Disorders of the Pharynx and Larynx

Table of Contents

• I - Disorders of the Nasopharynx
• A. Nasopharyngeal Collapse

• Introduction, Etiopathogenesis, Clinical Presentation, Diagnosis, Treatment

• B. Dorsal Displacement of the Soft Palate

• Introduction, Etiopathogenesis, Physiological Implications, Clinical Presentation, Diagnosis, Treatment, Epiglottic Augmentation, Tension and Thermal Palatoplasty, Hogan and Palmer’s Llewellyn Procedure Modification, Laryngeal Tie-Forward

• C. Retropharyngeal Abscess

• Introduction, Clinical Presentation and Diagnosis, Treatment

• II - Disorders of the Larynx
• A. General Considerations

• Anatomical Considerations, Etiology, Physiological Considerations, Diagnosis

• B. Laryngeal Hemiplegia

• Introduction, Management of Laryngeal Hemiplegia

• C. Arytenoid Chondritis
• D. Fourth Branchial Arch Defects (4-BAD)
• E. Laryngeal Cyst
• F. Hyperkalemic Periodic Paralysis (HPP)
• G. Epiglottic Abnormalities
• H. Subepiglottic Cyst
• I. Neoplasia of the Nasopharynx and Larynx

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I - Disorders of the Nasopharynx

A. Nasopharyngeal Collapse

1. Introduction

Nasopharyngeal collapse and/or narrowing is a rare but frustrating condition which causes an upper airway obstruction in horses. This obstruction generally affects the rostral two-thirds of the nasopharynx, but the caudal part of the nasopharynx may also become reduced in diameter leading to a varying degree of obstruction. Although the condition can be suspected from the associated upper respiratory noise, the diagnosis is confirmed by endoscopy or videoendoscopy.

2. Etiopathogenesis

Anatomically, the nasopharynx is a muscular tube (unsupported by bone or cartilage) that directs the flow of air to and from the trachea. It is lined with pseudostratified columnar ciliated epithelium and goblet cells. There is also a large amount of lymphoid tissue organized as the nasopharyngeal tonsils and a network with groups of lymphocytes called follicles. These provide a local defense mechanism by mucus secretion which can entrap inhaled substances and by local immunoglobulin production from its lymphoid tissue [1].

The location of the nasopharynx is at the entry of the airway and a defense function explains the high rate of pharyngeal inflammation. The nasopharynx can become inflamed because of exposure to inhaled allergens, inhaled particles, viral or bacterial agents, or as a result of an autoimmune reaction (i.e., purpura). In addition, mechanical factors such as nasal obstruction may lead to greater subatmospheric pressure during inspiration leading to nasopharyngeal edema. In the acute and subacute state, inflammation interferes with the neuromuscular function of the nasopharynx. Chronic inflammation of the nasopharynx is endemic in a certain region (southern USA) and results in the formation of cicatrix that might physically compromise the nasopharyngeal diameter (Fig. 1).

Figure 1. Nasopharyngeal cicatrix (courtesy of Dr. Peter Rakestraw, Texas A & M University).

Acute and subacute nasopharyngeal inflammation and edema is rarely significant enough to be obstructive, but can interfere with the nasopharynx ability to resist collapsing inspiratory pressure and maintain airway patency. This is because the innervation and/or muscle tone of the intrinsic nasopharyngeal musculature (as a result of inflammation) exhibit decreased activity; and its role is to dilate and stabilize the nasopharynx. The mechanism responsible for increased activity of these nasopharyngeal dilators is a chemical drive as well as a sensory mediated afferent input of the upper airway by the airflow and associated pressure [2]. This afferent feedback to the central nervous system (CNS) results in stimulation of the nasopharyngeal and other upper airway muscles to resist the collapsing pressure. Experimentally this nasopharyngeal collapse can be reproduced by desensitizing the larynx; the location of the afferent reflex mediated bilaterally through the internal branch of the cranial laryngeal nerve, itself a branch of the vagal nerve. Factors that could affect the efferent arc included many muscular diseases such as equine protozoal myelitis, botulism, inflammatory myopathy, and also certain medication such as muscle relaxants and sedatives. Failure of the nasopharyngeal musculature to maintain respiratory patency of the upper airway can result in rostral, dorsoventral, lateral or circumferential decrease in diameter of the nasopharynx [3]. This manifests itself as a functional deficit that, except in severe cases, is only seen during exercise. Physiologically, this nasopharyngeal collapse results in increased impedance (resistance) during inhalation. In severe cases, it can result in severe dyspnea and lead to disease associated with inspiratory resistive breathing [4].

In the rostral half of the nasopharynx, collapse of the nasopharynx is seen as the soft palate billowing dorsally into the airway. This distinct cause of nasopharyngeal collapse is associated with dysfunction of the rostral aspect of the soft palate. This is apparently due to a specific dysfunction of the tensor veli palatini muscles [5]. The neuromuscular dysfunction of this muscle results in the inability of the tensor veli palatini to stabilize the rostral half of the soft palate to resist the collapsing pressure during inspiration. As a result, the rostral half of the soft palate billows into the airway and obstructs airflow creating an inspiratory noise. Some authors feel that this dysfunction is a prelude to dorsal displacement of the soft palate (DDSP). Although these two anomalies may be seen in association with each other, they do not appear to be causally related. Indeed, experimentally, complete dysfunction of the rostral soft palate resulting in billowing of the soft palate does not lead to DDSP [5].

Collapse of the lateral walls of the nasopharynx is a rare cause of airway obstruction whose pathophysiology is not established. Some causes of lateral wall collapses are static and include masses or swelling in adjacent structure. Some horses have a congenital narrow nasopharynx which increases air velocity through the nasopharynx and decreases pressure thus causing a suction effect (a Venturi effect as described in Bernoulli’s principle). There are no known treatments for this abnormality at this time.

Circumferential nasopharyngeal collapse is seen as a result of complete instability of the nasopharynx [6]. The entire nasopharynx collapse during inhalation resulting in a severe airway obstruction and varying degree of respiratory noise proportional to the degree of collapse. This is also sometimes seen in horses recovering from anesthesia, presumably because of the depressing effects of anesthetic agents on the intrinsic musculature of the nasopharynx.

Collapse of the caudal third of the nasopharynx is usually manifested by a collapse of the roof of the nasopharynx. This is most commonly seen in horses with guttural pouch disease, such as empyema and tympanitis. This can be suspected by the collapse limited to the dorsal aspect of the nasopharynx and can be unilateral or bilateral depending on the extent of the guttural pouch disease. Also, retropharyngeal lymph node enlargement as seen in Streptococcus equi infection can depress the dorsolateral wall of the nasopharynx. Recently, it has been shown that dysfunction of the stylopharyngeus muscle also can result in collapse of the roof of the nasopharynx [7]. The stylopharyngeus muscle is attached on the medial aspect of the distal section of the stylohyoid bone and can be seen upon videoendoscopy of the guttural pouch. It inserts on the roof of the nasopharynx, thus stabilizing the dorsal aspect of the nasopharynx. On rare occasions, neoplasia affecting the nasopharynx or other mass-occupying lesions adjacent to or invading the nasopharynx reduces the lumen of the nasopharynx.

3. Clinical Presentation

There are multiple presentations of this disease ranging from acute respiratory distress to exercise intolerance at various levels of exercise intensity (Fig. 2). Invariably, the complaint is exacerbated with a more flex position of the head. The most common presentation is that of exercise intolerance with an upper respiratory noise. The noise (when it can be characterized) occurs during inspiration. When circumferential nasopharyngeal collapse occurs at exercise, it is usually in young (2-year-old) horses and is associated with a respiratory noise, which is repeatable at the same level of exercise intensity.

Acute respiratory crisis (similar to laryngospasm) is the rarest presentation. These horses can suffer from a severe inspiratory obstruction that can lead to pulmonary edema and hemorrhage if untreated. A loud inspiratory sound is heard associated with this dyspnea.

Figure 2. Videoendoscopic image of the nasopharynx of a horse during exercise. Note that the roof of the nasopharynx (arrows) obstructs the view of the corniculate process of the respective arytenoid cartilage.

4. Diagnosis

The diagnosis is made by physical examination of the upper airway to eliminate other causes of airway obstruction. The functional patency of the nasal cavity can be evaluated by placing a cupped hand in front of each nostril and estimating the airflow. The flow of air should be symmetrical. No asymmetry or deformity of the head (nasal cavity and sinuses) is appreciated. Because some of the causes of nasopharyngeal collapse are related to upper airway inflammation/infection, signs of upper airway inflammatory disease should be recognized. These included elevation of systemic temperature, enlargement and/or pain of the regional lymph nodes (intermandibular space and retropharyngeal), and presence and character of the nasal discharge.

Endoscopic/videoendoscopic exam at rest focuses on signs of upper airway inflammation such as exudates in the nasopharynx and/or from the guttural pouch. Prior to endoscopic/videoendoscopic exam, sedation should be avoided if possible. Indeed, sedation relaxes the musculature of the nasopharynx, making it less able to resist sub-atmospheric pressure during inhalation. This leads to false diagnosis of nasopharyngeal collapse. Sedation should be used with great caution in horses with respiratory distress because it can exacerbate the degree of airway obstruction. Likewise if respiratory distress increases during the endoscopic/videoendoscopic examination, the exam should be terminated and consideration for performing a tracheostomy before further examination should be made.

