CURRICULUM VITAE

Qualifications
MB BS (Qld), FRCS ( Edin), FRANZCO

Appointments Current
Consultant QEDIC (Queensland Electrodiagnostic & Imaging Clinic)
Hospital Accreditation
     Eye Tech Day Surgeries, Brisbane
     Queensland Eye Hospital, Brisbane

Memberships

RANZCO
International Society of Electrophysiology of Vision;
Royal Australian & New Zealand College of Ophthalmologists
Paediatric Specialist Group RANZCO
Strabismus Society RANZCO

Past Appointments
Visiting Specialist Mater Children's Hospital 1970-2000
Visiting Specialist Mater Hospital 1970-1985
Consultant NeuroSensory Unit , Brisbane 1979-2005
Senior Specialist, Mater Children's Hospital 1980-1998
Consultant Ophthalmologist ORBIS 1990-1992
Consultant Ophthalmologist, Marfans Clinic, Prince Charles Hospital 1993-2018
:Chairman, Royal Australian and New Zealand College Ophthalmologists- P SIG 1993-2013

Current Private Practice
Valley Eye Specialists ,53 Ballow St, fortitude Valley, Qld
Oxford Eye Clinic, I Victoria St, Balmoral

Special Interest Areas
Strabismus.
Paediatric Eye disorders; learning disorders.
Visual Electrophysiology including Retinal Dystrophies
Adult Strabismus.
Marfan’s Syndrome

Awards
Ida Mann Lecture 1998

CONJUNCTIVITIS
| Conjunctivitis in older children presents no unusual diagnostic problems. Aetiological factors may be:-

  1. Bacterial Conjunctivitis

Clinical Findings :
-Red eyes – usually bilateral, sore (but not painful)
- Muco-purulent discharge

Diagnosis - Gram stain and culture
Therapy - Eye toilets + Local antibiotic drops second hourly

2. Viral Conjunctivitis (adenovirus) Adeno Viral Conjunctivitis

Clinical Findings
- Frequently unilateral initially
- Red eye
- Watery discharge
- Tender preauricular lymph node
- Follicles visible on tarsal conjunctival
Diagnosis
– Clinical features + Culture (e.g. Adeno Virus)
Therapy
- Supportive
- Hot Spoon bathing

3.Allergic Conjunctivitis- Spring catarrh, vernal conjunctivitis

Clinical Findings                                                                              
- Itchy eye, Rubbing of eyes
- Watery discharge
- No injection
- Cobblestone papillae on tarsal conjunctival   PAPILLAE
- Beware of Photophobia or reduced vision –This signifies corneal involvement and possible serious loss of vision!   CORNEAL ULCERATION
due to Keratitis
Diagnosis
– Eosinophils in conjunctival scraping
Therapy
- Minor case –trial with vasoconstrictors- Naphcon A, Albalon A
- Mast Cell Stabilisers-Patanol . Effectivity is limited in children. Drops must be used regularly 3 or 4 times daily even when asymptomatic to stabilise Mast Cells. They are of no value used only when symptoms occur because they take some time to have an effect. Compliance with these medications is extremely poor and I find their practical value is minimal.
-Local steroid drops- Continue to be the most effective available topical medication for severe Vernal conjunctivitis. Their use requires monitoring because of their possible effect on Intra Ocular Pressure. I have often seen vision lost as a result of failure to control Allergic Keratoconjunctivitis because of fears regarding steroid use. Steroid raised pressure in children is rare, I have not seen vision lost from this complication in childhood. Monitor the dose of steroids, adjusting the dose according to the response. There is usually a gradual reduction in the number of applications required and eventual cessation in teenage life.

