Vet Clin Equine 19 (2003) 159167

Disorders of the pharynx

Eileen K. Sullivan, DVMa,*, Eric J. Parente, DVMb
Department of Clinical Sciences, Colorado State University, College of Veterinary Medicine and Biomedical Sciences, James L. Voss Veterinary Teaching Hospital, Fort Collins, CO 805231620, USA b Department of Clinical Studies, University of Pennsylvania, School of Veterinary Medicine, Kennett Square, PA, USA
a

Congenital disorders of the pharynx Choanal atresia Choanal atresia is a disorder resulting from failure of the bucconasal membrane to perforate during embryologic development [1] and is rare in horses [2]. The bucconasal membrane then forms a partial or complete separation between the caudal nasal cavity and the pharynx [1]. Choanal atresia can occur as a unilateral or bilateral condition and is recognized most often in the neonate. Unlike what is reported in people and llamas, the obstruction in horses is not bony. Clinical signs include severe dyspnea and decreased air movement from each aected nostril. When both nasal passages are aected, emergency tracheotomy is necessary shortly after birth to maintain airway patency. Endoscopic examination and contrast radiography can be used to demonstrate the imperforate septum. The bucconasal membrane can be excised surgically through a nasal ap or transnasally using endoscopic guidance. Stents to minimize stricture should be considered after bucconasal membrane excision [3], but, to date, there are no long-term reports of recovery to athletic function, and it is presumed that stricture is common. More recently, the authors have used a technique of frequent bougienage, which seems promising. Cleft palate (palate hypoplasia) A cleft palate may be suspected when milk drains from a newborn foals nostrils shortly after initial nursing eorts. Diagnosis is conrmed by either
* Corresponding author. E-mail address: esulliv@lamarcolostate.edu (E.K. Sullivan). 0749-0739/03/$ - see front matter 2003, Elsevier Science (USA). All rights reserved. doi:10.1016/S0749-0739(02)00071-8

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oral palpation of the defect or by endoscopic examination. The resulting oronasal defect can predispose the foal to failure of passive transfer, malnutrition, and aspiration pneumonia [4]. If the palate defect is small, foals may mature without denitive diagnosis from 6 weeks to 7 years of age, although eventual soundness is jeopardized by the defect [58]. When severe, surgical repair is the necessary treatment and should be performed as early as possible to close the oronasal stula and prevent secondary complications. Mandibular symphysiotomy is the most common surgical approach to palate repair [4]. Complications after surgical repair include aspiration pneumonia, mandibular osteitis or nonunion, and dehiscence failure of the palatal repair [9]. Despite successful treatment of the oronasal defect, pharyngeal function may still be compromised, precluding athletic function as an adult. Concurrent congenital facial deformities are known to occur with cleft palate and include cyclops [10] and nasal septal deviation [6]. The presence of additional congenital abnormalities must always be investigated. Pharyngeal cysts Pharyngeal cysts have been identied in the dorsal pharyngeal wall and soft palate but occur most commonly in the subepiglottic region. Subepiglottic cysts are thought to be embryologic remnants of the thyroglossal duct [11], although a traumatic origin has been postulated [12]. Cysts located on the dorsal pharyngeal wall may be congenital and result from a persistent remnant of the craniopharyngeal duct or Rathkes pouch [11]. Cysts, usually evident at a young age, can occur in any breed and have been more commonly reported inmaale horses [13]. Clinical signs include abnormal upper airway noise, cough, exercise intolerance, nasal discharge, dysphagia, and aspiration pneumonia. Foals with cysts involving the soft palate may develop dorsal displacement of the soft palate (Fig. 1). A pharyngeal cyst may be suspected based on history and clinical signs, but endoscopic and radiographic examination is necessary to conrm the diagnosis. Contrast radiography after oral administration of barium sulfate can be helpful is isolating pharyngeal cysts located on the soft palate [14]. Surgical excision of the cyst can be accomplished through laryngotomy, pharyngotomy, or a transoral or transnasal approach. Noncontact laser ablation can also be successful and obviate the need for a surgical incision. Rostral displacement of the palatopharyngeal arch Typically, the larynx protrudes through the intrapharyngeal ostium, which is bordered caudally by the palatopharyngeal arch. Rostral displacement of the palatopharyngeal arch is a congenital anomaly that induces pharyngeal dysfunction. Horses may display clinical signs of dysphagia, persistent cough, abnormal upper respiratory noise, and aspiration pneumonia

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Fig. 1. A lateral skull radiograph with persistent displacement of the soft palate. The epiglottis can be seen below the cyst. An esophageal feeding tube is present.