The degree of pharyngeal inflammation is important to evaluate (Table 1) [8]. The normal adult pharynx is grade I (Fig. 3). Pharyngeal grade II is normal for 2-year-old horses (Fig. 4). Grade III pharyngitis (Fig. 5) are often seen in association with other abnormalities such as epiglottic flaccidity and DDSP. Pharyngeal grade of IV should dictate considerations for tracheostomy. The guttural pouch should also be evaluated to assess the size of the pharyngeal lymph node in the ventral floor of the medial compartment (Fig. 6).

Figure 3. Pharyngeal grade I: only a few small whitish follicles are seen over the dorsal walls of the nasopharynx. This is the normal status.

Figure 4. Pharyngeal grade II - Numerous small whitish follicles, interspersed with occasional hyperemic follicles are extending ventrally over the lateral nasopharyngeal walls. This is commonly seen in 2-year-olds.

Figure 5. Pharyngeal grade III - hyperemic follicles located close together, covering the entire dorsal and lateral walls of the nasopharynx often associated with nasopharyngeal abnormality such as flaccid epiglottis as in this case.

Figure 6. Enlarged lymph node adjacent to the pharyngeal branch of the vagal nerve in a horse with DDSP.

After the examination of the nasopharynx and larynx is complete, one can obstruct both nostrils and observe for nasopharyngeal collapse. If the horse has been sedated for examination or received topical local anesthesia of its larynx, holding the respiration is of no diagnostic value and yields a false-positive result. Except in severe cases, the diagnosis is generally made by videoendoscopy during treadmill exercise (Fig. 2). If the videoendoscope is placed too far caudally in the nasopharynx, rostral and mid-nasopharyngeal collapse may be missed. Note, there can be a mild collapse of the roof of the nasopharynx that occurs normally during exercise. This is thought to be a "ballistic effect" associated with the head movement. The authors feel that, in normal horses, the roof of the nasopharynx can collapse ventrally and mask the view of the arytenoid cartilages obstructing less than 10% of the rima glottidis. If a recording of the respiration is obtained at the same time as the videoendoscopy, one can see that this dorsoventral collapse occurs at the end of expiration presumably as the head suddenly stops its ventral displacement. This is different from the clinically significant nasopharyngeal collapse that occurs during inspiration and obstructs the upper airway.

5. Treatment

For the most common presentation of nasopharyngeal collapse (i.e., exercise intolerance), a course of anti-inflammatory therapy is indicated if inflammation of the upper airway is present. Considerations should be given for a 30 day course for either of the following treatments: prednisolone (0.6 mg/kg BID, PO for 14 days, 0.6 mg/kg SID, PO for 14 days, and 0.6 mg/kg PO every other day for 14 days). Alternatively, dexamethasone can also be used in a shorter protocol (30 mg, IV or PO for 3 days SID, 20 mg, IV or PO for 3 days SID, 10 mg, IV or PO for 3 days SID, 10 mg, IV or PO EOD for 3 treatments). Some horses seem to respond to increasing the interval between competition, yet maintaining training to allow for "increased fitness of upper airway musculature". Unless severely affected, young horses improve as they mature, probably a result of decreased airway inflammation or increased tone of the nasopharynx musculature.

Horses with rostral instability of the soft palate have been reported to respond to a procedure resulting in stiffening of the rostral aspect of the soft palate. This has been performed on the ventral aspect of the soft palate by surgical resection of a wedge of mucosa and submucosal tissue followed by apposition of the remaining tissue (tension palatoplasty) [9,10] or by cauterization (thermal palatoplasty) [11]. Stiffening can also be performed from the nasopharynx by laser (Tim Greet, personal communication, September 2003).
The procedures are performed as follows:

a. Tension Palatoplasty

The procedure’s intent is to reduce dorsal billowing of the soft palate by stiffening the ventral aspect of the soft palate [9,10]. The horse is placed under general anesthesia in dorsal or lateral recumbency, with or without nasotracheal intubation. After placement of a mouth gag, through an oral approach with long-handled scissors (Fig. 7a), an elliptical incision is made in the oral palatine mucosa starting 1 - 2 cm caudal to the hard palate and extending caudally 1 cm past the palatopharyngeal arch (Fig. 7b). The palatine mucosa and submucosal tissue down to the aponeurosis of the soft palate is resected (Fig. 7c). Care must be exercised not to invade the aponeurosis as a palatal fistula could occur. The palatine mucosa is re-apposed using 0 polyglactin 910 in a simple interrupted pattern (Fig. 7d). Postoperatively, horses are fed mashes, wet hay and return to work. They are administered phenylbutazone for 3 to 5 days and trimethoprim sulfas. Training can be resumed in 2 - 3 weeks (the procedure can be repeated in four weeks (a procedure termed maximum tension palatoplasty) to further increase the tension in the soft palate). There are some reports of inappetence after surgery for up to one week in some horses, but the incidence of this complication varies between surgeons and therefore, could be associated with the degree of tissue resected.

Figure 7a. Tension palatoplasty procedure. Oral view of normal rostral soft palate of a horse. (Courtesy of Dr. TJ Ahern).

Figure 7b. Tension palatoplasty procedure. Island of palate is grasped by a hemostat and removed using a long handle curved scissors. (Courtesy of Dr. TJ Ahern).

Figure 7c. Tension palatoplasty procedure. Defect in the ventral aspect of the rostral soft palate after resection. (Courtesy of Dr. TJ Ahern).

Figure 7d. Tension palatoplasty procedure. Suturing of the defect in soft palate (Courtesy of Dr. TJ Ahern).

b. Thermal Palatoplasty

This procedure’s goal is similar to tension palatoplasty, but is obtained after thermal injury to the ventral aspect of the rostral palate [11]. The procedure is done as follows. The horse is anesthetized using an intravenous agent and a mouth gag is placed. A protective instrument is used to protect the tongue during the procedure. Using a heated metal instrument, the ventral surface of the soft palate from the hard palate extending caudally to 2 cm rostral to the palatopharyngeal arch, is cauterized (Fig. 8a and Fig. 8b). Postoperatively, horses are fed mashes, wet hay and return to work. They are administered phenylbutazone for 3 to 5 days and trimethoprim sulfas. Training can resume in 3 weeks. The main reported advantage of this technique is decreased postoperative pain as compared to the tension palatoplasty.

Figure 8a. Thermal palatoplasty procedure. Appearance of the rostral aspect of the soft palate immediately after cautery. (Courtesy of Dr. P Dixon, Royal (Dick) School of Veterinary Studies).

Figure 8b. Thermal palatoplasty procedure. Many months post cautery. (Courtesy of Dr. P Dixon, Royal (Dick) School of Veterinary Studies).

c. Laser Palatoplasty

This procedure’s goal is similar to tension palatoplasty, but is obtained after thermal injury to the dorsal aspect of the rostral palate. The procedure is done as follows. The horse is sedated and topical anesthesia applied to the nasopharynx with special emphasis to the rostral aspect of the soft palate. The laser fiber [Diode laser or neodymium: yttrium aluminum garnet (ND:YAG)] is passed through the biopsy channel, and the rostral half of the soft palate is cauterized using a laser contact technique. The fiber contacts the soft palate for 1 - 2 seconds at 2 - 4 mm intervals along the rostral half of the soft palate. Routine laser safety precautions must be used, including protective eyewear appropriate for the respective laser wavelength and laser signs restricting entry into the operating theater to ensure safety of all personnel.

Horses with mass occupying disease involving the nasopharynx require treatment directed at the primary cause of the collapse - surgical drainage of abscess. In horses with acute respiratory distress as the presenting complaint, a temporary tracheostomy should first be placed. Systemic anti-inflammatory agents such as flunixin meglumine (1 mg/kg, BID) or naproxen (22 mg/kg, PO, BID for 2 days, 22 mg/kg, PO, SID for 2 days then 22 mg/kg PO every other day), DMSO (1 g/kg, IV, SID), and dexamethasone (40 mg, IV, SID for 2 - 3 days, then tapering dose) can be administered as needed. Every effort should be made to identify and remove the source of allergens (i.e., paint fumes, new feed, new housing, etc.). In addition, a review of medications given to the animal in the previous 2 months may lead one to identify the cause of this unusual complication. One should remember that diseases causing severe vasculitis such as purpura could create this problem, so appropriate serum titers and vaccination history for equine viral arteritis and strangles are indicated.

B. Dorsal Displacement of the Soft Palate (DDSP)

1. Introduction

Displacement of the soft palate refers to the soft palate being displaced over the epiglottis instead of its normal subepiglottic position. This may present as a permanent anomaly or as an intermittent disease. In the former, dysphagia may be part of the clinical problem. Intermittent DDSP is purely a respiratory ailment. In certain cases, intermittent and permanent DDSP are just different gradation of the same denervation problem of the soft palate (palatinus muscles). This chapter will focus on DDSP as it relates to impairment in respiratory function.

2. Etiopathogenesis

The horse is an obligate nasal breather because of the anatomical configuration between the larynx and soft palate. Although DDSP was first proposed by Quinlan to be a manifestation of paresis or paralysis of the soft palate [12], Cook proposed that DDSP was truly a dislocation of the larynx [13]. Anatomically, Cook pointed out that the larynx is placed into the intra-pharyngeal ostium in a buttonhole type of relationship where the larynx is the button and the soft palate (i.e., more precisely the intra-pharyngeal ostium), the buttonhole (Fig. 9).