4. Neonatal Conjunctivitis
Conjunctivitis in the neonate may be a sight threatening condition.                                                                                   GONOCOCCAL CONJUNCTIVITIS
Severe Purulent conjunctival infection in this age group can result in corneal involvement and even rupture.
Aetiological Agents:
- Gonococcal – (classical but rare) culture
- Other Bacteria – culture, gram stain
- Chlamydia – smear; REMEMBER PNEUMONITIS
- Herpes simplex – culture

Therapy :
- Admit to hospital
- Hourly eye toilets
-Hourly antibiotic drops
-Appropriate systemic antibiotics
Prompt adequate therapy in patients with neonatal conjunctivitis should prevent corneal complication and permanent visual impairment.

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CORNEA

Clinical Features A corneal lesion from any cause results in :- pain, photophobia and a red eye
- Vision may be reduced
Examination
- Inspection using magnification may reveal corneal opacities, a corneal foreign body, Dendritic ulcer ; a corneal ulcer stained fluorescein ; corneal abrasion or erosion ; corneal abrasion stained ; corneal Scar (alkali)

- Inspection after staining with fluorescein will demonstrate any epithelial defect.

Lesions include:

Herpetic Keratitis (Dendritic Ulcer): Herpes simplex infection results in a branching ulcer Dendritic ulcer     herpetic-dendritic-ulcer                     Dendritic Ulcer stained
Therapy
– Oc Acyclovir
Complications - recurrence
- corneal scarring
- iritis and deep keratitis
NOTE: Corticosteroids are contra indicated for they cause rapid progression and can lead to corneal perforation.

Corneal Abrasion: A geographic area of epithelial loss.                                                                                      Corneal abrasion

Therapy: – occlusion with a firm pad results in rapid resolution

Corneal Foreign Body: Corneal FB Will be noted on inspection or following fluorescein stain             CORNEAL fb

Therapy: – Amethocaine drop for anaesthesia and removal with a fine hypodermic needle
- Occlude until ulcer has healed

Viral Keratoconjunctivitis: Associated with the conjunctivitis may be a punctate keratitis with subepithelial infiltrates

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REFRACTION IN CHILDREN
Infant’s eyes tend towards the hypermetropic side of normal. The incidence of myopia is low in preschool children but increases in childhood. Click for causes of myopia
Astigmatic refractive errors are common in neonates but frequently resolve within the first six months of life.
Refraction of children of all ages is possible. This is performed following the instillation of drops (atropine or cyclopentolate) to paralyse the ciliary muscle. This enables a measurement of the ocular refractive state to be made objectively using the retinoscope. Subjective refraction becomes practicable from the age of 7 years. (click on pictures below for enlargement)

Hypermetropia   Myopia     Astigmatism  click pictures to enlarge

Correction Of Refractive Errors
Spectacles can be prescribed from an early age if high myopia is present or if hypermetropia precipitates an accommodative squint. Small refractive errors do not require spectacle correction. Children are not assisted in any way by the prescription of weak spectacles.
Where the refraction is different in each eye amblyopia may occur (anisometropic amblyopia), requiring the prescription of spectacles.
Contact lenses
Daily wear soft contact lenses are well tolerated by older children and can be prescribed for recreational or cosmetic purposes.
Extended wear soft contact lenses are suitable for the correction of gross refractive errors in infancy (see Congenital Cataract). They require removal for cleansing on a regular basis.
Pinhole Vision
In older children the best corrected vision may be determined by testing visual acuity through a pinhole. If vision is not improved in this manner the visual loss is not due to refractive error.
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NEURO-OPHTHALMOLOGY: OPTIC ATROPHY

AetiologicaL FACTORS in Children
- Hydrocephalus
- Hereditary (dominant, recessive, or x-linked)
- Space occupying lesions (intracranial, orbital)
- Heavy metal poisoning (lead, arsenic)
- Secondary to papilloedema
- Cerebral DegenerationsClinical Findings

FINDINGS
- Diminished vision
- Pupil reaction to light reduced
- Marcus Gunn Pupil – (consensual reaction greater than direct)
- Pallor of optic disc and reduced vessels on disc.
- Visual field changes

