A rare case of zolendronate infusion complication leading to glaucoma filtration surgery.

Zolendronic acid is a nitrogenous biphosphonate commonly used as an intravenous infusion for the management of Paget's disease, osteoporosis, and hypercalcemia of malignancy. We report a rare and challenging complication of zolendronate infusion: unilateral acute anterior uveitis followed by persistently raised intraocular pressure despite being on four different classes of antiglaucoma medication. The challenge was that the patient required topical steroid to treat her uveitis in the background of known glaucoma with corresponding steroid response. She eventually underwent a left phacotrabeculectomy augmented with 5-fluorouracil. Four weeks postoperatively she developed an encapsulated bleb and underwent needling with 5-fluorouracil. This case highlights the importance of having a high index of suspicion for anterior uveitis in patients with a red and painful eye after initiating biphosphonate therapy. Caution should also be exercised when prescribing biphosponates to glaucoma patients.

Intraocular pressures after ketamine and sevoflurane in children with glaucoma undergoing examination under anaesthesia.

AIM: For accurate intraocular pressure (IOP) measurement in very young children examination under anaesthesia (EUA) may be necessary. Most anaesthetic agents used for EUA have some effect on IOP. We compared IOPs in children after ketamine and sevoflurane anaesthesia. METHODS: Consecutive patients with definite or suspected glaucoma, uncooperative for reliable IOP measurement in clinic and requiring EUA, were included in this study. IOPs were measured after intramuscular injection (5 mg/kg) or intravenous injection (2 mg/kg) of ketamine using a Perkins applanation tonometer. Three measurements were taken from each eye. The IOPs were rechecked after sevoflurane, given for maintenance anaesthesia. Mean IOPs were used for analysis. Paired t test was used to assess the differences in IOPs for the whole group and one-way ANOVA for the three subgroups (ketamine IOP <20, 20-30, >30 mmHg). RESULTS: The records of eight patients (16 eyes) were available for review. The mean age was 55.42 (SD 25, range 26-89) months. Seventy data-points from both eyes (35 EUAs) were used for the analysis. The mean IOP after sevoflurane (17 (SD 10) mmHg) was statistically lower than after ketamine (24.4 (SD 12.7) mmHg, p<0.001). The percentage difference was 28.5 (SD 20.8; 95% CI 23.5 to 33.4)). The difference between the subgroups was not statistically significant (p = 0.192). CONCLUSION: Sevoflurane lowers the IOP significantly compared with the IOP measured after ketamine. This difference is independent of the IOP level. It may be important to use ketamine as the induction anaesthetic agent when accurate IOP measurement is necessary during EUA for children.

Isolated bilateral trigeminal neuropathy in sarcoidosis presenting with neurotrophic corneal ulcers.

Sarcoidosis is a multisystem granulomatous disease that may affect various organs. Nevertheless, involvement of the trigeminal nerve is exceedingly uncommon. This report presents a rare case of isolated bilateral trigeminal neuropathy presenting with neurotrophic corneal ulcers. The patient was treated with topical chloramphenicol and lubricants, as well as botulinum toxin injection to the upper eyelid to induce ptosis. Our case illustrates the importance of recognizing that bilateral corneal ulceration might be a manifestation of sarcoidosis. Physicians should be aware of this rare association, when treating sarcoidosis patients with eye related symptoms.

A hypothesis to suggest that light is a risk factor in glaucoma and the mitochondrial optic neuropathies.

The authors propose that light entering the eye interacts with retinal ganglion cell (RGC) axon mitochondria to generate reactive oxygen intermediates (ROI) and that when these neurons are in an energetically low state, their capacity to remove these damaging molecules is exceeded and their survival is compromised. They suggest that in the initial stages of glaucoma, RGCs exist at a low energy level because of a reduced blood flow at the optic nerve head and that in the mitochondrial optic neuropathies (MONs), this results from a primary, genetic defect in aerobic metabolism. In these states RGCs function at a reduced energy level and incident light on the retina becomes a risk factor. Preliminary laboratory studies support this proposition. Firstly, the authors have shown that light is detrimental to isolated mitochondria in an intensity dependent manner. Secondly, light triggers apoptosis of cultured, transformed RGCs and this effect is exacerbated when the cells are nutritionally deprived. Detailed studies are under way to strengthen the proposed theory. On the basis of this proposal, the authors suggest that patients with optic neuropathies such as glaucoma or at risk of developing a MON may benefit from the use of spectral filters and reducing the intensity of light entering the eye.