Hiten G. Sheth

Outcome of Raised Intraocular Pressure in Uveitic Eyes with and without a Corticosteroid-Induced Hypertensive Response

PURPOSE To compare the management and outcome of raised intraocular pressure (IOP) in uveitis patients with a corticosteroid hypertensive response and those who are noncorticosteroid responders and to determine the impact of intraocular corticosteroid use on IOP in uveitic eyes. DESIGN Retrospective study. METHODS Eight hundred and ninety-one uveitis patients were observed in a specialized clinic over 3 months. The main outcome measures were frequency, characterization, management, and outcome of uveitis-related ocular hypertension and glaucoma. RESULTS Of 891 patients with uveitis, 191 (275 eyes) had IOP elevation (21.4%). Of these, 95 (34.5%) eyes had glaucoma. IOP elevation attributed to corticosteroid-response (61.1%) was controlled more easily than that resulting from other causes (38.9%), requiring fewer eye drops (mean, 2.06 vs 2.52; P = .009) and less filtration surgery (8.9% vs 22.4%). Among eyes with uveitis and raised IOP, elevated IOP developed in 18 eyes (6.5%) after intravitreal triamcinolone, including 64.7% to 30 to 39 mm Hg and 35.3% to 40 mm Hg or more. Prostaglandin analogs were used in 49.2% of 246 eyes; no increase in inflammation was seen in these eyes. CONCLUSIONS In this tertiary center series, most instances of raised IOP were attributable to corticosteroid response. Raised IOP induced by corticosteroid response was controlled more easily and less often resulted in optic nerve or visual field changes of glaucoma. Although intravitreous triamcinolone was associated with substantial risk of corticosteroid-response IOP elevation, all cases were controlled medically without experiencing glaucomatous injury. Prostaglandin-induced uveitis was not observed despite extensive use of prostaglandin IOP-lowering agents.

A prospective study of change in visual function in patients treated with pegylated interferon alpha for hepatitis C in the UK

Background: Hepatitis C virus and interferon treatment have been associated with retinopathy. Baseline and ongoing assessment by ophthalmologists have therefore been advocated in previous studies. Our experience suggests that the incidence is low, with no or negligible impact of pegylated interferon alpha on actual visual function. This study was conducted to determine whether ophthalmic assessment is necessary in such patients. Methods: The study was a prospective case series of 52 patients (104 eyes). Visual acuity, contrast sensitivity, colour vision, visual field by perimetry and fundal assessment were measured at baseline and at 3 and 6 months post commencement of interferon alpha treatment. Results: Forty-two men and ten women were followed. No patients reported any subjective visual symptoms. The mean changes in right and left logarithmic minimal angle resolution (LogMAR) visual acuity were negligible between baseline and 6 months (0.05 (SD 0.13) and 0.10 (SD 0.12), respectively). Mean changes in contrast sensitivity and colour vision were also negligible. Of all eyes monitored by serial perimetry for the full follow-up period and deemed to have reliable tests, none developed visual field defects. One patient appeared to develop nasal field defects within 3 months of commencing treatment but failed to attend for repeat testing. No patients developed optic disc changes or permanent fundal changes over the follow-up period. Conclusion: In contrast to previous studies in America and south-east Asia, our findings based on a UK cohort suggest that routine ophthalmic screening is not essential for patients with hepatitis C treated with pegylated interferon alpha who have no subjective visual complaints.

Cystoid macular edema and visual loss as sequelae to interferon alpha treatment of systemic hepatitis C

Hepatitis C virus infection and interferon treatment may be associated with retinopathy but visual function is generally unaffected. This paper reports the rare occurrence of unilateral macular edema with visual loss. We present an interventional case report with fundus photograph and optical coherence tomography (OCT). A 48-year-old white male with hepatitis C, treated with a six-month course of pegylated interferon alpha and ribavirin, complained of gradual reduction in the vision of his left eye. Visual acuities were 20/16 right and 20/400 left with clinical examination and OCT confirming cystoid macular edema. This report shows that cystoid macular edema may rarely occur in association with hepatitis C infection and/or interferon therapy. Physicians and ophthalmologists should be alert to this potential but infrequent association as the resultant visual loss is a significant potential complication that should be discussed when obtaining informed consent for interferon treatment.

Nature of subretinal fluid in patients undergoing vitrectomy for macular hole: a cytopathological and optical coherence tomography study.