[15]. In some cases, the primary clinical sign is abnormal upper respiratory noise [16]. Treatment options are limited, because concurrent anomalies, such as absence of the cricopharyngeal muscle, deformed thyroid cartilage, absence of the cricothyroid articulation, and degeneration of the recurrent laryngeal nerve, can accompany the palatopharyngeal arch displacement [17]. Successful surgical laser ablation of the displaced palatal tissue has been performed; however, the prognosis for athletic performance remained poor [18]. Pharyngeal trauma Trauma to the pharynx may manifest as external swelling, dyspnea, dysphagia, or unusual upper respiratory noise. Diagnostic tools, such as astute physical examination, radiography, and upper airway endoscopy, may elucidate both the source of trauma and extent of pharyngeal damage. Potential origins of pharyngeal trauma include external lacerations, puncture wounds, and blunt trauma. Another potential origin of pharyngeal trauma is foreign body penetration. Pharyngeal foreign bodies are most commonly composed of wood or metal [19], although, historically, anthelmintic boluses administered by a balling gun have been implicated [20]. Obligate anaerobic bacterial infections may result in foreign bodies penetrating the mucosa, and anaerobic commensals may gain access to deeper pharyngeal tissues [21]. Radiographic examination is the diagnostic tool of choice with metallic foreign bodies [22]. In most horses, surgical removal of pharyngeal foreign bodies is necessary before clinical signs can be resolved [22].

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Iatrogenic causes of pharyngeal trauma include laceration secondary to nasogastric intubation. Trauma may be caused by forceful initial insertion or prolonged intubation and can result in signs of ptyalism, dysphagia, and coughing [23]. It may be difcult to differentiate between pharyngeal and esophageal trauma based on clinical signs alone without the use of endoscopic examination [23]. Clinical signs associated with pharyngeal perforation may not be evident for several weeks after the initial trauma, when secondary abscesses form [24]. Treatment regimens may include esophagostomy to allow enteral feeding or gastric decompression if required. Although rare, iatrogenic laceration of the soft palate can occur when transnasal approaches are used to correct epiglottic entrapment. Fullthickness lacerations of the soft palate have been repaired successfully in adult horses after inadvertent division [25]. Nasopharyngeal cicatrix may develop as a result of scarring and inammation secondary to pharyngeal trauma. In many horses, the underlying traumatic incident is not readily apparent at the time of endoscopic examination, although other abnormalities seen concurrently include abnormal or deformed epiglottic and arytenoid cartilage [26]. Concurrent clinical signs include upper respiratory noise and exercise intolerance. Nasopharyngeal cicatrix may not be the primary cause of respiratory impairment, although when it is implicated, surgical correction may be attempted [27]. In more severe cases, permanent tracheostomy is recommended [24].

Pharyngeal dysfunction Dorsal displacement of the soft palate Dorsal displacement of the soft palate (DDSP) can be intermittent or persistent. Horses with persistent DDSP exhibit exercise intolerance and upper respiratory noise and may or may not cough and be dysphagic. Diagnosis is conrmed on endoscopic examination after failure to see the epiglottis during a prolonged examination and frequent attempts to correct the displacement after swallowing. The etiology of persistent displacement versus intermittent displacement seems to be dierent and therefore should be addressed accordingly. Occasionally, persistent displacement is observed with concurrent epiglottic entrapment. This should be suspected if there is bulging of the palate from the epiglottis, minimal dysphagia, and no other neurologic decits. Infrequently, the edge of the entrapment can be recognized separate from the edge of the palate (Fig. 2). Radiographs may conrm this diagnosis, and resolving the entrapment surgically resolves the displacement problem. Persistent displacement associated with more signicant dysphagia and neurologic problems has a poorer prognosis, and therapy is aimed at resolving the underlying neurologic dysfunction. Intermittent DDSP (IDDSP) is a signicant performance-limiting problem in horses that is only evident during exercise. Often, a presumptive

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Fig. 2. Concurrent displacement of the soft palate and epiglottic entrapment. Both the edge of the entrapment and the edge of the palate can be discerned.

diagnosis and treatment are based on historical information of poor performance, abnormal respiratory noise, resting or postexercise endoscopic examination, and lack of other clinical ndings. Although the cause of this disorder is unknown, epiglottic hypoplasia, malformation, and neuromuscular dysfunction have been proposed [28]. More recent information from a study of IDDSP during high-speed treadmill endoscopy provides evidence that IDDSP occurs in multiple forms and can be associated with other dynamic respiratory abnormalities [19]. Furthermore, many horses had no structural abnormalities noted on resting endoscopic examination and no history of making an abnormal respiratory noise [19]. Although the diagnosis of IDDSP is not easy, IDDSP may be suspected if the epiglottis appears small or accid on endoscopic examination and the upper airway noise reported during exercise is consistent with this diagnosis. Transient displacement of the soft palate during resting endoscopic examination is an incidental and insignicant nding if DDSP is not suggested in the history [19,29]. Horses that are predisposed to IDDSP may develop palate displacement on occlusion of the external nares during a standing examination, because this maneuver mimics the exercise examination by creating negative pressure in the pharynx [30]. It has long been suspected

