- Email: [email protected]
Disorders of the pharynx
Vet Clin Equine 19 (2003) 159–167
Disorders of the pharynx Eileen K. Sullivan, DVMa,*, Eric J. Parente, DVMb a
Department of Clinical Sciences, Colorado State University, College of Veterinary Medicine and Biomedical Sciences, James L. Voss Veterinary Teaching Hospital, Fort Collins, CO 80523–1620, USA b Department of Clinical Studies, University of Pennsylvania, School of Veterinary Medicine, Kennett Square, PA, USA
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 affected nostril. When both nasal passages are affected, 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 flap 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 foal’s nostrils shortly after initial nursing efforts. Diagnosis is confirmed by either * Corresponding author. E-mail address: [email protected] (E.K. Sullivan). 0749-0739/03/$ - see front matter Ó 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 definitive diagnosis from 6 weeks to 7 years of age, although eventual soundness is jeopardized by the defect [5–8]. When severe, surgical repair is the necessary treatment and should be performed as early as possible to close the oronasal fistula 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 identified 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 Rathke’s 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 confirm 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 difficult 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 inflammation 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 confirmed 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 different 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 deficits. Infrequently, the edge of the entrapment can be recognized separate from the edge of the palate (Fig. 2). Radiographs may confirm this diagnosis, and resolving the entrapment surgically resolves the displacement problem. Persistent displacement associated with more significant dysphagia and neurologic problems has a poorer prognosis, and therapy is aimed at resolving the underlying neurologic dysfunction. Intermittent DDSP (IDDSP) is a significant 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 findings. 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 flaccid 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 insignificant finding 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 significant correlation between ulceration of the palate and displacement during highspeed treadmill endoscopy has not been supported [19]. Given the difficulty in diagnosing and differentiating the cause of IDDSP, moderate success with numerous treatments is not surprising. Use of a tongue tie can be beneficial 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 flaccid epiglottis can improve an individual horse’s 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 antiinflammatory 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, definitive 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 findings 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 [45–47]. 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 influenza virus have been implicated in horses developing acute signs of infectious upper respiratory disease [48]. Nasopharyngeal swab samples are helpful in identification 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 identified. 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.
References [1] Freeman D. Nasal passages. In: Beech J, editor. Equine respiratory disorders. Philadelphia: Lea & Febiger; 1991. p. 253–74. [2] Raphel C. Endoscopic findings in the upper respiratory tract of 479 horses. JAVMA 1982;181:470–3. [3] Hogan PM, Embertson RM, Hunt RJ. Unilateral choanal atresia in a foal. JAVMA 1995;207:471–3.
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[4] Gaughan E, DeBowes R. Congenital diseases of the equine head. Vet Clin North Am Equine Pract 1993;9:93–110. [5] Bertone J, Traub-Dargatz JL, Trotter G. Bilateral hypoplasia of the soft palate and aryepiglottic entrapment in a horse. JAVMA 1986;188:727–8. [6] Haynes P, Qualls W. Cleft soft palate, nasal septal deviation, and epiglottic entrapment in a Thoroughbred filly. JAVMA 1981;179:910–3. [7] Mason T, Speirs V, Maclean A, et al. Surgical repair of cleft soft palate in the horse. Vet Rec 1977;100:6–8. [8] Pouret E. Practical aspects of the treatment of difficult wound. Equine Vet J 1973;5:52–5. [9] Bowman K, Tate L, Evans L, et al. Complications of cleft palate repair in large animals. JAVMA 1982;180:652–7. [10] Crowe W, Swerczek T. Equine congenital defects. Am J Vet Res 1985;46:353–8. [11] Proudman C, Knottenbelt D, May S, et al. Soft palate hypoplasia in a horse. Vet Rec 1991;129:284–6. [12] Richardson J, Lane J, Day M. Congenital choanal