Figure 9. Schema showing that the larynx is placed into the intrapharyngeal ostium in a buttonhole type of relationship where the larynx is the button and the soft palate (i.e., more precisely the intrapharyngeal ostium), the buttonhole (Courtesy of Dr. RP Hackett).

We do know that the role of the nasopharynx is to maintain the patency of the airway through wide swing in airway static pressure (-50 cm of H20 to +30 cm of H20) [14] while allowing peak airflow of up to 90 L/sec. To resist these pressure swings, the nasopharynx has neither cartilage nor bony walls and thus, must use neuromuscular coordination to prevent nasopharyngeal collapse or DDSP. The current understanding of DDSP is that DDSP can occur as a result of intrinsic or extrinsic factors.

Intrinsic causes refer to all factors that affect the anatomical or neuromuscular control of the nasopharynx, specifically the soft palate. These include:

• Mechanical: Palatal or subepiglottic cysts or any mass on the caudal edge of the soft palate or under the epiglottis, that by their mere size and location, prevent the soft palate from resting in a subepiglottic position.
• Neuromuscular: Relates to dysfunction of the palatal muscles (palatinus, levator and tensor veli palatini). This is observed in unfit horses that have apparently not been able to develop sufficient palatal/nasopharyngeal strength to resist airway pressure swings at exercise. Palatal muscle dysfunction might be due to inflammation (myositis) or injection of foreign substances into the soft palate preventing the soft palate’s musculature from contracting normally during exercise. Damage to the innervation of these muscles (Fig. 10) has also been reported with inflammatory disease of the medial compartment of the guttural pouch, where the pharyngeal branch of the vagal nerve gets exposed to inflammatory processes or masses (Fig. 9) [15]. Any damage to the proximal portion of the vagal nerve could also affect the tone of the palatal musculature. In addition, there are many receptors in the nasopharynx and larynx that sense temperature and pressure change and is important sensory impulses to reflexive increased tone during exercise [2]. Blockage of these receptors has been shown experimentally to result in nasopharyngeal instability and DDSP [2]. Therefore, it is possible that disease affecting this receptor’s function can be a cause of DDSP.
  A note should be made here of the role of the epiglottic cartilage on the stability of the soft palate at exercise. Although an association has been made between the short/flaccid epiglottic cartilage and DDSP, it remains to be proven that there is a causal relationship between the two [16,17]. The association is made because of endoscopic observation as shown in Fig. 5 and Fig. 11, and DDSP. However, experimentally, epiglottic retroversion that occurs after temporary denervation of the hyoepiglottic muscle results in lack of contact between the epiglottis cartilage and the soft palate, but not in DDSP [17]. This is further emphasized by the lack of clinical predictive value of flaccid epiglottic cartilage in yearling and racing performance in Thoroughbred racehorses [18].

Figure 10. Pharyngeal branch (arrow) of the vagal nerve as it courses runs in the ventral surface of the medial compartment of the guttural pouch.

Figure 11. Flaccid epiglottis occurring during treadmill exercise in a 4 year old female Standardbred.

Extrinsic Causes of DDSP Include:

The musculature that affects the position of the hyoid bone and/or larynx plays a role in the pathophysiology of the DDSP [19,20]. Excessive traction on the larynx applied by the strap muscles is thought to result in DDSP [13]. More recently, the position of the hyoid apparatus has been added as relevant to the occurrence of DDSP [19]. It follows that any disorder that affects the extrinsic musculature and its innervation or neural control may result in DDSP. Extrinsic musculature refers to the muscles which affect the position of the hyoid apparatus and the larynx such as geniohyoid, genioglossus, thyrohyoid, hyoepiglottic, as well as the strap muscles (omohyoid, sternohyoid and sternothyroid) [19,20].

3. Physiological Implications

DDSP submits the horse to resistive breathing during exhalation. The soft palate is elevated during exhalation, thus obstructing the airflow. During inhalation, the soft palate moves ventrally such that little or no airflow obstruction occurs. Mechanically, this has been shown to significantly increase airway impedance during exhalation with no effect or a decrease in impedance during inhalation [15,21]. The net effect of this obstruction is impairment in ventilation so that exercise-induced hypoxemia is increased and hypercarbia occurs [21,22].

4. Clinical Presentation

Typically, horses present with a complaint of impaired performance and upper respiratory noise. It is thought that DDSP occurs near the end of maximal exercise intensity, but it is seen earlier in some horses and at less than maximal exercise [23]. Furthermore, some DDSP are not seen until after the horse slows down after exercise and therefore, may be of no clinical significance [23]. Because of the immediate marked effect of DDSP on ventilation, decreased performance is seen soon after its occurrence and is more obvious in horses performing at maximal exercise intensity. Respiratory noise associated with DDSP resembles a flutter or "snoring noise" coming from the back of the throat. However, the sound is not always present or reported by the trainer/owner. We estimate approximately 20% of horses are "silent displacers".

Some trainers report that DDSP occurs as a result of a sudden event during the end of competition. It appears that if the concentration of the animal can be maintained, (i.e., there is no change in demand placed in the horse), the horse will not experience DDSP and compete successfully.

5. Diagnosis

Physical examination during hyperpnea in horses with DDSP revealed open mouth breathing during exhalation as air is directed through the oropharynx. This causes the cheeks to billow. During normal breathing at rest, no abnormality is noted on physical examination of the head or neck. There are a few endoscopic/videoendoscopic findings suggestive that DDSP is occurring at exercise. These findings are suggestive of DDSP if noted in unsedated horses, because of the relaxing effect of sedation on the nasopharynx musculature.

First, an abnormal epiglottis (flaccid epiglottis, short or hypoplastic) or a deviated epiglottis to one side is supportive of a diagnosis of DDSP (although the association is not causal). It is important to note that the role of a normal epiglottis is unknown such that DDSP can occur regardless of the epiglottis conformation. Likewise, abnormal epiglottis does not imply that DDSP will occur. Some horses are permanently displaced at rest, thus preventing examination of the epiglottis. In those horses, other means of evaluating the epiglottis and the subepiglottic tissue includes radiography (Fig. 12), and general anesthesia with manual palpation of the larynx.

Figure 12. Radiograph of nasopharynx; note position of the soft palate dorsal to the epiglottic cartilage.

The most important observation is the position and morphology of the soft palate. At rest, the position of the soft palate dorsal to the epiglottis despite multiple swallow is suggestive of DDSP. Note: Some horses will replace the soft palate if the twitch is removed.

A complete endoscopic/videoendoscopic exam should also look for reasons or causes for DDSP; the contour of the caudal soft palate should be evaluated for masses or cysts. Passing the endoscope in the proximal aspect of the trachea will lead to temporary displacement of the soft palate in most horses. Another means of inducing DDSP, is to hold the respiration during endoscopy. Both these techniques should allow examination of the caudal edge of the soft palate for a few seconds. Observation of an ulcer on the caudal edge of the soft palate (Fig. 13) is also suggestive that DDSP occurs during exercise.

Figure 13. Soft palate displacement with ulceration. Note that the outline of the epiglottic cartilage cannot be seen.

One should also evaluate the subepiglottic tissue. Granulation tissue and subepiglottic cysts/masses (Fig. 14a and Fig. 14b) cause a mechanical barrier to normal subepiglottic position of the soft palate. This may not be observed unless one uses a forceps to lift the epiglottic cartilage. The horse is first sedated with detomidine and butorphanol to effect and 50 cc of local anesthetic applied to the epiglottic cartilage and surrounding tissue through the biopsy channel of the videoendoscope. The epiglottis is then elevated either using the forceps as a finger to lift the epiglottis or by grasping the subepiglottic tissues . The epiglottic cartilage itself should not be grasped by the forceps.

Figure 14a. Subepiglottic ulcer in a 2 year old Thoroughbred filly.

Figure 14b. After application of local anesthesia, the epiglottic cartilage has been lifted showing the extent of the ulcer/granuloma.

The guttural pouch should also be examined for evidence of masses near the pharyngeal branch of the vagus nerve. This is crucial if any dysphagia is present. Finally one should be aware of DDSP post-laryngoplasty in horses with significant aspiration regardless of the degree of abduction. The cause of DDSP is unclear in these circumstances, but is probably secondary to the degree of tracheal contamination, and is not necessarily due to primary soft palate disease.

A definite diagnosis of DDSP can be made by endoscopic/videoendoscopic examination at exercise, but this method is not available to many veterinarians. Experimental sound analysis is a new promising method for field diagnosis of DDSP [24,25]. These methods require further validation studies, but should increase the ability of veterinarians to make this diagnosis.

In general practice, the authors feel that the diagnosis of DDSP is made with four levels of confidence.

Level 1: History suggestive of DDSP and endoscopic/videoendoscopic confirmation of DDSP during exercise.

Level 2: History suggestive of DDSP and endoscopic/videoendoscopic observation of DDSP after training and exercise.

Level 3: History suggestive of DDSP and endoscopic/videoendoscopic observation of DDSP at rest persisting despite 2 or more attempts to swallow.