Investigations
- Visual Evoked Potential - (of particular value in children too young to measure vision or visual fields.)
MRI Scan is necessary

Note: Optic Atrophy requires a full neurological investigation

Abnormal Pupillary Reactions

Anisocoria: – ( unequal pupils) is present in about 20% of the normal population

Pathological Anisocoria
- Large pupil – 3rd nerve paresis – associated with 3rd neve paresis -fails to constrict with light
- Small pupil – sympathetic paralysis (Horner’s Syndrome)
- Mydriasis may also occur because of eye drops, some plants and trauma.
- Horner’s Syndrome – Miosis, Ptosis, Enophthalmos, anhydrosis
If this occurs before two years of age Heterochromia of the Iris results.
Congenital Horner’s commonly occurs due to birth trauma but occasionally may be due to a mediastinal tumour (eg neuroblastoma.)

Afferent Pupillary Defect -Marcus Gunn Pupil, Swinging light test.                        
If Reaction to direct light< consensual reaction.   = Optic nerve dysfunction          video

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RETINA
Retinitis Pigmentosa
An inherited disorder of pigment epithelium and receptor cells (recessive, dominant or x-linked inheritance)
Clinical Findings
- Night blindness, constricted visual fields                                                RP
- Often good central vision, but constricted fields
- Retinal pigmentation – bone spicule
- Optic atrophy and retinal artery attenuation
- Electroretinogram is abnormal from an early age- before there is any other evidence of abnormality erg information

Management
No therapy is available at present
But research is evaluating a variety of Genetic therapies which offer promise for the future

Associated disorders
- Refsum’s Syndrome – R.P., deafness, elevated blood phytamic acid
- Bardet Biedl Syndrome – R.P., & obesity metal retardation, hypogonadism,
- Ushers syndrome – R.P. & deafness

Macular Dystrophies
Stargardt's Macular Dystrophy – decreased vision, pigmentary macular change (“beaten- bronze” appearance) with or without yellow fleck deposits. Recessively inherited.
Diagnosis Confirmed with Pattern ERG

Vitelliform Macular Dystrophy
– an “egg yolk appearance” at the macula. Dominantly inherited.
Diagnosis Confirmed Normal ERG but abnormal EOG

Retinopathy Of Prematurity
Infants born prematurely have an incompletely vascularized retina. The exposure of this immature retina to high oxygen concentrations may result in abnormal vascular development.

In the acute phase an arterio-venous mesenchymal shunt is present in the peripheral retina at the junction of the vascularized and non-vascularised zones. This may be visible ophthalmoscopically as an elevated ridge.

If the condition progresses intravitreal fibrovascular proliferation may occur progressing even to an exudative retinal detachment.
Ophthalmic Review:  Infants at risk require ophthalmic examination . Those at risk are – less than 1000 gms at birth, severely ill babies, especially babies who required supplemental oxygen.
Treatment: with laser or cryopexy can control these changes in most infants.

Chronic changes secondary to contracture of this fibrovascular tissue may result in retinal folds, dragging of the optic disc, and even traction retinal detachment. This retinal detachment and fibrous tissue can be seen as a white retrolental opacity – retrolental fibroplasia.

Supplemental oxygen levels should be restricted to a that level which is adequate to maintain cerebral and other vital functions.  Arterial oxygen levels must be monitored.  But even with the greatest care retrolental fibroplasia still occurs. Improved paediatric care has resulted in changing the goalposts. In 1980 babies of 2000gm or less required review. Today children of birthweight greater than 1000gm rarely are found to be significantly affected. 

