Christopher M Stewart

Comparison of grafted and non‐grafted patients with corneal astigmatism undergoing cataract extraction with a toric intraocular lens implant

Background:  Toric intraocular lenses (IOLs) are advocated as an effective treatment for both regular corneal‐based astigmatism and cataract in both non‐penetrating keratoplasty and penetrating keratoplasty (PK) patients. The aim of this analysis is to compare postoperative outcomes for both PK and non‐PK patients to determine whether or not the past PK is relevant when calculating the appropriate IOL and predicting the postoperative results.

Late-onset persistent Descemet's membrane detachment following uncomplicated clear corneal incision cataract surgery.

We report the case of a 76‐year‐old man who developed a late‐onset Descemets membrane detachment (DMD) 5 months after uncomplicated cataract surgery. Despite two air tamponade procedures that initially appeared successful, the DMD continued to return. After careful examination it was found that a surgical entry wound may have been scarred open (fish‐mouthing), which continually promoted Descemets membrane to detach. Excision of the abnormal scar led to an almost complete resolution of the DMD. To our knowledge, this is the first report of a pathological (fish‐mouthing) entry wound causing a persistent, late DMD. We discuss the reasons why the management of late DMDs requires careful consideration.

Key Issues When Reconstructing Extensive Upper Eyelid Defects With Description of a Dynamic, Frontalis Turnover Flap.

Reconstruction of full thickness, total upper eyelid defects represents a significant challenge in terms of recreating an upper eyelid which has acceptable cosmesis and a degree of dynamic function. Options include bridging, eyelid-sharing techniques (e.g., Cutler-Beard), or nonbridging techniques such as an anterior lamella-based flap combined with a posterior lamella free graft or a “sandwich flap.” The success of these techniques depends on the size of the defect, postoperative cosmesis and whether or not the upper eyelid still has a degree of dynamic function to avoid ptosis and exposure keratopathy. The authors present an innervated frontalis turnover flap supporting anterior and posterior lamella grafts as a reconstructive solution for an extensive upper eyelid defect. This technique is cosmetically acceptable, preserves local tissues, and maintains a degree of dynamic function, which keeps the patient’s eye comfortable and does not adversely affect visual acuity.

Bronchial artery aneurysm: a rare, undescribed cause of Horner syndrome: Letter to the Editor

Bronchial artery aneurysms are a rare and asymptomatic but potentially fatal condition. We present the first described case in the literature of an acute onset Horner syndrome secondary to a bronchial artery aneurysm. A 65-year-old man was referred for a new rightsided ptosis, which had occurred in the last 3months. Hewas otherwise asymptomatic, had not suffered any trauma previously and had no medical comorbidities. On examination, best-corrected visual acuity was 6/6 right and 6/6 left. A 1-mm right ptosis (compared with left side) was noted (Fig. 1). Levator function and ocular motility were normal. Anisocoria was seen with no associated iris heterochromia. The right pupil was miotic when compared with the left (Fig. 1), and this was accentuated in the dark. Apraclonidine 1% (Alcon, Surrey, UK) was used to pharmacologically confirm a suspected right Horner syndrome. Thirty minutes post-instillation in both eyes, there was reversal of the anisocoria, which confirmed the diagnosis (Fig. 2). A CT-angiogram (CTA) (aortic arch/carotid protocol) demonstrated a torturous right bronchial artery with an irregular lumen, which represented a small, partially thrombosed aneurysm. This was at the level of the T4 vertebra, immediately anterior to the right sympathetic chain (Figs 3, 1). The patient underwent an endovascular procedure to have the aneurysm treated shortly after the diagnosis was made. Horner syndrome or ‘oculosympathoparesis’, was first described by Johann Horner in 1929. It classically presents with ipsilateral blepharoptosis and pupillary miosis. The sympathetic supply to the eye is a threeneuron chain that follows a long and circuitous route. First-order neurons originate centrally in the thalamus and descend to synapse at the level of C8 to T2 in the interomediolateral spinal cord. Second-order neurons then emerge in the upper thoracic ventral nerve roots (mainly T1) to join the sympathetic chain and ascend to synapse in the superior cervical ganglion. There is a degree of variation at the thoracic level where the second-order neurons emerge from to enter the sympathetic chain. The bronchial arteries are located anteriorly adjacent to the sympathetic chain in the upper thoracic levels. Third-order neurons exit the superior cervical ganglion and form a plexus surrounding the internal carotid artery (ICA) to ascend to the eye. Causes of Horner syndrome are classified as first order (central), second order (pre-ganglionic) and third order (post-ganglionic) and can cause serious