Level 4: History suggestive of DDSP and supportive observations: flaccid, short epiglottis associated.

6. Treatment

Treatment of horses with DDSP is first a management adjustment. The horse’s degree of fitness should be increased and tack modification such as tongue-tie and figure-eight noseband should be first tried. An external device which prevents caudal movement of the basihyoid and larynx during exercise has been investigated in experimentally-created DDSP. It was found to be effective in preventing DDSP during exercise in 13 of 14 trials [26]. The device termed the throat support device (TSD, Vet-Aire, Inc, Ithaca, NY, USA, www.Vet-Aire.com.) †† also appears to be effective on the racetrack in preventing DDSP during racing. Further investigations are needed to quantitate the effectiveness of this external device.

If no upper airway infection is present, yet inflammation is noted in the guttural pouch or if marked inflammation of the nasopharynx is present, then one should consider a course of anti-inflammatory agents such as: prednisolone (0.6 mg/kg BID, PO for 14 days, 0.6 mg/kg SID, PO for 14 days, and 0.6 mg/kg PO every other day for 14 days) and topical anti-inflammatory agents (throat spray 20 cc BID made up of glycerin 250 ml, 250 ml DMSO 90%, nitrofurazone 500 ml, and 50 ml of prednisolone (25 mg/ml). This medical treatment is also the treatment of choice for DDSP associated with epiglottitis.

There are many surgical options likely due to the high number of pathways leading to DDSP. Some feel that DDSP is also associated with immaturity such that surgical treatment should not be considered in horses 2 years of age or younger.

Surgical treatment should first be directed at the primary cause of DDSP if identified. For example, DDSP associated with a palatal or subepiglottic cyst, should be treated by resection of the cyst. This may be done under endoscopic/videoendoscopic guidance using laser or cautery or through a laryngotomy.
The following describes the most common surgical treatment for DDSP:

a. Staphylectomy

Under general anesthesia, the horse is placed in dorsal recumbency, and a nasotracheal intubation is performed. A 10 cm ventral midline incision is made extending from the thyroid cartilage to the mid-aspect of the cricoid cartilage. The incision is extended through the subcutaneous tissue. The paired sternohyoid muscles are bluntly separated on the midline. A laryngotomy is performed via incision of the cricothyroid ligament extending from the cricoid cartilage to the thyroid cartilage. Care should be taken not to incise the thyroid or the cricoid cartilage. The caudal free edge of the soft palate is identified, and a crescent section of the soft palate (0.5 - 0.75 cm at the midline and tapering to each side) is resected using Satinsky scissors.
The cricothyroid membrane is re-apposed using #0 polyglactin 910 in a simple continuous pattern. Again, one should avoid placing suture in the cartilage to minimize the results of granulomas. Closure of the rest of the laryngotomy is optional, however, in the authors’ impression it is of little benefit and could add to the morbidity rate. Postoperatively, parenteral anti-inflammatory agents are given for 3 days and antibiotics for 5 days. Training can resume in 2 - 3 days in a Standardbred and 2 - 3 weeks in a Thoroughbred.
Complications can be observed if the soft palate resection is too large; and the seal barrier is disrupted between the oropharynx and nasopharynx which allows food particles and water to enter the nasopharynx. This causes signs of tracheal or pulmonary aspiration. Furthermore, if the soft palate is transected such that it is too short, it leads to expiratory airflow reaching the ventral surface of the soft palate and causing DDSP.

b. Strap Muscles (Sternothyroideus and Sternohyoideus) Transection

With a standing horse sedated and its head elevated in a cross-tie, a local anesthetic is infiltrated into the junction of the mid and proximal cervical area. A 10 cm ventral midline skin incision is made and extended through the subcutaneous fascia to expose the sternohyoid muscle. Using curved forceps, each sternohyoid muscle is undermined and transected at its proximal section. The muscle section distal to the transection site is grasped, pulled cranially, and transected encompassing approximately 15 cm of distal muscle. After resection of the sternohyoid muscle, the smaller sternothyroid muscles are exposed on the ventral surface of the trachea. A section of each of these muscles is resected in the same fashion. The skin is closed in an appropriate fashion.

If resection of the omohyoid muscle is elected, the horse must be placed in dorsal recumbency under general anesthesia. The omohyoideus is separated from the linguofacial and jugular vein and resection is done as described for the sternothyroid/hyoid muscles. Careful evaluation and ligation of all vessels is made, and the subcutaneous and skin is closed after placement of Penrose drains.

Postoperatively, a pressure bandage is applied (if omohyoid resection was done), anti-inflammatory agents are given for 3 days, and antibiotics for 5 to 7 days. The horse is kept in a stall with daily hand walking for 2 weeks. Training can be resumed 2 weeks after surgery.

Complications are usually minor in severity and are related to incisional seromas or abscesses requiring appropriate drainage. This latter complication is more common if the omohyoid muscles are removed. No long term complications are notable except for the cosmetic defect associated with the lack of strap muscle at the operated site. However, resection of the sternothyroid and sternohyoid muscles has been observed to result in an increase in inspiratory tracheal pressure in experimental normal horses [27].

c. Combined Staphylectomy and Sternothyroideus Muscles Transection

This technique was introduced by Dr. Llewellyn [28]. The horse is placed under general anesthesia in dorsal recumbency, and nasotracheal intubation is performed. A 10 cm ventral midline incision is made centered on the cricoid cartilage. The incision is extended through the subcutaneous tissue. The paired sternohyoid muscles are bluntly separated on the midline. They are retracted laterally, and the blunt dissection is carried onto the lateral caudal aspect of the thyroid cartilage to expose the sternothyroid muscle tendon of insertion on the thyroid cartilage. Transection is performed 1 cm caudal to the tendon insertion to prevent inadvertent incision of the vascular pedicle. Removal of a section of the muscle and its tendon is optional. The procedure is done bilaterally. A laryngotomy and staphylectomy are then performed as described above.
Postoperatively, parenteral anti-inflammatory agents are given for 3 days. Training is often resumed in 2 - 3 days in Standardbreds and 2 - 3 weeks in Thoroughbreds.

7. Epiglottic Augmentation

This procedure was developed because of the association of flaccid epiglottis and DDSP [29]. The procedure’s purpose is to stiffen the epiglottic cartilage of horses. This procedure is less commonly done at this time. The horse is prepared and positioned as described for a staphylectomy. After a laryngotomy, the epiglottic cartilage is inverted into the lumen of the larynx by grasping the ary-epiglottic fold on one side with Allis forceps. Often the epiglottis gets trapped under the soft palate and must be dislodged by elevating the larynx with an Army-Navy retractor placed at the cranial aspect of the incision underneath the epiglottis. Using a hand-over-hand placement of Allis forceps, the epiglottis is inverted, exposing the ventral surface of the epiglottis. Three to seven ml of Teflon paste (Mentor Polytef® paste for injection, Mentor O&O, Inc., Norwell, MA, USA.) is injected submucosally. The authors preferred one midline injection of 3 ml of Teflon paste followed by digital redistribution/flattening on the ventral surface of the epiglottis. Postoperatively, parenteral anti-inflammatory agents are given for 5 - 7 days. Training can resume in 2 - 6 weeks.

8. Tension and Thermal Palatoplasty

Tension palatoplasty [9,10] and Thermocautery palatoplasty [11] have been previously described (nasopharyngeal collapse). Their rationale is based on the belief/observation that billowing of the rostral aspect of the soft palate precedes DDSP. This is not supported by current experimental data in normal horses, and it is not performed by the authors.

All these surgical procedures have been associated with a 60±5% success rate; and there is a significant recurrence rate 3 - 4 months later in horses that had originally improved.

The following two procedures have been reported to have a success rate ranging from 81 to 92%, but still required the test of time before widespread application.

9. Hogan and Palmer’s Llewellyn Procedure Modification

After the horse receives a bilateral sternothyroid muscle resection instead of a staphylectomy, a laser is used to induce fibrosis on the caudal aspect of the soft palate . The stiffening that results is thought to increase the intrinsic strength of the caudal soft palate so it is able to resist pressure changes [29].

Horses undergoing transendoscopic laser cautery of the soft palate are sedated and restrained in stocks. The endoscope is passed through the nasal passage into the nasopharynx, and a local anesthetic is applied topically. The laser fiber is passed through the biopsy channel, and the caudal free margin of the soft palate is cauterized using a laser contact technique. The fiber contacts the soft palate for 1 - 2 seconds at 2 - 4 mm intervals along the entire caudal free margin and extending 1.5 cm rostrally (Fig. 15). Routine laser safety precautions must be used, including protective eyewear appropriate for the respective laser wavelength and laser signs restricting entry into the operating theater to ensure safety of all personnel.

Figure 15. Post lasering of the caudal edge of the soft palate (Courtesy of Dr. P Hogan, New Jersey Equine Clinic).

10. Laryngeal Tie-Forward

We have performed this procedure [31] based on experimental data suggesting that the optimal position of the larynx during exercise is slightly dorsal to the basihyoid bone [19]. The principle of the procedure is to fix the larynx forward rather than preventing caudal traction by strap muscle resection.

