David S. Hull

Ocular rosacea : Signs, symptoms, and tear studies before and after treatment with doxycycline

OBJECTIVE To examine ocular signs, symptoms, and results of tear analysis in patients with cutaneous rosacea before, during, and after doxycycline therapy. DESIGN Before-after trial. SETTING General community. PATIENTS OR OTHER PARTICIPANTS Thirty-nine patients with cutaneous rosacea underwent dermatologic and ocular examinations, testing of tear break-up time, and Schirmer testing at baseline and 4, 8, and 12 weeks. Six patients did not complete the study. Baseline tear break-up time and results of Schirmer test were compared with those of 13 patients without rosacea who were matched for age and sex. INTERVENTION Patients with rosacea were given doxycycline, 100 mg daily for 12 weeks. MAIN OUTCOME MEASURE Statistically significant (P, .05) improvement in tear break-up time. RESULT The most frequent ocular symptoms were dryness, itching, blurred vision, and photosensitivity, all of which improved significantly with treatment. All patients had signs of ocular disease, most commonly erythema and telangiectasia, meibomian gland dysfunction, and ciliary base injection. Significant improvement (P,.05) for scales, erythema and telangiectasia, ciliary base injection, bulbar injection, papillary hypertrophy, and punctate epithelial erosions was seen. Average tear break-up time for the patients with rosacea was 5.7 seconds, which improved to 10.8 seconds after 12 weeks of treatment (P = .007). Baseline tear break-up time was significantly lower than for the comparison group of normal subjects (P = .001). There was no correlation between severity of cutaneous disease and ocular disease. CONCLUSIONS All patients with cutaneous rosacea had some degree of ocular involvement. Tear break-up time is abnormal in patients with rosacea. Ocular erythema and telangiectasia, meibomian gland dysfunction, and short tear break-up time in patients with cutaneous rosacea are indicators of ocular rosacea. Doxycycline, 100 mg daily, will improve ocular disease and increase the tear break-up time.

Computer-simulated eye surgery : a novel teaching method for residents and practitioners

PURPOSE To describe an eye surgery simulator that uses a computerized graphic display to allow ophthalmic surgeons of all experience levels to enhance their surgical skills. METHODS The eye surgery simulation environment consists of a high-speed computer graphics workstation, a stereo operating system, a wrist rest, and a position tracking stylus connected to force feedback motors. The surgeon views computer-generated images of the eye and surgical instruments through the stereo operating system and controls the position and orientation of the chosen surgical instrument by moving the stylus. During the simulated instrument-tissue interactions, three feedback motors generate component force feedback along three orthogonal axes connected by thin rigid bars to the tip of the stylus. RESULTS The current proof-of-concept system provides a method for rapid learning experiences in a living eye simulation. Procedures can be recorded for playback and analysis, as well as for examination of techniques from different viewpoints (e.g., from inside the eye). Four simulated surgical instruments are available for use (scalpel, forceps, scissors, and phacoemulsifier). CONCLUSION Eye surgery simulation offers both beginning and experienced ophthalmic surgeons an opportunity to learn new techniques and skills and achieve a satisfactory level of proficiency before use of that procedure in the operating room. When fully developed, this system should shorten the learning curve for new surgeons (i.e., residents) and offer an opportunity for practice before doing a difficult case or development of new techniques by experienced surgeons. The goal of replacement of current standard training methods for surgeons awaits further refinement and adjustment of the model.

Corneal Endothelial Permeability after Anterior Chamber Silicone Oil

One of six silicone oils, differing in both viscosity and manufacture, was infused into the anterior chambers of rabbit eyes. Polydimethylsiloxane oil, 5000 cps, caused an increased corneal endothelial permeability to inulin and dextran at 24, 96, and 168 hours after placement into the eye. Intraocular pressures were slightly elevated in the experimental eyes, compared with contralateral controls, at 24 and 144 hours after infusion. The effects of five other oils on corneal endothelial permeability were examined 168 hours after infusion. All oils increased permeability and caused thinning of endothelial cells, together with the appearance of a retrocorneal membrane, except Dow Corning Medical Fluid 360. The results indicated that contact of most silicone oils with corneal endothelium rapidly induces physiologic and morphologic changes.

Possible Relationship of Ethylene Oxide Exposure to Cataract Formation

We examined 12 men whose work involved exposure to ethylene oxide sterilizers after one sterilizer developed a leak. Only the four men who had worked on the leaking sterilizer developed neurologic abnormalities. Three of them also developed cataracts, and one required bilateral cataract extractions. Four men, two of whom had not worked on the leaking sterilizer, had increased central corneal thickness with normal endothelial cell counts.

Rabbit corneal endothelial permeability in the presence and absence of adenosine and glutathione

Rabbit corneal endothelial fluxes of sodium, bicarbonate, inulin, and dextran have been measured in ambient solutions containing either 0.5 mM adenosine alone (A), 0.3 mM glutathione alone (G), both adenosine and glutathione, or neither adenosine nor glutathione. Addition of A alone to a solution lacking both additives caused a decrease in both Jstrendo and Jendostr sodium fluxes coupled with an increase in Jstrendo net. Addition of G alone caused no effect, whereas addition of A and G together caused a decrease in both Jstrendo and Jendostr sodium fluxes and a large increase in Jstrendo net. Addition of A or G caused an increase in Jstrendo bicarbonate flux, but no change in Jendostr flux. Addition of A and G caused an increase in both Jstrendo and Jendostr bicarbonate flux and a decrease in Jstrendo net. None of the solution variations caused an alteration in either inulin or dextran permeability. Since both A and G influence Jstrendo net bicarbonate and sodium transport, this may provide an explanation of the beneficial effects of these compounds on the endothelium to both enhance and prolong corneal thickness and hydration regulation.