Bronchial artery aneurysm: a rare, undescribed cause of Horner syndrome

Bronchial artery aneurysms are a rare and asymptomatic but potentially fatal condition. We present the first described case in the literature of an acute onset Horner syndrome secondary to a bronchial artery aneurysm. A 65-year-old man was referred for a new rightsided ptosis, which had occurred in the last 3months. Hewas otherwise asymptomatic, had not suffered any trauma previously and had no medical comorbidities. On examination, best-corrected visual acuity was 6/6 right and 6/6 left. A 1-mm right ptosis (compared with left side) was noted (Fig. 1). Levator function and ocular motility were normal. Anisocoria was seen with no associated iris heterochromia. The right pupil was miotic when compared with the left (Fig. 1), and this was accentuated in the dark. Apraclonidine 1% (Alcon, Surrey, UK) was used to pharmacologically confirm a suspected right Horner syndrome. Thirty minutes post-instillation in both eyes, there was reversal of the anisocoria, which confirmed the diagnosis (Fig. 2). A CT-angiogram (CTA) (aortic arch/carotid protocol) demonstrated a torturous right bronchial artery with an irregular lumen, which represented a small, partially thrombosed aneurysm. This was at the level of the T4 vertebra, immediately anterior to the right sympathetic chain (Figs 3, 1). The patient underwent an endovascular procedure to have the aneurysm treated shortly after the diagnosis was made. Horner syndrome or ‘oculosympathoparesis’, was first described by Johann Horner in 1929. It classically presents with ipsilateral blepharoptosis and pupillary miosis. The sympathetic supply to the eye is a threeneuron chain that follows a long and circuitous route. First-order neurons originate centrally in the thalamus and descend to synapse at the level of C8 to T2 in the interomediolateral spinal cord. Second-order neurons then emerge in the upper thoracic ventral nerve roots (mainly T1) to join the sympathetic chain and ascend to synapse in the superior cervical ganglion. There is a degree of variation at the thoracic level where the second-order neurons emerge from to enter the sympathetic chain. The bronchial arteries are located anteriorly adjacent to the sympathetic chain in the upper thoracic levels. Third-order neurons exit the superior cervical ganglion and form a plexus surrounding the internal carotid artery (ICA) to ascend to the eye. Causes of Horner syndrome are classified as first order (central), second order (pre-ganglionic) and third order (post-ganglionic) and can cause serious

Bilateral subretinal abscesses: the first case of disseminated Nocardia beijingensis in Australia

1. Maekawa S, Shiga Y, Kawasaki R, Nakazawa T. Usefulness of novel laser speckle flowgraphy-derived variables of the large vessel area in the optic nerve head in normal tension glaucoma. Clin Experiment Ophthalmol 2014; 42: 887–9. 2. Aizawa N, Kunikata H, Yokoyama Y, Nakazawa T. Correlation between optic disc microcirculation in glaucoma measured with laser speckle flowgraphy and fluorescein angiography, and the correlation with mean deviation. Clin Experiment Ophthalmol 2014; 42: 293–4. 3. Kawasaki R, Wang JJ, Rochtchina E, Lee AJ, Wong TY, Mitchell P. Retinal vessel caliber is associated with the 10-year incidence of glaucoma: the Blue Mountains Eye Study. Ophthalmology 2013; 120: 84–90.