The procedure is performed with the horse placed under general anesthesia in dorsal recumbency, and endotracheal intubation is performed. A ventral midline skin incision is made extending from the basihyoid bone caudally to the cricoid cartilage. The sternohyoideus (ST) muscles are bluntly separated exposing the ventrolateral aspect of the larynx and basihyoid bone. The ventral aspect of the basihyoid bone is exposed using a curette to remove the local attachment of the ST muscles. A 3.2 mm hole is drilled into the basihyoid bone taking care not to injure the vascular structure on the dorsal surface of the basihyoid bone. A nonabsorbable suture (No. 2 or 5 polyblend) is placed through the drill hole into the caudolateral aspect of each lamina of the thyroid cartilage. After the sutures are tied, the larynx is moved dorsally and rostrally (Fig. 16). The correct rostral position of the larynx is obtained when the rostral aspect of the thyroid cartilage is dorsal to the basihyoid and 0.5 cm rostral to the caudal aspect of the basihyoid bone. In the first clinical report, the procedure has been performed in 117 horses, and the success rate appears to be approximately 80 - 82%. Further experience is needed to determine the value of this procedure and its recurrence rate.

Figure 16. Laryngeal tie-forward. Two sutures have been placed, one on each side between the left or right wing of the thyroid cartilage and a hole drilled in the basihyoid bone.

C. Retropharyngeal Abscess

1. Introduction

Retropharyngeal abscesses are an infectious disease usually affecting young horses following upper airway infection. The primary manifestation of the disease is related to the site of primary infection (i.e., upper airway coughing and nasal discharges), but some animals present for acute dyspnea as the sole presenting complaint. Following upper airway infection, the organism may settle into the retropharyngeal lymph node and form an abscess. Although any infection affecting the upper airway can be followed by abscessation of the retropharyngeal lymph node, Streptococcus equi is the most frequent causal organism. Therefore, a proper isolation procedure should be used in the workup of any animals with retropharyngeal abscess. An alternative cause of retropharyngeal abscess includes trauma to the caudal aspect of the nasopharynx or cranial esophagus. Any surgery to the area, such as laryngoplasty, could also result in a retropharyngeal abscess.

2. Clinical Presentation and Diagnosis

A history of recent upper airway infection in weanlings and yearlings, more often strangles, is often present in animals with retropharyngeal abscessation. Sometimes the owner/manager will report a louder breathing noise in the preceding days. Physical examination usually reveals a depressed or at least quiet individual with a loud inspiratory noise and a various degree of dyspnea. When examining any horse with dyspnea, the clinicians must be prepared for an emergency tracheostomy. One should remember that sedation will increase the nasopharyngeal collapse and thus, could worsen the dyspnea.

Mild (1°C) elevation of temperature and mild elevation in heart rate are usually present. Nasal discharge, sometimes purulent, is seen and the intermandibular lymph nodes are enlarged. The Viborg’s triangle may be distended, but usually no abnormality is noted retropharyngeal unless deep palpation or ultrasound examination is used.

Endoscopic/videoendoscopic examination must be done carefully in a dyspneic animal. It may be prudent to first perform a temporary tracheostomy prior to initiating the endoscopic/videoendoscopic exam. A strong indicator of a retropharyngeal mass is a unilateral depression and collapse of the nasopharynx. In addition, there may be a unilateral depression of the ipsilateral arytenoid cartilage. Any condition that results in unilateral guttural pouch distension (infection, tympany) could give the same endoscopic/videoendoscopic picture and should be ruled out. Therefore, evaluation of the guttural pouch endoscopically/videoendoscopically or radiographically is important. Radiographic evaluation is less stressful to a dyspneic animal than guttural pouch endoscopy/videoendoscopy. Ultrasound examination is then done to determine the extent and characteristic of the retropharyngeal abscess: a single mass or a multi-lobulated structure. Ultrasound-guided aspiration in the Viborg’s triangle may allow confirmation of the presence of an abscess (Fig. 17).

Figure 17. Aspiration of retropharyngeal abscess with a 14 gauge catheter. Note that this is performed above the linguofacial vein on this horse, but it would be preferable to perform this procedure under ultrasonographic control and by entering the skin below the linguofacial vein to avoid inadvertent contamination of the parotid gland.

If the animal is dyspneic, a tracheostomy is first performed, then the animal is sedated and ultrasound-guided aspiration of the mass is done to confirm the diagnosis and identify the bacterial agent.

3. Treatment

In all cases where dyspnea at rest is present, a temporary tracheostomy is indicated. If the abscess is ill-defined or multiloculated, a course of nonsteroidal anti-inflammatory agents and systemic antibiotics (including penicillin G) should be instituted. The antibiotherapy can be realigned once the results of bacterial culture and sensitivity become available.

If the abscess is well encapsulated and located within the floor of the guttural pouch (Fig. 6), the abscess could be drained using laser [32]. This procedure is done with the horse standing and sedated initially with a combination of detomidine (5 mg) and butorphanol (5 mg) for a 450 kg horse, followed with 1 or 2 repeated detomidine (2 mg) injections as needed. Topical anesthesia is then applied through the biopsy channel of the endoscope on the abscess in the medial compartment of the guttural pouch. A solution containing 50 cc of lidocaine hydrochloride and 10 cc of a 0.15% solution of phenylephrine can be used. Using a diode or a ND:YAG laser, an incision is made over the abscess. Using a 0.5 mm sterile Teflon catheter inserted through the biopsy channel of the endoscope the abscess cavity is lavaged with physiological saline. This entire procedure must be done carefully because the pharyngeal branch of the vagal nerve runs in the ventral surface of the medial compartment of the guttural pouch (Fig. 10). Damage to this nerve may result in dorsal displacement of the soft palate and/or dysphagia.

Postoperatively, the horse should be muzzled for a few hours because anesthesia applied to the guttural pouch could have reached the pharyngeal branch of the vagus or the vagal nerve and lead to temporary dysphagia.

In a retropharyngeal abscess beyond the confine of the guttural pouch, invasive surgical drainage of the retropharyngeal lymph node abscess is the optimal treatment. The surgery is complicated by the important adjacent neurovascular bundles. If one does not proceed carefully, significant morbidity such as dysphagia and hemorrhage can occur.

Under appropriate general anesthesia, the animal is placed in lateral recumbency with the affected side uppermost. An 18 gauge needle is inserted ventral to the linguofacial vein and directed toward the abscess. Ultrasound guidance facilitates this procedure. If not previously done, once the abscess has been sampled, intraoperative antibiotics can be administered. Once the needle has entered the abscess, a 5 cm skin incision is made ventrally to the linguofacial vein and centered on the needle. Using curved Mayo scissors, the incision is extended toward the tip of the needle using blunt dissection only. Once the abscess is entered, digital examination of the abscess is done and multiloculated abscesses are converted to a single large cavity. The incision may need to be enlarged to get better drainage. However, this should be done very conservatively because of the proximity of important neurovascular structures and the inability to identify them because of the extensive fibrosis surrounding the abscess. Enlargement is only done from within the incision by inserting the closed curved Mayo scissors into the incision and opening them. The abscess site is then lavaged with physiological solution.

After surgery, the horses received systemic antibiotics mainly to minimize the possibility of cervical cellulites, secondary to exposure of purulent exudates to local tissue. The area is flushed daily and petroleum jelly or vitamin A and D ointment applied ventrally around the incision to prevent scalding. Recurrence rate is very low. If Streptococcus equi was the causative agent, proper containment procedures should be used.

II - Disorders of the Larynx

A. General Considerations

1. Anatomical Considerations

The larynx is a complex organ that serves as a conduit between the pharynx and the trachea. A healthy larynx dilates to facilitate increased airflow during exercise, closes during swallowing to prevent aspiration of foreign material into the trachea and also serves as an instrument for phonation. It is comprised of three unpaired (cricoid, thyroid, and epiglottic) cartilages and two paired (arytenoid) cartilages. These cartilages articulate with each other and their relative positions are controlled by the intrinsic muscles of the larynx. Clinically, the most significant of the intrinsic laryngeal muscles is the paired m. cricoarytenoideus dorsalis which serve to abduct the arytenoid cartilages and produce sustained abduction during exercise. All of the intrinsic muscles of the larynx except for the m. cricothyroideus are innervated by the recurrent laryngeal nerves. The extrinsic muscles of the larynx move the larynx as a whole and play a rather complex role in the control of laryngopalatal function [33].

The cricoid, thyroid and the bodies of each arytenoid cartilage are composed of hyaline cartilage. There is a pattern of progressive mineralization of these hyaline cartilages as the horse ages. The epiglottis as well as the corniculate processes of the arytenoid cartilages are composed of elastic cartilage. During the first two years of life, at least, there appears to be a maturation process of the epiglottic cartilage with changes in histological composition as well as changes in endoscopic appearance [34]. The corniculate process is the most cranial and endoscopically visible component of the arytenoid cartilage proper while the cuneiform cartilage is fused with the epiglottic cartilage (Fig. 18). The corniculate processes and the epiglottis are "buttoned" into the nasopharynx through the ostium intra-pharyngeum which acts as the "buttonhole" [13] (Fig. 9 and Fig. 19). During normal respiration, both at rest and at exercise, the caudal margin of the soft palate is maintained in a subepiglottic position, thus ensuring streamlined nasal breathing. In the normal horse, the only time that the soft palate should be positioned dorsal to the epiglottis is during swallowing.