Background:  Outer retinal defects (ORDs) may occur after surgical closure of full thickness macular holes (FTMH) and be associated with delayed visual recovery. This may be due to the nature of the subretinal fluid (SRF) cuff and/or the loss of retinal elements.

Ocular features of Sjogren–Larsson syndrome

Sjogren–Larson syndrome is a rare autosomal recessive neurocutaneous disorder characterized by a triad of intellectual disability, spastic diplegia or tetraplegia and congenital ichthyosis with associated ocular features, which include pigmentary changes in the retina. The usual presentation of crystalline maculopathy is from the age of 1–2 years onwards. Herein, a case of Sjogren–Larson syndrome in a 25‐year‐old woman is presented to highlight the ocular findings.

Pole to Pole Intraocular Transit of Tarantula Hairs—An Intriguing Cause of Red Eye

This intriguing case report provides novel images and a description of the anterior and rarer posterior segment findings seen in ocular inflammation associated with tarantula spider hair exposure. We present an interventional case report of a 9-year-old boy who presented with a red, sore eye. Slit lamp examination revealed right eye injection, multiple small hairs at differing levels of the cornea with associated opacities and inflammation within the anterior and posterior segments of the eye. Only after detailed and repeated questioning did the aetiology become apparent. Conservative management in the form of topical steroid and antibiotics was commenced and he did well with no obvious sequelae in the medium term. Healthcare personnel (and indeed pet shop owners, arachnid enthusiasts and even parents) should be aware of the potential ocular complications of tarantula hair exposure and clinicians should perhaps specifically ask about pet-keeping when presented with an unusual red eye.

Development of full-thickness macular hole despite previous posterior vitreous detachment and vitrectomy for retinal detachment: two cases.

Purpose To report the delayed development of idiopathic full-thickness macular hole in eyes with previously documented complete posterior vitreous detachment that were vitrectomized during surgery for rhegmatogenous retinal detachment. Methods Two interventional case reports with serial color fundus photographs and optical coherence tomography scans. Results Case 1: A 62-year-old man underwent vitrectomy cryoretinopexy and intraocular gas tamponade for rhegmatogenous retinal detachment associated with a complete posterior vitreous detachment. Three years later, he developed a full-thickness macular hole in the same eye. Peeling of the inner limiting membrane and gas tamponade resulted in complete closure of the macular hole with improvement in visual acuity. Case 2: A 70-year-old man presented with a macula-off inferior retinal detachment and counting fingers vision. Vitrectomy cryoretinopexy to a single tear, and gas tamponade was successful and acuity improved to 6/9. He subsequently developed retinal redetachment associated with a new retinal tear and was treated by further vitrectomy and gas. He developed a full-thickness macular hole in the same eye 2 years later with acuity dropping to 1/60. Conclusions Macular hole formation may occur in the context of vitrectomized eyes. These observations support the hypothesis that anteroposterior vitreomacular traction, while traditionally implicated, is not always essential for the development of macular holes.

Lipid lowering drugs in diabetes: lipid lowering has ophthalmic benefits.

EDITOR—Lipid lowering treatment in diabetes has ophthalmic benefits.1 Diabetic maculopathy is a common cause of loss of sight in diabetic patients and is characterised by retinal oedema and lipid exudates. The use of atorvastatin in diabetic maculopathy has recently been shown in a randomised controlled trial to decrease visible lipid exudates and …