Effects of calcium channel blockers on rabbit corneal endothelial function

The effects of calcium channel antagonists and agents that alter intracellular Ca2+ mobilization on corneal endothelial function have been examined. All experiments, except where specifically designated, were performed in the continuous presence of extracellular Ca2+. Verapamil (at 50 microM) increased the swelling rate of corneas bathed in normal Ringer solution whereas nifedipine and diltiazem (both up to 100 microM) were without effect. The nifedipine analog nisoldipine caused corneal swelling at 10 microM and 50 microM but nimodipine was without effect. When briefly exposed to a Ca(2+)-free solution corneal swelling was enhanced after subsequent exposure to 50 microM verapamil in normal Ringer but not after 50 microM diltiazem in normal Ringer, indicating that Ca2+ entry from the bathing solution into the cell was important and was apparently impeded by verapamil. Cadmium (0.6 and 1 mM) but not nickel (up to 250 microM) caused swelling of corneas bathed in normal Ringer. A Ca2+ channel agonist, BAY-K-8644, alone did not influence corneal thickness but when presented to the endothelium with 50 microM verapamil the swelling rate was much reduced compared to verapamil alone. The agonist, therefore, presumably maintained some Ca2+ channels open in face of the Ca2+ channel blocker. An agent that inhibited the release of intracellular Ca2+ stores (TMB-8) caused an initial corneal swelling over the first 1.5 hr of perfusion but thereafter had no effect on corneal thickness. In the presence of continued extracellular Ca2+ one explanation for the results is that modulation of intracellular Ca2+ by agents that alter plasma membrane transfer of Ca2+ influences apical junction permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

Photodynamic alteration of cornea endothelium: Relation to bicarbonate fluxes and oxygen concentration

Corneas were mounted in flux chambers and endothelial bicarbonate fluxes were determined following sensitization of endothelial cells with 5 . 10(-6) M rose bengal and exposure to light. Corneas exposed to light demonstrated an increased passive bicarbonate flux compared to corneas not photosensitized. Active bicarbonate flux was reduced after 5 min of light exposure, but not after 1 min of light exposure. The increase in passive bicarbonate flux was prevented by the addition of 200 microgram/ml catalase to the bathing solution; however, catalase had no effect on the photodynamic alteration of active flux. Neither 10 mM ascorbic acid nor 1.012 gram/l glutathione prevented the photodynamically induced increase in passive flux. Perfusion of corneas with 5 . 10(-6) M rose bengal dissolved in a sucrose-substituted Krebs-Ringer bicarbonate solution with a PO2 of 124 +/- 4.0 mmHg and exposed to light swelled at rates more rapid than corneas treated in a similar fashion but perfused with a solution with a PO2 of 20 +/- 4.6 mmHg. This study demonstrated that photodynamically induced corneal endothelial cell alteration results in increased passive bicarbonate flux, a time-dependent decrease in active bicarbonate flux, is oxygen dependent, and is at least in part secondary to H2O2 produced by the dismutation reaction of the superoxide free radical.

BSS and BSS-plus: effect on corneal endothelial ionic and non-ionic fluxes.

Rabbit corneas were mounted in water jacketed chambers and the endothelial surface perfused with either BSS (Balanced Salt Solution) or BSS-Plus for 3 hr. Unidirectional and net fluxes of sodium were similar in both groups of corneas. Bicarbonate fluxes in BSS-Plus were statistically similar to those in Krebs-Ringer solution. Bicarbonate fluxes could not be determined with BSS because the solution does not contain bicarbonate. In addition, there was no statistically significant alteration of inulin or dextran permeability when comparing perfusion with BSS and BSS-Plus. From this study it appears that BSS and BSS-Plus are comparable in their ability to maintain corneal endothelial physiologic function during in-vitro perfusion. This is in contrast to previous work which showed that BSS-Plus induced less endothelial morphologic change than BSS. It is concluded that morphologic alterations may be more sensitive parameters of endothelial stress than are fluxes and permeabilities.

Rose bengal induced corneal swelling: relation to inciting wavelength

Cornea endothelial cells sensitized with rose bengal and exposed to light demonstrated a wavelength dependent alteration in physiological response. Corneas exposed to 549 millimicron swelled at rates similar to controls exposed to identical energy levels of incandescent light. Corneas exposed to 451, 500, 612, and 651 millimicron swelled at rates less rapid than corneas exposed to similar energy levels of incandescent light. The photodynamically induced physiological alteration of cornea endothelial cells approximately paralleled the spectral curve of rose bengal with its peak at 550 millimicron.

Rabbit corneal endothelial physiologic and morphologic characteristics following storage in MK medium and K-Sol

Abstract Rabbit corneas were stored for 3, 7, 10 or 14 days in MK medium or K‐Sol. Corneas were thinner immediately following removal from K‐Sol than following removal from MK medium at all time periods studied. Following 3 days of storage, corneas stored in both solutions showed similar temperature reversal characteristics. Corneas stored for 7 and 10 days in MK medium also temperature reversed, whereas those stored in K‐Sol did not. Corneas stored for 14 days in both solutions swelled following mounting in the specular microscope. Endothelial cell morphology was similar following storage in MK medium and K‐Sol at all time periods studied. It is postulated that a persistant osmotic gradient is present across the endothelium following storage in K‐Sol. This osmotic gradient occurs because of retention of chondroitin sulphate in the corneal stroma thereby preventing early temperature reversal.