Ophthalmology

To the Editor: Retinal screening is crucial to the prevention of vision loss from diabetic retinopathy. The recent National Eye Health Survey highlighted a gap in screening rates between Indigenous Australians (aged ≥ 40 years) and non-Indigenous Australians (aged ≥ 50 years),1 providing a foundation on which to target future eye health services. While acknowledging the budgetary and logistical constraints of such a large-scale study, we are concerned that another at-risk group — younger adults with type 2 diabetes who are aged 18–49 years — was not included in the National Eye Health Survey. The past two decades have seen a global increase in the incidence of type 2 diabetes in youth and young adults, with younger age being an independent risk factor for the development of diabetic retinopathy.2 In Australia, about 130 000 people with type 2 diabetes who are aged < 50 years are registered on the National Diabetes Services Scheme.3 However, there are no population-level data available regarding retinal screening rates in this age group. A decade ago, a survey of young Australian adults with type 2 diabetes (aged 16–35 years) reported a 55% retinal screening rate.4 Given the small, self-selected sample, this is likely an overestimate and compares unfavourably with the non-Indigenous rate of 78% reported for adults aged ≥ 50 years in the National Eye Health Survey.1Moreover, our qualitative research has shown that young adults aged 18–39 years who have type 2 diabetes face different psychosocial challenges and barriers to retinal screening compared with their older counterparts aged ≥ 40 years.5 Younger adults with type 2 diabetes require targeted, tailored intervention, which can only be provided if accurate, population-level data are available for this group. As Foreman and colleagues1 acknowledge, diabetic retinopathy is the leading cause of vision loss in working age adults — a situation with potential for considerable social and economic burden. The absence of current eye examination data for younger Australians with type 2 diabetes increases the risk that their needs will be neglected in future evidence-based policy and program delivery initiatives. We urge the Australian Government and other stakeholders to extend future population-level surveys (and other research and policy initiatives) to include all adults with diabetes.

Amelia J Lake · Jessica L Browne · Jane Speight

In reply

Joshua Foreman · Stuart Keel · Mohamed Dirani

To the Editor:We thank Tong and colleagues1 for their report on a patient with schizophrenia and clozapine-induced maculopathy, and for highlighting this under-recognised condition. Both typical2 and atypical3 antipsychotic drugs have been reported to cause widespread retinopathy; more recently, there have been reports of rare cases of retinal damage localised to the macula (maculopathy) due to both typical4 and atypical1,5 antipsychotics. The classical hypothesis for widespread pigmentary retinopathy is that drugs are absorbed by melanin in the retinal pigment epithelium (RPE) and act as photosensitisers to damage the RPE. This results in loss of RPE support functions of overlying photoreceptors, which secondarily degenerate. An alternative hypothesis,2 supported by histological and animal studies, is that the problem begins in photoreceptors, with drug-induced blockade of retinal dopamine receptors followed by photoreceptor and subsequent RPE cell loss. Neuroleptic retinal drug toxicity typically involves pigment disruption in the RPE, but the dopamine hypothesis allows for broader combinations of RPE and/or photoreceptor damage. The reasons for the development of maculopathy in some patients, rather than a widespread retinopathy, are not known. This phenomenon is seen in other ocular drug toxicities, particularly hydroxychloroquine. Most drug-induced retinal toxicities are bilateral and symmetrical; asymmetrical cases have rarely been reported. The patient reported by Tong and colleagues is atypical with apparently unilateral macular changes.1 Significant differential diagnoses for unilateral macular pigment and photoreceptor changes include age-related and secondary to retinal conditions, such as central serous chorioretinopathy, inflammatory retinopathies and trauma. Maculopathy limited to the outer neuroretina may occur with the use of other drugs (eg, poppers maculopathy).6 Also, schizophrenia is known to cause illness-related retinal changes in the neuroretina but not in the RPE.7 We agree that patients taking psychotropic medications benefit from a multidisciplinary approach when ocular symptoms and signs develop.

Heather G Mack · RC Andrew Symons

In reply

Jessica Y Tong · Amy Pai · Stephanie H Young

To the Editor: A 53-year-old woman experienced rapid onset of left eyelid pain, swelling and purulent discharge (Box 1). She presented to our eye hospital 3 days later and, on assessment, the lids were exquisitely tender, inflamed and difficult to open. There was chemosis, microcystic corneal oedema with Descemet membrane folds and moderate inflammation in the anterior chamber. Visual acuity was 6/24 in the left eye and 6/9 in the right eye. Ocular motility appeared normal. The severe inflammation and visual impairment raised concerns for post-septal orbital cellulitis. A computed tomography scan showed severe pre-septal stranding only (Box 2). A diagnosis of left pre-septal cellulitis and keratoconjunctivitis was made. She was given intravenous ceftriaxone 2 g daily, intravenous flucloxacillin 2 g four times a day, topical chloramphenicol 0.5% four times a day and regular eye washings. Microscopy found gram-negative diplococci, and polymerase chain reaction testing was positive for Neisseria gonorrhoeae. The patient denied history of sexually transmissible infection. A urine and serum sexually transmissible infection screen for N. gonorrhoeae, Chlamydia trachomatis and blood-borne viruses was negative. Treatment was rationalised to intravenous ceftriaxone 1 g daily, with a single 1 g dose of oral azithromycin. The patient had dramatic improvement over 4 days, and visual acuity improved to 6/7.5 at discharge (Box 3). One week later, the infection had predominately resolved. N. gonorrhoeae typically produces a hyperacute unilateral conjunctivitis. While the source of infection in this patient is unclear, in most cases infection is acquired via sexual transmission and reaches the conjunctiva through hand–eye auto-inoculation.1,2 The bacteria can invade the corneal epithelium, producing keratitis and corneal melting necessitating therapeutic keratoplasty.1,2 Gonococcal periorbital infection is rare, with only three cases of pre-septal cellulitis and two cases of post-septal cellulitis reported.3 All patients were successfully treated with parenteral antibiotics. N. gonorrhoeae has increasing antimicrobial resistance, creating a therapeutic challenge. The Australian Gonococcal Surveillance Programme has shown an emerging resistance to ceftriaxone — the antibiotic of choice — from 0.6% in 2006 to 5.4% in 2014.4 Azithromycin resistance occurs in 2.4% of strains.4 The Australian Therapeutic Guidelines recommend treatment of N. gonorrhoeae with parenteral ceftriaxone and oral azithromycin, for bactericidal synergy and cotreatment for C. trachomatis. When presented with pre-septal cellulitis and purulent keratoconjunctivitis, the clinician should be vigilant for a sight-threatening N. gonorrhoeae infection. Box 1 – Lid inflammation and purulent discharge at onset, 3 days before presentation Box 2 – Contrast-enhanced computed tomography scan showing significant pre-septal subcutaneous stranding (blue arrow) and severe conjunctival chemosis (yellow arrow) Box 3 – Marked improvement in periorbital inflammation after 3 days of antibiotic therapy, with residual conjunctival injection

Shivesh Varma · Nathan Wong · Jwu Jin Khong

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Uma Jatkar · Mitchell D Anjou · Hugh R Taylor