Figure 18. Normal laryngeal anatomy (cadaver larynx): CPLA - corniculate process of the left arytenoid cartilage. SP - pillar of the soft palate. AEF - left aryepiglottic fold. VC - left vocal cord. E - epiglottis.

Figure 19. In this view of the cadaver larynx, the epiglottis is no longer visible as a result of a dorsal displacement of the soft palate. The dotted circle outlines the border of the ostium intrapharyngeum or "buttonhole" of the soft palate.

2. Etiology

Etiologic categories for diseases of the larynx include acquired, congenital and developmental. Some of the diseases in each of these categories have suspected or proven heritability. Acquired diseases of the larynx are most common and include laryngeal hemiplegia, arytenoid chondritis, entrapment of the epiglottis and deformity of the epiglottis [35]. Congenital diseases of the larynx are encountered much less frequently. Congenital conditions of the larynx proper include fourth branchial arch defects (4-BAD), laryngeal cyst and polymyopathy of the laryngeal musculature, associated with hyperkalemic periodic paralysis, a heritable condition seen in heavily muscled Quarter Horses [36-39]. Although not a disease of the larynx proper, subepiglottic cyst, arising from remnants of the thyroglossal duct, can interfere with epiglottic and soft palate function and produce airway obstruction. A common developmental abnormality that is encountered, particularly in young Thoroughbreds intended for racing, is hypoplasia of the epiglottis [16].

3. Physiological Considerations

Diseases of the larynx, can produce or have the potential to produce airway obstruction and, occasionally, dysphagia (or both). Obstructive lesions of the larynx often produce an abnormal respiratory noise and they limit airflow which leads to early fatigue and poor performance in the exercising horse. These obstructive conditions are most likely to be diagnosed in their early stages in performance horses while in the sedentary horse, laryngeal disease may go unnoticed or undiagnosed such that the lesions may be very advanced before the condition is recognized and diagnosed.

4. Diagnosis

In a horse suspected of having an upper airway obstruction, part of the physical examination should include external, digital palpation of the larynx (Fig. 20). Palpation may reveal muscular or cartilaginous asymmetry or anatomical anomalies of the laryngeal cartilages. The muscular process of the left arytenoid cartilage may feel more prominent in a horse with atrophy of the left cricoarytenoideus dorsalis muscle [40]. Minimal digital pressure on both muscular processes (arytenoid depression test) may elicit an abnormal (primarily inspiratory) respiratory noise in horses with unilateral laryngeal paralysis and will induce a much louder noise and respiratory distress in a horse with bilateral paralysis. In some horses with unilateral arytenoid chondritis, there may be a palpable enlargement over the dorsal larynx on the affected side but the muscular process may be indistinct. Horses that have endoscopic evidence of either right or left laryngeal paralysis but do not have a clearly defined muscular process on the affected side when palpated, are not good candidates for laryngoplasty. The "slap test" has been described as an ancillary method for evaluating arytenoid function but it adds little useful information in most horses with laryngeal disease [41]. It is possible to evaluate the function of the left recurrent nerves using electrodiagnostics [42]. Again, this seems to have little if any clinical value.

The skin ventral to the larynx and ventral and parallel to the linguofacial vein should be inspected carefully for the presence of scars which indicate that there has been previous surgery. These scars can be difficult to detect and may require that the hair be clipped and shaved in order to see them. The jugular veins should also be examined for patency. Occasionally, laryngeal hemiplegia is associated with perivascular inflammation and jugular thrombophlebitis. (Fig. 21).

Figure 20. Digital palpation of the larynx.

Figure 21. Left jugular vein (LV) thrombosis which has resulted in prominent collateral venous circulation.

The definitive diagnosis of laryngeal obstructive disease is made on endoscopic/videoendoscopic examination. A description of grades (I - IV) of arytenoid movement is listed in Table 2. It is preferable to perform the endoscopic examination in the standing, unsedated horse in order to best evaluate laryngopalatal function. Sedation can produce nasopharyngeal relaxation and can alter the responsiveness of the arytenoid cartilages. A nose twitch can be used for restraint. In the normal horse, the arytenoid cartilages should appear symmetrical and be capable of maximal abduction following stimulation (Fig. 22). This is best assessed in the resting horse after swallowing or during nasal occlusion. Except during swallowing, the caudal border of the soft palate should be in a subepiglottic position. Most abnormal laryngeal conditions can be diagnosed at rest but in some horses, the resting endoscopic findings present an interpretive challenge, such as a horse with arytenoid asynchrony where the question is whether the arytenoid movement is grade II (asynchronous but normal, capable of complete abduction) or grade III (incapable of complete abduction) [43] (Fig. 23).

Figure 22. Endoscopic view of the normal larynx showing maximal and symmetrical abduction of both arytenoids. Note: Maximal abduction is sustained during exercise.

Figure 23. At rest, it appears that the left arytenoid cartilage does not maximally abduct (arrow). This was later confirmed with treadmill videoendoscopy.

It may be necessary to work those horses on a high speed treadmill and perform simultaneous videoendoscopy in order to better evaluate arytenoid function under stress. Intermittent conditions such as dorsal displacement of the soft palate and entrapment of the epiglottis as well as axial deviation of the aryepiglottic folds, nasopharyngeal collapse and epiglottic retroversion may only be observed during exercise (Fig. 24) [44]. Another endoscopic oddity that is occasionally encountered is arytenoid overlap or "infolding" of the arytenoids at their articulation on the dorsal midline of the larynx (Fig. 25). In some horses, this infolding becomes more exaggerated with nasal occlusion at rest or on the treadmill, to the point where the laryngeal opening becomes significantly narrowed and air begins to leak between the aryepiglottic folds and the pillars of the soft palate producing a loud, abnormal noise. This condition is seen more frequently in show horses that have a great deal of poll flexion. Videoendoscopy during high speed treadmill exercise is useful for evaluating the significance of arytenoid articulation anomalies.

Figure 24. Epiglottic retroversion in a horse during treadmill exercise. Note: The ventral aspect of the epiglottic cartilage is visible.

Figure 25. Abnormal arytenoid "infolding" (arrows) on midline that became more accentuated with nasal occlusion.

In a horse with an unknown medical history, the lumen of the larynx should be examined carefully during the endoscopic examination for mucosal scars that are evidence of previous surgery such as a laryngotomy, ventriculectomy or ventriculocordectomy. Scarring of the vocal cord area, without evidence of a laryngotomy incision would suggest that a fiberoptic guided laser surgery was performed (Fig. 26aand Fig. 26b).

Figure 26a. Left laryngeal hemiplegia with scarring of the left vocal cord.

Figure 26b. A close up view of the scarred left vocal cord (LVC). Note the absence of a ventral laryngeal mucosal scar which would suggest that a fiberoptic guided laser procedure produced the scarring.

B. Laryngeal Hemiplegia

1. Introduction

Horses can develop unilateral or bilateral paralysis of the arytenoid cartilages, with left sided paralysis being, by far, the most common. Idiopathic left sided laryngeal paralysis develops as a result of a progressive demyelination of the left recurrent laryngeal nerve (Fig. 27). The resultant neurogenic atrophy of the intrinsic musculature results in a loss of both arytenoid abductor and adductor muscle function (Fig. 28) [45]. The term idiopathic is used because the cause of the disease, in most horses, is not evident [35]. However, a genetic predisposition should always be considered [46,47]. An anatomic predisposition for left laryngeal paralysis has been suggested because the left recurrent laryngeal nerve is longer and therefore more susceptible to axonal transport failure than the right recurrent laryngeal nerve. This has contributed to the notion that long necked horses were at greater risk for developing left laryngeal paralysis. Other known causes of damage to the recurrent laryngeal nerve include: inflammation as a result of perivascular injection of an irritating substance intended for the jugular vein; trauma as a result of an injury or surgery of the neck; guttural pouch mycosis; strangles abscessation of the head or neck and pressure from neoplasms or masses in the neck or chest. Organophosphate toxicity, plant and lead poisonings, and diseases of the central nervous system (CNS), specifically the brain stem, can also produce laryngeal hemiplegia. Whenever bilateral laryngeal paralysis is diagnosed, CNS disease should be suspected, particularly Equine Protozoal Myeloencephalitis (in North America).

Figure 27. Idiopathic, complete paralysis of the left arytenoid cartilage (LA).

Figure 28. Cadaver larynx showing atrophy of the left cricoarytenoideus dorsalis muscle (LCAD) in a horse affected with left laryngeal hemiplegia.

Idiopathic laryngeal hemiplegia (ILH) can affect a horse of any age although the incidence seems to be highest in young horses. Foals are rarely affected. Large breed horses are more commonly affected than small breed horses or ponies with the incidence in some Draft breed populations approaching 50% [48]. A study of ILH in Thoroughbred sales yearlings showed the incidence to be no less than 2.75% [49]. It is quite likely that the incidence in the entire Thoroughbred yearling population is considerably higher. The progression of the idiopathic form of the disease from normal to an obstructive lesion occurs generally over 3 - 4 months but there are some horses where the disease progresses to complete arytenoid paralysis within a 4 - 6 week period.

