phenylalanine diet, serum enzymes, and in a worst-case scenario, a liver transplant.

A differential diagnosis of pseudo-dendrites can be complex and the possibility of the following conditions needs to be examined: acanthamoeba keratitis, fungal keratitis, tyrosinaemia, ocular rosacea/blepharitis including a reaction to Staphylococcus aureus, and exposure to toxins (rarely to CL care products). A differential diagnosis between pseudo-dendrites and herpes simplex keratitis (HSK) can be based on the presence or absence of the following pseudo-dendrite properties: no dendrite terminal bulbs, corneal sensitivity remaining normal, and the dendrites staining poorly with fluorescein. HSK has terminal bulbs, a loss of corneal sensitivity, and the lesions stain well.

The discussion then changed to fundal haemorrhages and haemorrhage-like lesions including: BRVO, diabetic retinopathy, hypertensive retinopathy, and leukaemia (four main types). Roth spots are also suggestive of leukaemia and have white centres because of the presence of white blood cells in places not intended.

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Foresto stated that around 50% of leukaemia cases have ocular involvement, and that it is not rare. It is also not a disease restricted to childhood, and most forms are more common in adults, with acute lymphoblastic leukaemia being the exception. Roth spots require urgent referral to a retinal specialist for management and they can exist concurrently in cases of diabetic retinopathy.

Vortex keratopathy/medication-induced verticillata and Fabry Disease were his next foci. Many common medications can induce a verticillata, but Fabry disease is an X-linked lysosomal disorder that can be fatal through its effects on the heart (cardiomyopathy) or kidneys (severe renal impairment). While medication-induced vortices can be resolved or improved by a change in medication, Fabry disease, which is usually asymptomatic, requires enzyme replacement therapy and possibly dialysis to prolong life.

KEYNOTE SPEAKERS

Andrew McKinnon

Anthony Maloof

Raf Ghabrial

Phillip Cremer

Julie Kiel

David Foresto

In a subset of his lecture titled ‘Old age is not a diagnosis’, Foresto tackled lid ptosis in the aged (senile ptosis or aponeurotic ptosis). In particular he focused on cases in which the pupil responses are not affected, and cases with the possibility that the patient might have Horner’s Syndrome, several causes of which can be fatal and in which the pupils’ responses can be abnormal.

In Horner’s cases, there can be ptosis, a lag of dilation after miosis, a normal or hyper-constriction on exposure to light, and sometimes an inability to sweat on the affected side of the face.

Those optometrists endorsed to use ophthalmic medicines are able to test for Horner’s using 0.5% apraclonidine. From 20 or more minutes after instillation, the pupil in a case of Horner’s will dilate. The situation is more complicated should the condition be bilateral, as it renders intraocular comparisons impossible.

Foresto closed his presentation with a review of persistent conjunctival lymphomas, those salmon-pink lesions that can occur almost anywhere on the eye. They are persistent, painless, can be subtle or large, and, in up to 30% of cases, are secondary tumours arising from a disseminated lymphoma.

His presentation revealed the plethora of traps for the young, and not-so-young, players that can confront a practitioner at any time.

Orbital and oculoplastic disorders

Ophthalmologist and now full-time oculoplastic surgeon, Clinical Associate Professor Raf Ghabrial, delivered a presentation on orbital and oculoplastic disorders. He commenced with an uncommon ptosis, congenital blepharophimosis, which is an inheritable characteristic of abnormally small interpalpebral apertures leading to an appearance of having small eyes. The condition can be corrected well by surgery.


He also covered; acquired ptosis, which usually presents with thin lids and a high skin crease in the upper lid, and is sometimes difficult (about 10% of cases) to achieve a post-surgical symmetrical outcome in; myopathic ptosis, wherein the levator palpebrae superioris (LPS) displays reduced function, leading to reduced upper lid retraction and a characteristic head-back posture required for the patient to see; ectropion, a common condition requiring surgery and usually a skin graft, in which the lower lid rolls out; and entropion, a common condition in which the lower lid rolls in, leading to tear film and ocular surface problems. The lashes of the lower lid abrade the anterior ocular surface, and treatment is similar to ectropion.