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TYPES OF STRABISMUS

1. Incomitant: The angle of deviation varies in different directions of gaze.  This occurs most commonly where there is paralysis of one or more extraocular muscles.
Causes:

a. Neurological - due to lesions of 3rd, 4th, or 6th cranial nerves caused by:

• Trauma- Tumour – (Intracranial)
• Infection
• Raised Intra-Cranial Pressure (6th Nerve Palsy)

b. Muscular – Direct involvement of the extraocular muscles by

• Trauma
• Tumour of the orbital or periorbital tissue
• Infection
• Muscular Anomaly – Dystrophy etc.

c. Neuro Muscular – Myasthenia Gravis

d. Congenital Conditions:

• Duane’s Retraction Syndrome
• Browns Syndrome
• Moebius Syndrome

In all these states the angle of squint varies, becoming maximal when an attempt is made to gaze in the direction of action of the paralysed muscle.  In children the eyes may fail to realign following temporary paralysis and a permanent comitant squint may occur.

Duane’s Syndrome
– The involved eye is unable to abduct and on adduction is retracted into the orbit.
Brown’s Syndrome
- The inability to elevate the eye in adduction
Moebius Syndrome
– Combined 6th and 7th nerve palsies.

2.Comitant Strabismus
The angle of squint is equal in all directions of gaze. There is no abnormality of function of extra ocular muscles but instead, incorrect co- ordination of binocular muscle function is present.
Types Of Concomitant Strabismus
- Esotropia (Convergent Squint) optical axes converge (A convergent squint)
- Exotropia (Divergent Squint) optical axes diverge (A Divergent squint)
- Hypertropia – (Vertical Squint) – One optical axis is deviated vertically.
- Latent Strabismus becomes apparent only on dissociation of the vision of the eyes (eg on covering one eye) and is termed a phoria (exophoria, esophoria, hyperphoria). This may become overt with fatigue, illness, or with lack of attention.
Causes of Comitant Strabismus
Hereditary :
a familial predisposition to develop strabismus may be inherited as an autosomal dominant trait.
Sensory Deprivation
A blind eye has no incentive to remain aligned. Therefore any condition which results in markedly reduced vision may cause a squint. E.g. Corneal Scarring, Cataract, Opacity of the Refractive Media, Retinal Lesion e.g. – Retinoblastoma, Retinal Detachment, Optic Atrophy, High Refractive Error.
Secondary To Paralytic Squint
Children have a tenuous hold on single binocular vision therefore they frequently do not manage to redevelop this following a paralytic squint.
Accommodative
The close anatomical and physiological link between accommodation and convergence causes the frequent excessive convergence (esotropia) in children who are hypermetropic i.e. because these children need to accommodate excessively to obtain clear vision they often break down and develop a convergent squint.      ACCOM SQUINT        
Unknown
No cause for the occurrence of strabismus will be found in many cases.

Anterior Uveitis – Iritis
Aetiology - often unknown
- auto immune disorders e.g. Stills’ Disease or ulcerative colitis
- secondary to corneal lesions
- tuberculosis, sarcoidosis

Acute Iritis
Symptoms- red, painful eye
- vision often reduced
- Signs: miosis (pupil may be irregular due to adhesions to the lens)
- cells visible in anterior chamber
- deposits of white cells on corneal endothelium
Therapy
- local steroids (Prednisone drop)
- mydriatics (atropine 1% drops)
Complications
- secondary glaucoma
- cataract
- vision loss

Chronic Iritis
Is often insidious but the examination demonstrates the features as above but the eye is white.

Chorio–Retinitis
Toxoplasmosis Retinitis –usually a focal chorio-retinal scar, frequently at the macula.
Toxocara Canis Retinitis – ocular manifestation of visceral larva migrans – nematode larva. A peripheral retinal granuloma may be seen associated with vitreo-retinal fibrosis and traction.




