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Biomedical subjects

C W Raker

Publications and source records attributed to C W Raker.

At least 19 recordsLinked to original sources

Xeroradiographic evaluation of the equine larynx.

The normal radiographic anatomy of the equine larynx was determine by use of xeroradiography and dissection. The body and laminae of the thyroid cartilage, the muscular process of the arytenoid cartilages, and the dorsal lamina and arch of the cricoid cartilage had radiographic evidence of mineralization (calcification) and/or ossification in clinically normal horses. There was a significant (P less than 0.01) increase in the degree of mineralization of the thyroid and arytenoid cartilages with advancing age. Horses with diagnosis of arytenoid chondrosis (arytenoid chondral dysplasia, arytenoid chondropathy) by use of endoscopy had radiographic changes that included: enlargement with increased density of the arytenoid cartilage region, abnormal patterns of mineralization (dystrophic mineralization or osseous metaplasia), abnormal contour of the corniculate process(es) and laryngeal masses, sometimes obliterating part or all of the lateral laryngeal ventricles.

Aging↗

Sternothyrohyoideus myectomy in horses: 17 cases (1984-1985).

Review of medical records of 78 horses admitted to the George D. Widener Hospital for Large Animals with dorsal displacement of the soft palate revealed 94% of these horses to have evidence of an intermittent abnormal "gurgling" respiratory noise at the time of exercise. Sternothyrohyoideus myectomy was used as a primary treatment for 17 of these horses, with a success rate of 58%. Anatomic dissection of 30 horses indicated that the midcervical region is the optimal site for sternothyrohyoideus myectomy to alleviate dorsal displacement of the soft palate.

Animals↗

Management of arytenoid chondropathy and failed laryngoplasty in horses: 75 cases (1979-1985).

By use of endoscopy, 75 horses with respiratory noise and/or exercise intolerance were determined to have structural arytenoid cartilage abnormalities (60 primary, 11 after previous laryngeal surgery), or failed left laryngoplasty (4 horses) for laryngeal hemiplegia in which the arytenoid cartilage still appeared normal. Eighty-eight percent of the horses were either Thoroughbred (54 horses; 72%) or Standardbred (12 horses; 16%) racehorses; only 9 horses (12%) had occupations not related to racing. Seventy-six percent of the racehorses were 2 to 4 years old; all non-racehorses were greater than 4 years old. The male:female ratio was approximately 2:1. Of the horses with cartilage abnormalities, 28 had left-sided involvement, 22 had right-sided involvement, and 21 had bilateral involvement. Sixty-two arytenoidectomies were performed, 58 for cartilage abnormalities (22 left, 19 right, 17 bilateral), and 4 for failed left laryngoplasties. Overall, 45% of the Thoroughbred racehorses that returned to racing after arytenoidectomy raced successfully (50% left, 75% right, 22% bilateral); only 20% of the Standardbreds were able to race. Seventy-five percent of non-racehorses were able to return to their previous use. Many horses were retired intentionally after surgery.

Animals↗

Dorsal glottic stenosis after bilateral arytenoidectomy in two horses.

Bilateral arytenoidectomy had been performed as treatment for bilateral arytenoid chondritis in 2 horses. After surgery, dorsal mucosal defects were associated with subsequent development of dorsal glottic stenosis in the 2 horses. When performing bilateral arytenoidectomy in the horse, care must be taken to eliminate dorsal mucosal defects that cross the midline. Failure to close these defects may result in glottic stenosis.

Animals↗

Complications during treatment of traumatic disruption of the suspensory apparatus in Thoroughbred horses.

A total of 19 Thoroughbred horses were treated for traumatic disruption of the suspensory apparatus, using either external support of the injured limb, removal of fractured proximal sesamoid bone fragments, metacarpophalangeal arthrodesis, compression screw fixation of the fractured proximal sesamoid bones, application of a cast-brace attached to a transfixation pin inserted through the third metacarpal bone, or combinations thereof. Major complications during the treatment of traumatic disruption of the suspensory apparatus were infection (9 of 19 horses, 47%), large cast sores (10 of 14 treated horses, 71%), laminitis (7 of 19 horses, 37%), and orthopedic implant failure or loosening (4 of 6 treated horses, 67%), which led to euthanasia in 16 of 18 cases with complete follow-up information. Increased pain and lameness signaled the development of such complications. In 7 of 9 cases with infection confirmed by microbiologic culture, the horse had received surgical treatment; in 6 of those 7 cases, the infection involved the surgical site. Postoperative wound infection developed in 4 of 7 cases when the surgery was performed within 18 days of injury. In 3 cases, septic metacarpophalangeal arthritis developed, but it was unrelated to surgical procedures. Implant failure or loosening and infection led to euthanasia in 5 of 6 horses treated by internal fixation to stabilize the metacarpophalangeal joint. Three of 6 attempts to perform metacarpophalangeal arthrodesis by application of a bone plate to the dorsal aspect of the joint resulted in implant failure after 45 to 101 days. Major complications did not develop in 2 horses that were treated successfully.

Animals↗

Epiglottic entrapment by arytenoepiglottic folds in the horse.

An abnormality of the epiglottis and arytenoepiglottic folds that caused epiglottic entrapment was diagnosed in 21 horses. Until recently, this entrapment was poorly understood. Definitive diagnosis of epiglottic entrapment can be made only by endoscopic examination of the epiglottis, arytenoepiglottic folds, and soft palate to differentiate the abnormality from dorsal displacement of the soft palate. Dorsal displacement of the soft palate is often associated with entrapped epiglottis. Epiglottic deformity, especially hypoplasia, is often associated with the entrapment. The abnormality was detected in horses 1 to 16 years old. Because of the relatively large number of young animals (11 being less than or equal to 2 years old), a congenital predisposition was suggested. This suggestion was strengthened by the fact that many of the horses had deformities of the epiglottis that were considered congenital. Because some of the horses had trained and raced satisfactorily before signs of upper airway obstruction developed, it was assumed that the abnormality may be a sequel to epiglottic injury.

Animals↗