Transient visual loss after seizures

Individuals with visual deterioration following a seizure may occasionally present to both general and ophthalmic emergency departments and can cause concern for both patient and clinician alike. Here, we describe two similar cases of young adults on treatment for epilepsy who developed significant bilateral visual loss after grand mal seizures. Full recovery of visual function to baseline was made in both cases. Case 1: A 28-year-old female nurse with known generalized epilepsy following a skull fracture 15 years previously and treated with phenytoin presented to eye casualty. She reported bilateral visual reduction following a witnessed grand mal seizure 1 day previously. On examination her visual acuities were 6/36 right and 6/24 left with reduced colour perception, achieving the demonstration plate and only 11/16 Ishihara colour plates in either eye. She had normal pupillary reactions and full visual fields to confrontation. Automated visual field testing was not available in the emergency eye clinic setting. A comprehensive anterior, dilated posterior segment, cranial nerve and neurological examination was normal. Blood pressure was 114/87 mmHg and blood sugar level was 6.2 mmol/L. A computed tomography brain scan did not reveal any abnormalities and no immediate treatment was recommended aside from checking her serum phenytoin level. At 1-week review, visual acuities had improved to 6/9 right and 6/6 left unaided with full return of colour perception. Slit-lamp and neurological examination remained normal. She reported that her ‘dark and foggy’ vision cleared over the days following her seizure with no residual subjective visual deficit. Case 2: A 37-year-old gentleman on treatment for idiopathic generalized epilepsy presented to eye casualty with persisting bilateral blurred vision subsequent to a grand mal seizure witnessed that morning. Past ophthalmic history included bilateral vitrectomy and pan-retinal photocoagulation for proliferative diabetic retinopathy due to insulin-dependent diabetes. His diabetic retinopathy had been inactive since 2005 and his visual acuity was recorded as 6/12 in the eye clinic 1 week before his casualty attendance. On examination visual acuities were reduced to 6/36 in each eye. His colour perception was reduced to the Ishihara demonstration plate and 9/16 of the colour plates in either eye. Visual field testing to confrontation was not performed as it was felt reliable diagnostic information would not be attained in view of known extensive pan-retinal photocoagulation scarring. He had normal pupillary reactions to light and no acute pathology was present in either eye. He was alert and orientated and cranial nerve examination appeared normal. His blood pressure was 130/ 80 mmHg and blood sugar level 10.9 mmol/L with no recent glycaemic instability on home testing. We elected to manage him by observation, and he gradually improved and at 2-week review visual acuities had returned to their original level of 6/12 unaided for each eye along with return of full colour perception. The mechanism of visual loss associated with seizures may be due to occipital epileptic activity but can also occur non-specifically following generalized convulsions. The precise mechanism in these cases is not known but most authors have suggested an ischaemic hypoxic theory. Experimental studies have demonstrated that clonictonic muscular contractions interfere with respiration and result in lactic acidemia, elevated plasma carbon dioxide levels and hypoxia. Furthermore, convulsions increase the oxygen requirements of the brain and aggravate any anoxia already present. As the macular area of the visual cortex of the occipital lobes are supplied by the terminal branches of the middle and posterior cerebral arteries and thus a watershed zone they are particularly sensitive to anoxia, which may manifest functionally as transient visual decline. Temporary reduction of visual function has also been described following cardiac arrests, head trauma, profound hypoglycaemia and meningitis. We believe the two cases described suffered an episode of transient cortical visual impairment as a result of an occipital ischaemic hypoxic insult. This presumably did not lead to actual cerebral infarction as there was no sign on clinical examination of cortical blindness. Further neuroimaging would have been indicated in the presence of progressing visual loss to exclude embolic lesions, haemorrhage and white matter morphological changes secondary to infarction with contrast enhanced magnetic resonance imaging. Specialist magnetic resonance imaging studies may have confirmed evidence of occipital ischaemia but as yet have not been reported, to our knowledge, in this setting. Indeed, brain perfusion spectroscopic scanning may also be diagnostic and has been used to demonstrate hypoperfusion in the occipital regions in a 19-month-old girl with post-ictal visual impairment. In summary, post-ictal visual reduction is a rare complication of generalized grand mal seizures or status epilepticus and can vary in severity and duration from days to months and is generally associated with full recovery of visual function. Clinicians should be aware of this unusual phenomenon so as to be able to offer reassurance to patients and avoid unnecessary investigations being commenced in the emergency setting.

Diplopia due to maxillary sinus mucocoele

Mucocoeles are cyst-like lesions of the paranasal sinuses, which may rarely erode through the bony orbit and so displace or compress orbital contents. Such patients may present to ophthalmologists and other health care professionals with diverse problems including facial pain and swelling, proptosis, double vision, ptosis, infra-orbital anaesthesia, epiphora and optic nerve dysfunction with reduced vision. We present an illustrated interventional case report of an 81-year-old gentleman with a 2-week history of swelling around the left lower eyelid and malar region associated with double vision both in the primary position and particularly downgaze. We discuss the aetiology, diagnosis and contemporary management of maxillary mucocoeles and also the Caldwell-Luc procedure. The article serves as a reminder that maxillary mucocoeles may slowly and covertly invade the orbit and should be considered in the differential diagnosis in patients presenting with proptosis, globe displacement and an orbital or adnexal mass.