Reconstruction of extensive medial canthal defects using a single V-Y, island pedicle flap

ABSTRACT The medial canthus represents one of the most challenging regions of the face to reconstruct due to the anatomical structures present, the concavity of the area, and the differences in skin texture. We present a case series of 11 patients whose defects were reconstructed with a single V-Y island pedicle flap running along the nasofacial sulcus. Our single-stage flap which modified and simplified a previously described technique achieves similar cosmetic and postoperative outcomes along with a high level of patient satisfaction in an area which can be reconstructed in a variety of ways, often with suboptimal results.

Acute Sickle Cell Orbitopathy Masquerading as Orbital Cellulitis

Sickle cell orbitopathy is a rare manifestation of a sickle cell crisis and can closely mimic orbital cellulitis, both clinically and radiologically. We present a case where a child presented with what was thought to be orbital cellulitis and was treated accordingly. Subtle radiologic features of sickle cell orbitopathy were initially overlooked, resulting in an incorrect diagnosis and a treatment delay for the patient. Correctly treated most cases resolve with no adverse affects, highlighting how important it is to consider acute sickle cell orbitopathy in the differential diagnosis of acute periorbital swelling in children with sickle disease.

Delayed recognition of Horner syndrome secondary to internal carotid artery dissection after scuba diving

mechanism that increases uveoscleral outflow. However, PG agents have several adverse effects, including induction of increased inflammatory cytokines, which results in intraocular inflammation. Cystoid macular edema, which is caused by a disruption of the blood-retinal barrier or by a disruption of the blood-aqueous barrier, has also been associated with the use of PG agents. We speculate that these actions of PG agents may be associated with increased VEGF levels. And many studies have reported that inflammation increases VEGF levels in systemic diseases. In the eye, although there have been studies reporting an association between VEGF and uveitis and that systemic immune suppressive agents resulted in decreased VEGF levels in the aqueous humor. However, few studies have characterized possible associations between ocular inflammation and levels of VEGF. Some previous studies have reported that VEGF plays a physiological role in neuroprotection and survival. Several studies reported increased blood flow and neuroprotection of retinal ganglion cells in animal models, and in an in vivo study of PG use, either alone or in combination with other drugs. More studies are therefore needed to further investigate the possible associations of PG agent use and neuroprotection conferred by VEGF or other factors. In summary, we showed increased VEGF concentrations in the aqueous humor of DM patients and glaucoma patients who used PG agents. However, it was unclear whether they played positive or negative roles in these patients. This will need to be decided by additional studies with larger cohorts.

Microbial keratitis in indigenous Australians

lens capsule. The solitary small vessel found in the fibrous component of the lesion also supports this conclusion. This entity must be distinguished from a progressive segmental congenital pupillary–iris–lens membrane with goniodysgenesis. Pupillary block requiring a peripheral iridectomy or iridotomy is not encountered in pupillary vascular remnants. Both a fibrous epiiridial membrane and an abnormal angle were not present in our case. Congenital pupillary strands that are occasionally seen to cross the pupil from one portion of the iris collarette to another are the most common form of persistent and stationary pupillary membranes. Such lesions can produce a focal opacity on the anterior lens. These membranes may partially occlude the pupil when they originate from multiple sites on the iris collarette, but do not necessarily attach directly to the lens. Representing a congenital, incomplete involution of the tunica vasculosa lentis which lasts from the third to sixth month of foetal life, persistent pupillary membranes can be tenacious. They are composed of fine fibrils or broad bands attached to the iris collarette on one side; the other end is either free-floating or attached to the lens. Iris stromal melanocytes cover the persistentfibrous scaffolding of the tunica vasculosa lentis, as revealed microscopically in our case. The lenses in similar cases can remain surprisingly clear after separation of the membrane. Alternatively, viscodissection may be adequate to break the lens attachments. The neodymium-doped yttrium aluminium garnet laser has been successfully employed to release pupillary membranes that interfere with vision.