Idiopathic right laryngeal hemiplegia is uncommon (Fig. 29). Instead, it is usually the result of an iatrogenic, perivascular reaction around the right jugular vein and there may be associated evidence of right jugular phlebitis or thrombosis. In addition to recurrent laryngeal nerve injury, some horses with a perivascular injection reaction (affecting either the right or left side) will also have Horner’s syndrome as a result of injury to the sympathetic nerve trunk which lies nearby (Fig. 30). Because right laryngeal hemiplegia is so uncommon, a horse with right arytenoid dysfunction should be carefully inspected for endoscopic or physical evidence of chondritis or congenital malformation of the larynx (4-BAD). The right guttural pouch should be examined for the presence of an erosive mycotic infection.

Figure 29. Paralysis of the right arytenoid cartilage (RA).

Figure 30. Right sided Horner’s syndrome. Note the sweating and mild ptosis on the right side of the horse’s head.

Bilateral laryngeal paralysis is rare and is usually associated with some type of central nervous system disease involving the nucleus ambiguous in the brain stem. It has been reported as a result of organophosphate toxicity [50]. Bilateral laryngeal hemiplegia can also be seen as a complication of surgery such as guttural pouch fenestration or cervical spinal fusion. Temporary bilateral arytenoid paralysis has also been reported following general anesthesia [51] and during encephalopathy associated with hepatic disease [92]. Some horses with bilateral laryngeal paralysis are close to asphyxiation and require an emergency tracheostomy. Others with less severe paralysis can breathe normally while standing but quickly become dyspneic with any type of activity or excitement, including attempts to perform endoscopy. Endoscopically, there is reduced movement of both arytenoid cartilages, with the degree of paralysis often being asymmetrical. The laryngeal opening may be reduced to a slit (Fig. 31). There are some horses that have obvious left laryngeal hemiplegia but have questionable ability to maximally abduct the right arytenoid cartilage. If the severity of the exercise intolerance is incongruous with a diagnosis of unilateral paralysis and the function of the opposite arytenoid is in question, then the horse should have a videoendoscopic examination while exercising on a high speed treadmill. In some horses with CNS disease, in addition to laryngeal paralysis, there is also pharyngeal paralysis and dysphagia.

Figure 31. Bilateral laryngeal paralysis.

2. Management of Laryngeal Hemiplegia

A horse that develops a neuritis of the recurrent laryngeal nerve and loss of abductor function on the affected side as a result of some type of injury, may regain neuromuscular function as inflammation subsides. However, this is a rare occurrence. One author (JTR) has seen function improve in two horses following right recurrent laryngeal nerve injury. If there is going to be any improvement it will likely be evident within 30 to 60 days.

In those horses that fail to respond to medical treatment and in all cases of idiopathic laryngeal paralysis, one should consider surgical treatment once performance has deteriorated to the point where the horse is no longer useful for its intended purpose. With some show horses, the complaint may be an objectionable noise rather than exercise intolerance. If the horse has diminished laryngeal function but still possesses considerable residual ability to abduct the left arytenoid (>70% abduction), the owner may be advised to wait until there is further loss of abductor function before performing a laryngoplasty, particularly if there is not an obviously palpable loss of the left cricoarytenoideus dorsalis muscle mass. This is because experience has shown that if a horse has a good deal of residual intrinsic laryngeal muscle function, the prognosis for laryngoplasty is reduced. These horses are more likely to suffer failure of laryngoplasty as a result of continuous movement of the muscular process against the prosthetic suture. Ipsilateral recurrent laryngeal neurectomy has been proposed as an ancillary procedure to laryngoplasty in these horses in order to eliminate the muscular cycling after placement of the prosthetic suture but to date, this has not been shown to be beneficial [52]. There can be some frustration associated with waiting until the horse becomes more affected because there is no predictable timetable for deterioration with idiopathic laryngeal hemiplegia. If it is determined on a high speed treadmill that the affected arytenoid can sustain abduction, albeit diminished, for the duration of an exercise test, the owner can be given the option of continuing to compete the horse at a less demanding level until the horse becomes a more suitable surgical candidate.

If there is dynamic collapse of the left arytenoid cartilage during the exercise test, there is little benefit to continued competition (Fig. 32and Fig. 33). Continuing to compete a horse that experiences repeated episodes of airway obstruction has some risk. These horses may become psychologically stressed and, in the racehorse, exercise induced pulmonary hemorrhage may be worsened as a result of the obstruction.

Figure 32. Dynamic collapse of the left arytenoid cartilage with axial deviation of both vocal cords during treadmill exercise.

Figure 33. In addition to dynamic collapse of the left arytenoid cartilage and axial deviation of both vocal cords during treadmill exercise, this horse also showed significant bilateral nasopharyngeal collapse (arrows).

Surgical Treatment of Left Laryngeal Hemiplegia

The most commonly recommended treatment for left laryngeal hemiplegia in performance horses is prosthetic laryngoplasty [35,53]. The goal of a laryngoplasty is to fix the left arytenoid cartilage in an abducted position. This is usually performed with a unilateral or bilateral sacculectomy or a left ventriculocordectomy as an ancillary procedure through a ventral laryngotomy incision or endoscopically, using a laser. A major benefit of these laser endoscopic laser techniques is that a laryngotomy incision is not required. Some of the complications associated with a laryngotomy can be avoided and aftercare is simplified.

The laryngoplasty technique performed today is quite similar, in principle, to the technique first described by Marks et al., in the early 1970’s [53]. Over the years, modifications of the original description have been reported and include the use of different suture materials for the prosthesis and the placement of more than one suture. Some surgeons feel that young horses (2 years old or less) are not good surgical candidates for laryngoplasty because the laryngeal cartilages are immature and less likely to provide holding power for the prosthetic suture which is placed through the cartilages and tied under tension. Research results, however, have not supported this contention [54,55]. There are also differences of opinion among surgeons with regard to the optimal degree of abduction that should be achieved with laryngoplasty. Certainly, in some horses the abduction produced by the laryngoplasty is related to aspiration, but in racehorses, for example it is important to produce at least moderate abduction in order to allow the airflows required for sustained, high speed performance.

Sacculectomy or ventriculocordectomy can be performed without laryngoplasty [35]. Recently, in North America, it has become popular to perform endoscope/videoendoscope guided laser sacculectomy or ventriculocordectomy on racehorses with Grade III left arytenoid movement. A major benefit of these laser techniques is that the procedure can be done standing and a laryngotomy procedure is not required [56]. In the absence of a laryngoplasty, these procedures produce some vocal cord and arytenoid stability and may alleviate some of the abnormal respiratory noise [57] but they do not produce arytenoid abduction, hence, significant mechanical impedance to airflow remains [58]. In horses with partial paralysis, there is often an initial improvement, particularly with noise reduction but ultimately, as the disease progresses and paralysis becomes more complete, many of these horses will require a laryngoplasty. It is the author’s (JTR) impression that the scar produced in the area of the saccule or vocal cord can compromise the effectiveness of the subsequent laryngoplasty by limiting abduction.

Nerve-muscle pedicle grafting was first reported in 1989 [59] and reported to have clinical efficacy for treatment of left laryngeal hemiplegia [60] but has not yet gained popularity, likely for two reasons: it has not been demonstrated to produce clinical results that are superior to those reported for laryngoplasty [61,62] and the convalescent time is six months or greater which is unacceptable to most owners and trainers. An advantage of the laryngeal reinnervation procedure is that there are fewer problems with aspiration of feed material.

Arytenoidectomy, for a time, was used as a primary treatment for left laryngeal hemiplegia, but fell out of favor because of poor results and postoperative complications. Experimental studies have shown that some airflow limitations still remain at maximal flow rates following partial arytenoidectomy [63]. One of the authors (NGD), however, prefers partial arytenoidectomy over laryngoplasty in some horses with Grade III arytenoid movement. The other author (JTR) prefers laryngoplasty as the first line of treatment of horses with Grade III arytenoid movement but partial arytenoidectomy does remain the treatment of last resort for failure of laryngoplasty.

In those racing jurisdictions where it is allowed, a tracheostomy tube can be placed and the stoma can be opened when the horse trains or races. A screen covering the tracheal opening limits the gross contamination of the trachea. There are very few race tracks left in North America that will allow a horse to run with a tracheostomy tube.

Surgical Treatment of Right Laryngeal Hemiplegia

Right laryngeal hemiplegia is treated in the same fashion as left laryngeal hemiplegia. The prognosis for right laryngoplasty is lower than that for left laryngoplasty simply because it is much more difficult for a right handed surgeon, even an experienced one, to perform the surgery in a "back-handed" fashion. Suture placement becomes difficult and less precise. Another reason why the results of a right laryngoplasty can be disappointing is the failure, preoperatively, to appreciate subtle anatomical malformations such as a "blunted" muscular process or a fourth branchial arch defect or to not recognize the subtle signs of arytenoid chondritis. These conditions will not respond well to laryngoplasty.

Surgical Treatment of Bilateral Laryngeal Paralysis - In most cases, horses with bilateral arytenoid paralysis can be improved with unilateral laryngoplasty. If the horse is dysphagic and already aspirating food material and saliva, a permanent tracheostomy is a better alternative to laryngoplasty. The procedure can be done on the standing horse. Bilateral laryngoplasty is generally contraindicated because of the great risk of aspiration pneumonia.

