Phosphate buffer in alkali eye burns as an inducer of experimental corneal calcification.

Corneal calcification is a common problem in severe inflammation, chronic glaucoma, renal disorders and other diseases with disturbed calcium and phosphorus metabolism. The pathogenesis of corneal calcifications in ocular diseases is not yet completely understood. We present a model of an induced corneal calcification by local treatment. In a double-masked experiment 16 rabbits underwent eye burn of one cornea followed by immediate rinsing (160 ml) with isotonic phosphate buffer (n=8) or saline solution (n=8) three time a day for 16 days. Tissues were excised, shock frozen and cut into 10 microm slices, freeze dried and coated with evaporated carbon. In the phosphate buffer group an early onset of corneal opacification occurred resulting in completely white corneas after 16 days, combined with corneoscleral ulceration. The other group showed similar corneal erosion and a little corneal ulceration, but no opacifications. The opacifications of the phosphate buffer group could be identified as calcifications by direct measurements of calcium and phosphate (by energy dispersive X-ray analysis on corneal samples). In conclusion, inappropriate application of phosphate leads to uncontrolled calcifications of the cornea after severe burns to the eye. This reflects clinically observed calcifications after eye burns and possibly the adverse side effects of phosphate buffered eye drops being applied in ophthalmology.

[Therapy of persistent erosion after severe chemical eye burn with the excimer laser]. / Therapie einer persistierenden Erosio nach schwerer Verätzung mit dem Excimer-Laser.

BACKGROUND: The course after severe eye burns is characterized by many complications which require a longlasting and intensive therapy. The success of treatment is menaced especially by superficial problems like persistent erosiones which occur also after keratoplasty. PATIENT: As a cause of persistent erosions, pathological changes of Bowmans' membrane are discussed. Therefore, it was removed by PTK (phototherapeutic keratectomy) in our patient, in order to allow better adhesion of the epithelium to the deeper, less changed layers. THERAPY AND OUTCOME: The patient suffered from a severe burn accident of his right eye with liquid cement. After proliferations were excised twice, we had to glue on a hard contact lens as an artificial epithelium due to a persistent erosion. Later, the development of a bacterial keratitis required keratoplasty. The epithelium remained intact for eleven months, but then an erosion arose and persisted for nine months. Therefore we performed a PTK and the epithelium closed subsequently within four days. CONCLUSION: The treatment of persistent erosions has been very difficult so far, and often procedures like artificial epithelium or even keratoplasty have been necessary. The astonishing course of our patient indicates, that PTK is a promising and less invasive therapy in these cases.

Modulation of esophageal peristalsis by alterations of body position. Effect of bolus viscosity.

Previous studies have demonstrated that nonviscous liquids traverse the esophagus more rapidly with the subject in the upright rather than the supine position. Conversely, similar studies have shown that viscous liquids traverse the esophagus at similar rates for both upright and supine positions. Our purpose was to define the motor correlates of these differing responses. Six normal volunteers were studied with an infused catheter system incorporating a Dent sleeve for monitoring lower esophageal sphincter pressure. The subjects were given a series of swallows of a water and a viscous (52 centipoise) bolus in both the supine and upright positions. In the upright position, the water bolus caused an increased velocity of propagation in the proximal esophageal segment that was associated with a shortening of lower esophageal sphincter relaxation time and reductions in amplitude and duration of contraction. No significant changes in the peristaltic wave were noted with the viscous bolus during alterations of body position. We conclude that the more rapid transit of a nonviscous water bolus through the esophagus in the upright position is reflected in specific alterations of esophageal peristaltic parameters. The possible mechanisms for these differing responses are discussed.

Effects of alterations in bolus viscosity on esophageal peristalsis in humans.

The effect of increased bolus viscosity on esophageal peristaltic function was studied in six healthy volunteer subjects. Intraluminal pressure events were measured with an infused catheter system and lower esophageal sphincter pressure was monitored continuously with a Dent sleeve. Boluses with viscosities of 2.5, 8.7, 48, and 860 centipoise (cP) were compared with a water bolus. Increasing bolus viscosity to 48 and 860 cP elicited a slowing of wave velocity, an increase in wave duration, and a prolongation of lower esophageal sphincter relaxation. The initial change noted at lower viscosities was an increased duration of contraction wave. Maximal changes were noted at the 48 cP bolus. In conclusion, increased bolus viscosity significantly alters human esophageal peristalsis. These changes may be mediated by esophageal stretch reflexes or by the intrinsic properties of the esophageal musculature or both.