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that horses affected with IDDSP develop an ulcer on the free border of the soft palate as a result of the frequent displacement and replacement that is evident on standing endoscopic examination [31], but a signicant correlation between ulceration of the palate and displacement during highspeed treadmill endoscopy has not been supported [19]. Given the diculty in diagnosing and dierentiating the cause of IDDSP, moderate success with numerous treatments is not surprising. Use of a tongue tie can be benecial to prevent caudal retraction of the larynx, thereby increasing palate contact with the epiglottis [29]. Surgical treatments of DDSP also target caudal retraction of the larynx by excising muscles that apply caudal retracting forces. The sternothyrothoideus myectomy provided a successful outcome in 58% [32] and 60% [33] of horses in two populations. Staphylectomy, thought either to stiffen the free edge of the palate or to enlarge the pharyngeal ostium physically, improved 60% of horses in a similar population [33]. Neodymium:yttrium (Nd:Yag) laser augmentation of the free border of the soft palate has also been used to induce scar tissue and discourage palatal displacement [34]. When applicable, augmentation of a accid epiglottis can improve an individual horses airway dynamics, and a 66% success rate is reported [31]. Younger horses that are suspected of having a primary neurogenic cause can also improve with rest and antiinammatory treatment [19]. Pharyngeal collapse Collapse of the dorsal pharyngeal wall during exercise is a performancelimiting problem causing upper airway noise during peak expiration. Although the etiology of pharyngeal collapse during exercise is unknown, pharyngeal neuromuscular paresis and other adjacent dynamic abnormalities, such as mild guttural pouch tympany, have been proposed [35,36]. When suspected, denitive diagnosis of pharyngeal collapse is made through use of videoendoscopic examination during treadmill exercise. In three populations of horses undergoing treadmill evaluation for poor performance or upper airway noise, the incidence of pharyngeal collapse was 3% [37], 8% [38], and 12% [39]. Because there is no known treatment for this disorder, the prognosis for athletic function is guarded [35].

Pharyngitis Pharyngeal lymphoid hyperplasia is commonly recognized in young horses. Many attribute pharyngeal lymphoid hyperplasia to a local immune response to inhaled or ingested antigens [40], because it increases on challenge to both acute bacterial and viral infections [41] and stabling [42]. Diagnosis is obtained through pharyngeal endoscopic examination. Surveys of endoscopic ndings within the upper respiratory tract of racehorses

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estimate the prevalence to be from 34.2% [43] in one population to as high as 89% [2] in another population. Multiple studies correlate prevalence and age, with younger horses having a higher incidence and severity [40,43,44]. Some authors have implicated pharyngeal lymphoid hyperplasia as a performance-limiting entity [11,41], although most now agree that this condition has little if any impact on the athletic ability of the horse or function of the upper respiratory tract, unless severe [4547]. The pharynx may play a role in both harboring and detecting etiologic agents of subclinical upper respiratory tract infection. The soft palate epithelium and tonsillar tissue have been implicated as sites of both initial penetration and maintenance of Streptococcus equi infections, serving as a reservoir for future transmission [43]. Equine herpesvirus and inuenza virus have been implicated in horses developing acute signs of infectious upper respiratory disease [48]. Nasopharyngeal swab samples are helpful in identication of the causative organism in acute upper respiratory tract infections. Organisms isolated from pharyngeal mucosa have also been implicated as etiologic agents in lower respiratory tract disease [49,50]. Fungal infections caused by Conidiobolus coronatus are also reported as etiologic agents in equine pharyngitis [51]. Topical antifungal and systemic fungal treatment is indicated in these cases.

Neoplasia Although rare, primary pharyngeal neoplasia occurs in the horse. Clinical signs include nasal discharge, increased upper respiratory noise, exercise intolerance, dysphagia, and generalized wasting. Lymphosarcoma and squamous cell carcinoma are the most common tumors identied. Although primary pharyngeal neoplasia is rare, extension of masses from neighboring anatomic regions, such as the oral cavity and sinus regions, occurs more frequently. Diagnosis of pharyngeal neoplasia is based on clinical signs, endoscopy, and pharyngeal radiography. Many times, masses are severely enlarged and tissue invasion is extensive at the time of diagnosis because of slow onset of clinical signs [52]. For this reason, medical and surgical treatment options are limited and are not attempted many times [52]. Treatment by intralesional injection or laser excision can be attempted.

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