restriction in 3 horses. Equine Vet J 1994;26:162–5. [13] Koch D, Tate L. Pharyngeal cysts in horses. JAVMA 1978;173:860–2. [14] Haynes P, Beadle R, McClure J, et al. Soft palate cysts as a cause of pharyngeal dysfunction in two horses. Equine Vet J 1990;22:369–71. [15] Cook W. Some observations on diseases of the ear, nose, and throat in the horse, and endoscopy using a flexible fiberoptic endoscope. Vet Rec 1974;94:533–41. [16] Goulden B, Anderson L, Davies A, et al. Rostral displacement of the palatopharyngeal arch: a case report. Equine Vet J 1976;8:95–8. [17] Klein H, Deegen E, Stockhofe N, et al. Rostral displacement of the palatopharyngeal arch in a seven-month-old Hanoverian colt. Equine Vet J 1989;21:382–3. [18] Blikslager A, Tate L, Tudor R. Transendoscopic laser treatment of rostral displacement of the palatopharyngeal arch in four horses. J Clin Laser Med Surg 1999;17:49–52. [19] Parente EJ, Martin BB, Tulleners EP, et al. Dorsal displacement of the soft palate in 92 horses during high-speed treadmill examination (1993–1998). Vet Surg 2002;31: 507–12. [20] Hamilton DP. Pharyngeal rupture in a horse. JAVMA 1973;162:466. [21] Moore R. Pathogenesis of obligate anaerobic bacterial infections in horses. Compend Contin Educ Pract Vet 1993;15:278–86. [22] Kiper M, Wrigley R, Traub-Dargatz J, et al. Metallic foreign bodies in the mouth or pharynx of horses: seven cases (1983–1989). JAVMA 1992;200:91–3. [23] Hardy J, Stewart R, Beard W, et al. Complications of nasogastric intubation in horses: nine cases (1987–1989). JAVMA 1992;201:483–6. [24] Rakestraw PC, Eastman TG, Taylor TS, Schumacher J, Wright L. Long-term outcome of horses undergoing permanent tracheostomy: 42 cases. In: 46th Annual Convention Proceedings of the American Association of Equine Practitioners. 2000. p. 111–2 [25] Holcombe S, Robertson J, Richardson L. Surgical repair of iatrogenic soft palate defects in two horses. JAVMA 1994;205:1315–7. [26] Rashmir-Raven A, DeBowes R, Douglas J, et al. What is your diagnosis? JAVMA 1991;198:1991–2. [27] McClure S, Schumacher J, Snyder J. Transnasal incision of restrictive nasopharyngeal cicatrix in three horses. JAVMA 1994;205:461–3. [28] Holcome S, Derkson F, Stick J, et al. Pathophysiology of dorsal displacement of the soft palate in horses. Equine Vet J Suppl 1999;30:45–8. [29] Haynes P. Dorsal displacement of the soft palate and epiglottic entrapment: diagnosis, management, and interrelationship. Compend Contin Educ Pract Vet 1983;5(Suppl): S379–89. [30] Heffron C, Baker G. Observations on the mechanism of functional obstruction of the nasopharyngeal airway in the horse. Equine Vet J 1979;11:142–7.
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[31] Tate LP, Sweeney CL, Bowman KF, et al. Transendoscopic Nd:YAG laser surgery for treatment of epiglottal entrapment and dorsal displacement of the soft palate in the horse. Vet Surg 1990;19:356–63. [32] Harrison I, Raker C. Sternothyrothoideus myectomy in horses: 17 cases (1984–1985). JAVMA 1988;193:1299–302. [33] Anderson J, Tulleners EP, Johnston JJ, et al. Sternothyrothoideus myectomy or staphylectomy for treatment of intermittent dorsal displacement of the soft palate in racehorses: 209 cases (1986–1991). JAVMA 1995;206:1909–12. [34] Strand E, Staempfli HR. Dynamic collapse of the roof of the nasopharynx as a cause of poor performance in a Standardbred colt. Equine Vet J 1993;25:252–4. [35] Holcome S, Ducharme N. Pharynx. In: Auer JA, Stick JA, editors. Equine surgery. 2nd edition. Philadelphia: WB Saunders; 1999. p. 337–49. [36] Stick J, Boles C. Subepiglottic cyst in three foals. JAVMA 1980;177:62–4. [37] Kannegieter N, Dore M. Endoscopy of the upper respiratory tract during treadmill exercise: a clinical study of 100 horses. Aust Vet J 1995;72:101–7. [38] Dart A, Dowling B, Hodgson D, et al. Evaluation of high-speed treadmill videoendoscopy for diagnosis of upper respiratory tract dysfunction in horses. Aust Vet J 2001; 79:109–12. [39] Martin B, Reef V, Parente E, et al. Causes of poor performance of horses during training, racing, or showing: 348 cases (1992–1996). JAVMA 2000;216:554–8. [40] Ahern T. Tonsillitis and tonsillar hypertrophy predisposing to pharyngeal dysfunction in the horse. J Equine Vet Sci 1997;17:232–4. [41] McAllister E, Blakeslee J. Clinical observations of pharyngitis in the horse. JAVMA 1977;170:739–41. [42] Holcome S, Jackson C, Gerber V, et al. Stabling is associated with airway inflammation in young Arabian horses. Equine Vet J 2001;33:244–9. [43] Stick J, Derkson F, Nickels F, et al. Upper airway videoendoscopy during exercise in poorly performing horses. In: Proceedings of the Annual Convention of the American Association of Equine Practitioners, 1991;36:431–8 [44] Raker C. Diseases of the pharynx. Mod Vet Pract 