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• Overview Of Paediatric Ophthalmology
• Specific Eye Conditions

| ANOPHTHALMOS & RELATED CONDITIONS

Acknowledgements: The information on this page is based on that of MACS (microphthalmos and anophthalmos society UK) webpage. The information is designed for the assistance of parents and others who are assisting anophthalmic children.
The MACS webpage offers further support and discussion facilities to these people and it is recommended that their site is visited. Click here to visit MACS (UK) Home Page
This society's webpage is an excellent one with appropriate information, advice and support for parents and relatives of anophthalmic children
Anophthalmia
Anophthalmia (anophthalmos) is a condition that means one or both eyes didn’t form during the early stages of pregnancy.
There are three groups of patients with this condition.
1. Primary anophthalmia is a complete absence of eye tissue due to a failure of the part of the brain that forms the eye.
2. Secondary anophthalmia occurs when the eye starts to develop and for some reason stops, leaving the infant with only residual eye tissue or extremely tiny eyes which can only be seen under close examination.
3. Degenerative anophthalmia the eye started to form and, for some reason, degenerated. One reason for this occurring could be a lack of blood supply to the eye.
Causes
Incidence: True anophthalmia occurs in around 1 in 100,000 births.
Microphthalmia and coloboma occur in around 1 in 10,000 births.
Aetiology: Genetic- 2/3.
Environmental factors- 1/3 (drugs, pesticides, radiation, toxins or viral causes).
Viruses that have been linked to these conditions are toxoplasmosis, rubella and certain strains of the flu virus.
Research into the cause or causes of these distressing conditions has intensified over the past few years. One day the cause will be identified and hopefully lead to a significant reduction in the amount of children being born with these conditions.

Microphthalmia
Microphthalmia (microphthalmos) is a condition in which the eye(s) started to form during pregnancy but for some reason stopped, leaving the infant with small eyes. The size of the eye can vary from child to child.
If very mild it can almost go unnoticed while very advanced cases or extreme microphthalmia are really the same as some forms of anophthalmia.
Distinguishing between extreme microphthalmia and anophthalmia in such a case can be achieved only by examining especially stained tissue under a microscope but such a diagnosis is not usually of much practical importance.

Coloboma
Coloboma (colobomas or colobomata).
The word "coloboma" comes from the Greek word that literally translates to "mutilation". In this condition there has been a failure of the closure of the optic fissure leaving a gap in some or all of the structures of the eye. This condition is usually (but not always) apparent because the pupil is mis-shaped. It can often be a ‘cats eye’ or ‘keyhole’ shape. Again, this condition can occur in varying degrees.
Complete coloboma- all of the structures of the eye are involved; these are the choroid, the retina, the optic disc, the ciliary body, the macular and the iris. Lens colobomas can also occur but it is very rare and the cause isn’t very well understood.

Related Conditions
Some other conditions associated with coloboma, anophthalmia and microphthalmia are:
Congenital cataracts, optic disk abnormalities, congenital cystic eye, microcornea and persistent hyperplastic primary vitreous.
Nanophthalmia. Although similar sounding to anophthalmia, it means that the eye looks normal in appearance but the eyeball is significantly shorter. This condition appears to be hereditary.

Treatment
There is no cure for these conditions.
Sometimes the child may have other conditions or complications that may require monitoring.
Prosthetic eyes can be fitted to the empty eye sockets. This may involve surgery to the socket to make it easier to fit the prostheses but also to promote the growth of the eye socket. Conformers, similar to balloons that can be expanded inside the socket, are sometimes used to further encourage the growth of the socket.
Prosthetics
Prosthetic eyes are usually made from acrylic. Sometimes porcelain is used if there’s an allergy to the acrylic. If there is any vision at all in an eye then a prosthesis will not normally be fitted until the child reaches 5 years old. This is because if that eye is covered up for long periods the brain will cease to recognise the signals, causing a ‘lazy eye’. It is also important to establish if there is any useful vision in the affected eye(s), which is most reliably done at a later age.
After the age of 5-7 years then the brain is able to compensate and no vision will be lost. As the child grows the prosthesis will need to be checked regularly for size, comfort and fit (usually 2–3 times a year). It also needs to be polished and checked for any damage such as sharp edges etc.

Please remember that each child is different and this information should not be used to make a diagnosis. Any diagnosis should be made by a qualified ophthalmologist.