Ossiculoplasty with J.B. Causse composite prostheses: our experience with 500 cases.

In ossicular pathology, many options are available when the restoration of the columellar effect is required. Autoplasty, heteroplasty and homoplasty have advantages and disadvantages, but considerable recent progress in development of the prosthesis has changed the state of the situation. 500 partial and total prostheses (Porp and Torp) of composite material (Flex HA and Teflon HA) designed by Jean-Bernard Causse and developed by Microtek, were used from January 1992 until December 1993. The authors present results at short and middle term involving all aspects of otologic surgery, as well as surgical techniques that were used.

Ossiculoplasty with composite prostheses. Overview and analysis.

Aeration of a mucosa-lined tympanic cavity is essential for a functioning middle ear. Extrusions of even the best-designed prostheses occur from abnormal middle ear conditions such as atelectasis, middle ear fibrosis, recurrent cholesteatoma, tympanic membrane perforation, and otitis media. Various polymers have been developed in an attempt to maximize prosthetic biocompatibility and ease of use while minimizing the chance of extrusion. One such polymer is a composite of hydroxyapatite and Silastic, known as Flex H/A. This material has been incorporated into two ossicular prostheses, the Universal Plus and the Causse Flex H/A prostheses. Certainly, refinements will continue to be made in the chemical makeup of the bioceramics in order to achieve optimal biocompatibility. In addition to biocompatibility, cost containment issues have influenced the development of ossicular prostheses. A universal prosthesis eliminates the need to stock multiple designs, thereby reducing the cost to institutions. One of the greatest challenges in the future will be to define the appropriate prosthetic design for optimal sound transmission. Consideration of prosthesis weight, head size, and footplate attachment are future research questions that need to be addressed in a scientific biologic model.

Neurokinin inhibition of cholinergic myenteric neurons in canine antrum.

Neurokinins regulate gastrointestinal motility by interacting with receptors on both muscle layers and on myenteric plexus neurons. To determine if specific neurokinin (NK) receptor agonists can mediate inhibitory effects on myenteric neurons, we studied the effect of the NK-1 agonist substance P methylester (SPME) and the putative endogenous NK-2 receptor ligand neurokinin A (NKA) on [3H]acetylcholine [( 3H]ACh) release induced by electrical field stimulation from muscle strips cut from the canine gastric antrum. SPME but not NKA caused a dose-dependent inhibition of stimulated [3H]ACh release in tissues containing the myenteric plexus. The inhibition was not seen in longitudinal muscle without myenteric plexus. Pretreatment of tissues with indomethacin or antiserum to vasoactive intestinal polypeptide (VIP) but not naloxone or adrenergic or cholingergic blockade abolished the SPME-induced inhibition. Exogenous VIP stimulated the release of prostaglandin E2 (PGE2) from full thickness strips, and both VIP and PGE2 inhibited [3H]ACh release induced by electrical depolarization. These findings suggest that NK-1 receptor agonists can selectively inhibit stimulated [3H]ACh release and that this inhibition may involve the release of VIP and PGE2 from neurons within the myenteric plexus.

Endoscopic biopsy can detect high-grade dysplasia or early adenocarcinoma in Barrett's esophagus without grossly recognizable neoplastic lesions.

There is uncertainty regarding the value of endoscopic biopsy surveillance in Barrett's esophagus because, in retrospective studies, some patients with high-grade dysplasia in endoscopic biopsy specimens have had unexpected advanced adenocarcinoma discovered at the time of esophageal resection. We compared the accuracy of preoperative endoscopic biopsy diagnoses with the final pathologic diagnoses in esophagectomy specimens in 4 patients who had both high-grade dysplasia and intramucosal carcinoma and 4 other patients who had only high-grade dysplasia preoperatively. The histologic lesions in all 8 patients were documented in intact mucosa with no gross evidence of neoplasia by endoscopy. The preoperative diagnoses were defined with an endoscopic biopsy protocol in which specimens were taken with large-channel biopsy forceps at least every 2 cm throughout the length of Barrett's epithelium. Final pathologic diagnoses derived from detailed analysis of the resected specimens confirmed high-grade dysplasia without carcinoma in 4 patients and intramucosal carcinoma in 2 patients. The remaining 2 patients with a preoperative diagnosis of intramucosal carcinoma had focal submucosal invasion by carcinoma in the resected specimens, but no involvement of the muscularis propria or adventitial lymph nodes. Because the natural history of high-grade dysplasia is not known, the decision to operate on patients with this lesion must be carefully weighed and individualized for each patient. Two of our patients who underwent esophageal resection for high-grade dysplasia without cancer died, one immediately postoperatively and the other 9 mo later after a postoperative stroke. Once intramucosal carcinoma is documented, surgery should be considered if the patient is an acceptable operative risk. We conclude that systematic preoperative endoscopic biopsy of intact mucosa in Barrett's esophagus can correctly detect high-grade dysplasia, either alone or in combination with early, treatable adenocarcinoma.

Validation of corrections for errors in collimation during measurement of gastric emptying of nuclide-labeled meals.

The study was undertaken to validate phantom-derived corrections for errors in collimation due to septal penetration or scatter, which vary with the size of the gastric region of interest (ROI). Six volunteers received 495 ml of 20% glucose labeled with both In-113m DTPA and Tc-99m DTPA. Gastric emptying of each nuclide was monitored by gamma camera as well as by periodic removal and reinstillation of the meal through a gastric tube. Serial aspirates from the gastric tube confirmed parallel emptying of In-113m and Tc-99m, but analyses of gamma-camera data yielded parallel emptying only when adequate corrections were made for errors in collimation. Analyses of ratios of gastric counts from anterior to posterior, as well as analyses of peak-to-scatter ratios, revealed only small, insignificant anteroposterior movement of the tracers within the stomach during emptying. Accordingly, there was no significant improvement in the camera data when corrections were made for attenuation with intragastric depth.

Error and corrections with scintigraphic measurement of gastric emptying of solid foods.

Previous methods for correction of depth used geometric means of simultaneously obtained anterior and posterior counts. The present study compares this method with a new one that uses computations of depth based on peak-to-scatter (P:S) ratios. Six normal volunteers were fed a meal of beef stew, water, and chicken liver that had been labeled in vivo with both In-113m and Tc-99m. Gastric emptying was followed at short intervals with anterior counts of peak and scattered radiation for each nuclide, as well as posteriorly collected peak counts from the gastric ROI. Depth of the nuclides was estimated by the P:S method as well as the older method. Both gave similar results. Errors from septal penetration or scatter proved to be a significantly larger problem than errors from changes in depth.

Motilin-independent ectopic fronts of the interdigestive myoelectric complex in dogs.

We have studied in four conscious dogs the relationship between circulating concentrations of motilin and the activity front (phase III) of the interdigestive myoelectric complex. During fasting, cyclic peaks of motilin secretion were concomitant in every instance with the initiation of activity fronts that began in the stomach or duodenum. When somatostatin was administered at doses of 5, 2.5, or 0.625 microgram x kg-1 x h-1 for 3 h, motilin concentrations were stabilized at lowered levels and no activity fronts occurred in the duodenum. Somatostatin also inhibited the stimulatory effects of exogenous motilin on the entire small intestine. During somatostatin infusion, however, ectopic fronts began in the jejunum and were propagated to the cecum despite low motilin concentration. After a 100-g meat meal, the cyclic increase of motilin was interrupted and no activity fronts were observed in the duodenum, but ectopic fronts started lower in the small intestine. Our study supports the hypothesis that motilin induces activity fronts in the canine duodenum, but it shows that ectopic fronts are not controlled by motilin.