FRANK J. MILNE STATE-OF-THE-ART LECTURE


triculocordectomy and ary-epiglottic folds with a la- ryngoplasty procedure. There was an association between laryngoplasty


and the development of EIPH and airway inflamma- tory disease in a case-cohort study.238 Both of these support the documentation of shorter racing career reported in the past.236 It has been proposed that the interference with the native protective mechanism of the larynx by the laryngoplasty predispose to pulmo- nary inflammation and fibrosis of the pulmonary pa- renchyma. Both factors are likely to increase the occurrence and severity of EIPH.


Failure to Maintain Abduction


The loss of abduction in the first 6 weeks post laryn- goplasty has been well described by the classical paper of Dixon et al, 2003.75 However, there is ample evidence that a Dixon laryngeal Grade III (modest abduction) is compatible with good athletic performance. Moderate abduction of the arytenoid 6 weeks after surgery is likely to be maintained and is sufficient for racing soundness (probably the hard- est clinical test of this treatment) if the arytenoid is stable during exercise and no other soft tissue col- lapse is present.291,292,294 This has led many investigations on various tech-


niques to improve the stability of the upper airways. They can be classified under the following:


1. Increased stability of the cricoarytenoid articulation240,242,243


2. Increasing stability of the suture-cartilage interaction244,295–299


3. Better abduction intra-operatively248,250


Laryngeal Collapse Without RLN There are many laryngeal collapses that resemble RLN prompting our human counterparts to suggest the term “laryngeal movement disorder.”300 The affected horses have no evidence of RLN yet exhibit laryngeal collapse during exercise (Fig. 13, A–C). The horses in Figure 13 all had arytenoid collapse during exercise without evidence of RLN. No ex- perimental or histopathological data was available to explain the collapse. The author hypothesized that in horses with the collapse represented in Fig- ure 13A, the corniculate process medialize into the airway because of a structural weakness at the junc- tion of the corniculate and body of the arytenoid cartilage. We have information of the elastic con- tent of the body of the arytenoid cartilage301 and propose that a greater percentage of elastic content at the junction cause the body and corniculate cartilage leads to the collapse seen during exercise. Although we have limited experience with this odd condition, these horses do not respond to laryngoplasty. Treat- ment at this time is still experimental. This form of collapse showed in Figure 13B has


been reported in the Norwegian cold blood trot- ter,95,302,303 and we have observed it in Saddlebred, Hackney pony, Warmblood and Thoroughbred race-


108 2016  Vol. 62  AAEP PROCEEDINGS


horses. Catherine Fjorbakk’s PhD thesis is an ex- haustive explanation of the condition.304 The condition is associated with poll flexion leading to an external compression of the larynx. This occurs be- cause poll flexion leads to a more cephalic position of the larynx and narrowing of the laryngeal diameter.303,304The source of the intra-mandibular ex- ternal compression of the larynx is not identified but is clearly obvious on the CT exam.304 Although some histopathological evidence ofRLNis present, the prev- alence of this histopathological lesion is similar to those of nonaffected controls.215 These animals do not respond well to ventriculocordectomy with or with- out laryngoplasty. A device that restricts poll flexion has been shown to resolve this problem.305 The form of collapse shown in Figure 13C has


been reported by at least three different groups98,221,306 and is not well understood. In a recent paper calling for a plea for consensus on no- menclature of upper airway obstruction, it was rec- ommended to refer to this condition as ventromedial luxation of the apex of the corniculate process of the arytenoid cartilage (VLAC).6 The condition may be unilateral or bilateral, may be obstructive or not, and can be observed in horses that also have RLN, although this is rare in the author’s experience. In humans, a similar endoscopic appearance is ob- served associated with a posterior (i.e., dorsal) cleft of the cricoid cartilage.307 A post-mortem exam has not been performed in any affected horses but an esophageal ultrasound was performed in one case and failed to detect a cricoid cleft. Barakzai has reported the post-mortem exam of an affected Clydesdale horse and has suggested that the condi- tion is due to an abnormally wide transverse ary- tenoid ligament.221 Treatment at this time is still experimental.


Arytenoid Chondritis


Horses affected with arytenoid chondritis present with various degrees of restriction or inability to abduct their affected arytenoid cartilage(s).219,251 The condition can be unilateral or bilateral. Cur- rent evidence of this condition is a result of a pro- gressive infection following mucosal injury to the body of the arytenoid cartilages.219,308,309 The cause of the direct mucosal trauma has been associ- ated with direct trauma from endoscopy, attempts at nasogastric intubation, inhaled foreign body (from dirt tract?), or more violent evidence of coughing when both vocal process contact each other.219,309– 311 Excessive vocalization has been hypothesized as a cause.308 The author has observed an associ- ation between subepiglottic lesions and these muco- sal lesions. By inspection it seems that the ventral- lateral edge of the epiglottis contacts the medial surface of the arytenoid cartilage and creates a mu- cosal ulceration (Fig. 14). Chondritis of the arytenoid cartilage is believed to


start with a mucosal ulcer, which extends through the basal membrane into the arytenoid cartilage.


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