The facial manifestations of Bell’s Palsy – decreased lid closure leading to exposure keratitis as well as brow droop – can be complicated further, sometimes months after the initial Bell’s Palsy, by signs of unusual and novel innervation (mis-wiring or synkinesis). This leads to unusual pouts, baring of teeth, and blowing of the cheeks.

Bell’s can be mild, which usually ‘resolves early’, or more serious, in which case some residual manifestations can still be present years later. Bell’s affects those aged 20–50, lasts hours to days, always affects the upper face, and has few or no associated symptoms.

It also needs to be differentiated from the facial effects of a (ischaemic) stroke. Stroke generally affects those aged 60 or over, lasts seconds to minutes, may or may not affect the upper face, and results in weakness, numbness, speech difficulties, slurred speech, diplopia, swallowing difficulties, vertigo and ataxia.

Because of our exposure to sun, eyelid tumours are relatively common. About 90% of skin malignancies are BCCs, while the remainder are SCCs, sebaceous gland carcinomas (rare), or melanomas. The loss of lashes (cilia) can also be significant.

Tumours at or near the inner canthus are often bigger than their surface appearance suggests which, when treated conservatively with at least a 2 mm margin beyond their maximum extent, can lead to a plastic surgery challenge at reconstruction time.

BCCs can be large, and Ghabrial showed a 9 mm diameter example on a lower lid which amounts to a ≥13 mm excision. This also leads to reconstruction challenges.

Reconstruction after the excision of a deeper tumour such as a BCC, may necessitate the ‘borrowing’ of lid tissue from the contralateral eye. A chalazion was classified as an eyelid tumour, albeit a benign condition.

Ghabrial also detailed some cosmetic procedures including a brow lift, noting that usually, lower lid procedures were not included in Medicare. The criteria to operate include the loss of the visual field due to lid position, and whether or not lid skin touches the upper lid lashes.

Assessment of the tear flow and drainage system is usually done with an inspection of the lower tear meniscus, a fluorescein dye disappearance (FDD) test, and/or a Jones Test. Generally, the practitioner is seeking symmetry of performance between eyes rather than absolute values.

The most common blockage site in tear drainage is in the lacrimal sac. Because it can be fatal if no antibiotic is available, dacryocystitis and its surgical treatment was covered in some detail, as was DCR (dacryocystorhinostomy) surgery for blockages in the nasolacrimal ducts. Some procedures use a Nd-YAG laser, as well as more conventional surgical tools.

The complexity and multifaceted nature of thyroid orbitopathy was also covered in some detail. To simplify the treatment pathways, a ‘one-stop shop’ approach to the disease has been established at Sydney’s RPA Hospital involving all relevant specialties. Effects on the optic nerve and the EOMs can be serious, even vision threatening, and the main stages of treatment after a diagnosis are orbital decompression, strabismus surgery, and lastly, eyelid surgery.

In some cases, orbital wall removal may be required to accommodate the swollen orbital contents, especially the EOMs. In addition to surgery, decompression can also involve the use of steroids, immunosuppression, and radiotherapy.

To affect a scar-less outcome, orbital floor surgery can be performed using an over the lower eyelid–under the globe approach. While strabismus surgery is likely to be conventional, eyelid retraction can be more difficult to achieve good results for. This is because the cause can be sympathetic overeaction of Müller’s muscle, fibrosis of the ‘retractors’, or the result of attempted upgaze against the restricted movement offered by the inferior rectus muscle.

Ghabrial closed with an overview of orbital tumours, trauma, and infections and their treatment, including the possibility of enucleation.


Part two of Lewis Williams’ report will cover the keynote address, delivered by noted ophthalmologist Dr Anthony Maloof, and the engaging presentation from Sydney neurologist Clinical Associate Professor Peter Cremer.

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