1976;57:396–400. [45] Bayly W, Slocombe R. Airflow mechanics in models of equine obstructive airway disease under conditions simulating exercise. Res Vet Sci 1997;62:205–11. [46] King C, Evans D, Rose R. Cardiorespiratory and metabolic responses to exercise in horses with various abnormalities of the upper respiratory tract. Equine Vet J 1994;26:220–5. [47] Timoney J. Shedding and maintenance of Streptococcus equi in typical and atypical strangles. In Proceedings of the Fifth International Conference. Lexington: University Press of Kentucky; Lexington, 1988. p. 28–33 [48] Mumford E, Traub-Dargatz J, Salman M, et al. Monitoring and detection of acute viral respiratory tract disease in horses. JAVMA 1998;213:385–90. [49] Bailey G, Love D. Oral associated bacterial infection in horses: studies on the normal anaerobic flora from the pharyngeal tonsillar surface and its association with lower respiratory tract and paraoral infections. Vet Microbiol 1991;26:367–79. [50] Del Piero F, Wilkins P, Timoney J, et al. Fatal nonneurological EHV-1 infection in a yearling filly. Vet Pathol 2000;37:672–6. [51] Tulleners E, Stick JA, Leitch M, et al. Epiglottic augmentation for treatment of dorsal displacement of the soft palate in racehorses: 59 cases (1985–1994). JAVMA 1997;221: 1022–8. [52] Jones D. Squamous cell carcinoma of the larynx and pharynx in horses. Cornell Vet 1994;84:15–24.
Disorders of the pharynx Eileen K. Sullivan, DVMa,*, Eric J. Parente, DVMb a
Department of Clinical Sciences, Colorado State University, College of Veterinary Medicine and Biomedical Sciences, James L. Voss Veterinary Teaching Hospital, Fort Collins, CO 80523–1620, USA b Department of Clinical Studies, University of Pennsylvania, School of Veterinary Medicine, Kennett Square, PA, USA
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 affected nostril. When both nasal passages are affected, 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 flap 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 foal’s nostrils shortly after initial nursing efforts. Diagnosis is confirmed by either * Corresponding author. E-mail address: [email protected] (E.K. Sullivan). 0749-0739/03/$ - see front matter Ó 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 definitive diagnosis from 6 weeks to 7 years of age, although eventual soundness is jeopardized by the defect [5–8]. When severe, surgical repair is the necessary treatment and should be performed as early as possible to close the oronasal fistula 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 identified 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 Rathke’s 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 confirm 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 difficult 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 inflammation 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 confirmed 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 different 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 deficits. Infrequently, the edge of the entrapment can be recognized separate from the edge of the palate (Fig. 2). Radiographs may confirm this diagnosis, and resolving the entrapment surgically resolves the displacement problem. Persistent displacement associated with more significant dysphagia and neurologic problems has a poorer prognosis, and therapy is aimed at resolving the underlying neurologic dysfunction. Intermittent DDSP (IDDSP) is a significant 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 findings. 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 flaccid 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 insignificant finding 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 significant correlation between ulceration of the palate and displacement during highspeed treadmill endoscopy has not been supported [19]. Given the difficulty in diagnosing and differentiating the cause of IDDSP, moderate success with numerous treatments is not surprising. Use of a tongue tie can be beneficial 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 flaccid epiglottis can improve an individual horse’s 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 antiinflammatory 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, definitive 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 findings 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 [45–47]. 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 influenza virus have been implicated in horses developing acute signs of infectious upper respiratory disease [48]. Nasopharyngeal swab samples are helpful in identification 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 identified. 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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