2017 Non-RLN Collapse - Recognition and Treatment

Introduction: There are many laryngeal collapses whom by the noise they created or their endoscopic appearance at exercise resemble RLN prompting our human counterparts to suggest the term “laryngeal movement disorder”.(1) The underlying pathophysiology of these laryngeal collapses is poorly understood in some cases and are the subject of hypothesis and not evidence-based data above level 4.

Objectives: Review our experiences on horses with dynamic laryngeal collapse at exercise with no significant evidence of recurrent laryngeal neuropathy at either Cornell clinic.

Methods: Cases were reviewed from the dynamic (treadmill or overground) from each electronic medical record (EMR) from 2010- 2017 and videoendoscopic images retrieved.

Results and discussion: Five presentations of laryngeal collapse were observed. Type I referred to horses where the corniculate process displaces medially into the airway because (hypothesis) of an apparent structural weakness at the junction of the corniculate and the body of the arytenoid cartilage. Indeed, we propose that a greater percentage of elastic content is present at the junction between the body and corniculate cartilage leading to the collapse at exercise. Although we have limited experience, these horses do not respond to a laryngoplasty as the same degree and location of collapse is observed after surgery since the collapse it is not due to a failure of abduction by the CAD muscle. Treatment at this time is still experimental.

Type II refers to bilateral laryngeal collapse has been reported in the Norwegian cold blood trotters,(2) and we have observed it in saddlebred, Morgan, Hackney pony, warmblood and Thoroughbred racehorses. Dr. Catherine Fjorbakk’s PhD thesis is an exhaustive explanation of the pathophysiology of the condition.(3,4) It is associated with poll flexion leading to an external compression of the larynx. This occurs because poll flexion leads to a more cephalic position of the larynx and narrowing of the laryngeal diameter. The source of the intra-mandibular external compression of the larynx is not identified but is obvious on the CT exam. Although some histopathological evidence of RLN is present, the prevalence of this histopathological lesion is similar to those of non-affected controls. These animals also do not respond well to ventriculocordectomy with or without laryngoplasty. A device that restricts poll flexion has been shown to resolve this problem.(5)

A more recently descripted form of laryngeal collapse is recognized with a ventro-medial luxation of the apex of the corniculate process of the arytenoid cartilage (VMAD).(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 observed associated with a posterior (i.e., dorsal) cleft of the cricoid cartilage. We have not performed a post mortem exam in any affected horses but have performed esophageal ultrasound 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 condition is due to an abnormally wide transverse arytenoid ligament. Treatment at this time is still experimental. Horses affected with this condition present with various degrees of restriction or inability to abduct their affected arytenoid cartilage(s). The condition can be unilateral or bilateral. Current evidence is this condition is a result of a progressive infection following mucosal injury to the body of the arytenoid cartilages. The cause of the direct mucosal trauma has been associated with direct trauma from endoscopy, attempts at nasogastric intubation, inhaled foreign body (from kickback on dirt track?), or more violent evidence of coughing when both vocal processes contact each other. Excessive vocalization has been hypothesized as a cause. The author has observed an association between sub-epiglottic lesions and these mucosal lesions: by inspection it appears that the ventral-lateral edge of the epiglottis can contact the medial surface of the arytenoid cartilage and creates a mucosal ulceration.

Type IV is arytenoid chondritis of the arytenoid cartilage is believed to start with a mucosal ulcer which extends through the basal membrane into the arytenoid cartilage. The etiopathogenesis was pursued in an experimental study where mucosal ulcers were created by nasotracheal intubation in 21 horses.(7) In 52% of these horses, the lesions were healed within one week and another in three weeks. None of the horses developed granuloma nor clinically evident chondritis. This is consistent with the clinical findings that these mucosal lesions are rare and only a small percentage of horses with mucosal injury progress to intraluminal granuloma or chondritis. Smith et al., 2006 reported in a large survey of 2317 New Zealand Thoroughbred racehorses during sales (range 15-24 months of age) only 33 horses (1.2%) had arytenoid mucosal lesions including five with overt chondritis. Horses with mucosal lesions were not statically different than control in terms of number of horses that raced. Kelly et al., reported on 3312 post sales endoscopies in Australian Thoroughbreds and 21 horses (0.63%) had arytenoid mucosal lesions.(8) Five of the 21 were known to develop intraluminal granulomas and only one of them developed chondropathy. The low percentage of mucosal ulcers progressing to arytenoid chondritis is also consistent with the low prevalence of chondritis in Thoroughbred racehorses ranging from 0.21 to 0.22%. Management was either by removal of granuloma or by a partial arytenoidectomy. The last type (Type V) of laryngeal collapse is laryngeal dysplasia- this is well described elsewhere.