Laryngoplasty: Technique - Prior to surgery, the horse should receive broad spectrum, intravenous antibiotics. Some surgeons also administer a non-steroidal, anti-inflammatory agent before surgery in order to minimize postoperative swelling. During induction of anesthesia, it is useful for the anesthetist to have a selection of endotracheal tubes of different diameters. Some horses with longstanding, complete arytenoid paralysis may be difficult to intubate with the standard sized tube and a smaller diameter tube may be necessary.

The laryngoplasty is performed under general anesthesia with the horse in lateral recumbency, affected side up [64]. It is very important that the head and neck are in an extended position to allow proper access to the larynx. A 10 cm skin incision is made just below and parallel to the linguofacial vein and centered over the larynx. The omohyoideus muscle is bluntly separated from the linguofacial vein, using scissors, and the loose fascia overlying the larynx is separated with digital dissection exposing the lateral and dorsal aspect of the larynx. It may be necessary to ligate and divide the vascular pedicle that originates from the linguofacial vein and enters the omohyoideus muscle. A malleable retractor is placed into the incision to allow for better access. This is held by an assistant on the side of the head opposite to the surgeon. The caudal border of the cricoid cartilage and the muscular process of the arytenoid are identified with digital palpation. The cricopharyngeus and thyropharyngeus muscle bellies are separated along their aponeurosis in order to expose the muscular process. Once the sites of suture placement, the caudo-dorsal border of the cricoid, where, conveniently, there is often a distinct "notch" to aim for and the muscular process of the arytenoid have been adequately exposed, the prosthetic suture is placed. A trocar point needle should be used for suture placement because it is less likely to break than either a cutting or a taper point needle. The type and size of the suture selected for the prosthesis is the surgeon’s choice. Almost all surgeons use a large caliber, non absorbable material. Passing the needle through the respective cartilages can be difficult, particularly if bleeding is obscuring the field. The surgeon usually relies more on digital than visual guidance. The suture is first passed through the cricoid cartilage. The needle point is nestled into the caudo-dorsal notch, "walked" off the caudal edge of the cricoid cartilage until it is just underneath the full thickness of the cartilage, and then with a turn of the wrist, the surgeon advances the needle through the cartilage and the needle point exits on the dorsum of the cricoid near midline, approximately 1.5 to 2.0 cm cranial to the point of penetration. The leading end of the suture is drawn under the cricopharyngeus muscle and then, using a smaller trocar point needle, is passed through the muscular process in a caudomedial to craniolateral direction. The caudal end of the suture is then drawn under the cricopharyngeus muscle. The suture is tied under tension producing abduction of the arytenoid cartilage (Fig. 34 and Fig. 35). Some surgeons have a videoendoscope in place during surgery in order to evaluate the degree of abduction achieved and this guides how much tension they place on the suture before it is secured. The arytenoid should no longer be resting on the endotracheal tube (approximately 24 - 26 mm diameter) and the target position is 75 to 80% of maximal abduction. Other surgeons do not use intraoperative videoendoscopy, having developed a "feel" for how tight to pull the suture that is based on surgical experience. Following placement of the prosthetic suture the cricopharyngeus and thyropharyngeus muscles are reapposed with simple interrupted sutures, the fascia adjacent to the linguofacial vein is sutured to the omohyoideus muscle with simple interrupted sutures and the skin is closed (Fig. 36).

Figure 34. Schematic showing the placement of the laryngoplasty suture (black lines) in a cadaver larynx.

Figure 35. Endoscopic appearance of the larynx following left laryngoplasty. The left arytenoid is in a fixed and abducted position.

Figure 36. The laryngoplasty incision (arrow) is situated just ventral and parallel to the linguofacial vein. The skin incision has been stapled. There is obvious drainage from the cranial part of the ventral laryngotomy incision has been left open to heal by second intention.

Reoperation for failure of laryngoplasty is a challenge. The same approach is made but it can be quite difficult because of scar tissue in the operative site. Scar tissue makes it difficult to identify and expose the surgical landmarks and tissue dissection is likely to produce a good deal of bleeding. Using sharp Metzenbaum scissors, the scar tissue between the thyroid cartilage and the muscular process is incised in order to mobilize the arytenoid cartilage. An effort should be made to locate and remove the laryngoplasty suture(s) from the previous surgery. They can often be located by digital palpation of the knot through the scar tissue. The dissection is extended caudal to the muscular process and into the cricoarytenoid joint to further increase arytenoid mobility. This dissection can be facilitated by using a small Senn retractor hooked over the wing of the thyroid cartilage to provide traction on the larynx and gain a better exposure of the muscular process. The new prosthetic suture is placed and tied under a good deal of tension to ensure some improvement in abduction. Prior to surgery, a videoendoscope can be secured in a position to view the larynx and the degree of improvement in abduction can be assessed. If there is no apparent improvement in the position of the arytenoid, the surgeon may wish to immediately proceed to an partial arytenoidectomy.

A sacculectomy or ventriculocordectomy is often performed as an adjunct to the laryngoplasty. The author (JTR) almost always performs a sacculectomy upon completion of the laryngoplasty. The horse is rolled into dorsal recumbency, a laryngotomy is performed, and a laryngeal burr is used to evert the saccule which is excised. It is important to remove the entire saccule and not leave a small pocket of mucosa that could still create turbulent airflow. There is some justification for performing a bilateral sacculectomy because there is a possibility of axial deviation of the vocal cord on the normal side if the laryngoplasty on the affected side fails to produce much abduction. In some horses, particularly those where it is perceived that the laryngoplasty has failed to produce the desired degree of abduction (as viewed through the laryngotomy incision) the vocal cord is also excised in order to further streamline the airway. Bilateral ventriculocordectomy is not recommended because of the risk of ventral laryngeal web formation [65]. The laryngotomy incision is not sutured and is left to heal by second intention.

Alternatively, the sacculectomy or ventriculocordectomy can be performed using an ND:YAG or diode laser with endoscopic guidance. This can be done while the horse is still under anesthesia or following recovery with the horse standing.

Laser Cordectomy [66] - The videoendoscope is passed through the right nasal passage to allow for a better view of the left vocal fold. The first incision must start at the ventral aspect of the vocal fold, beginning 1.5 cm caudal to the rostral edge of the vocal fold. The incision is made in a caudal to rostral plane until the rostral edge of the vocal fold is reached. The videoendoscope is withdrawn and then passed through the left nostril and a grasping forceps is passed through the right nostril. The vocal cord is tensed in it’s midportion and incised vertically in a proximal to distal direction starting 3 - 4 mm distal to the vocal process of the arytenoid cartilage. After excision of the vocal cord, one can lase the abaxial wall (sacculectomy) of the remaining ventricle although the author (NGD) does not routinely perform this procedure.

In the first few days following laryngoplasty and sacculectomy performed via a laryngotomy, most horses have some degree of dysphagia when eating and may have a mild fever. Water, saliva and food particles may drain from the laryngotomy incision. Hay should be fed on the ground. Postoperative dysphagia usually improves within days of surgery, particularly with the administration of non-steroidal anti-inflammatories. A rare occurrence is the horse that simply cannot tolerate the laryngoplasty and the resultant aspiration of food, coughing and inappetance becomes a threat to the horse’s health. In such horses, a second surgery is necessary in order to remove or loosen the laryngoplasty suture.

Most horses develop a seroma at the laryngoplasty site that is self limiting and subsides within two weeks following surgery. If the horse develops a fever in conjunction with the seroma becoming larger, antibiotic treatment should be initiated and it may become necessary to drain the seroma. It is possible for the seroma to become infected without having the infection involve the prosthetic suture. Therefore, if the seroma is opened and left open to drain, great care should be taken to minimize further bacterial contamination of the area, for example with flushing. Infection of the prosthetic suture can lead to failure of the prosthesis to maintain abduction, infection of the arytenoid cartilage, chondritis and fistula formation (either into the lumen of the larynx or externally at the incision site). Infection of the prosthetic suture with a fistula forming into the lumen of the larynx is usually a result of penetration of the lumen of the larynx during suture placement. Once the prosthetic suture becomes infected the only way to resolve the infection completely is to remove the suture.

Following a laryngoplasty and sacculectomy, the horse should receive 30 to 45 days of stall rest with handwalking only for exercise before resuming training. Hay should always be fed on the ground to reduce the chances of aspiration while swallowing. Initially, at least, most horses will cough intermittently while eating.

In some horses, the postoperative coughing persists and is reflective of a more serious and chronic aspiration problem. Although horses that have a great deal of postoperative abduction (Fig. 37a) are at greater risk for developing this problem, it can also occur in horses that have only modest abduction. This would suggest that in addition to the obvious inability of the horse to protect its airway during swallowing as a result of over-abduction, there may be other factors such as neurologic dysfunction or perhaps foreign body reaction to the suture material that can also contribute to dysphagia. These horses cough excessively when eating and during exercise, particularly when they begin to exercise. There may be food staining at the nostrils. Endoscopically, food material is visible in the trachea, often extending as far distal as the bifurcation of the trachea (Fig. 37b). The amount of tracheal food contamination can vary greatly. In addition, some develop a secondary problem with intermittent dorsal displacement of the soft palate while they are coughing. As training intensifies, there may be repeated episodes of fever as a result of low grade aspiration pneumonia. Surprisingly, very few of these horses develop pleuropneumonia but their performance suffers greatly and generally they have a short-lived racing career.

Figure 37a. The left arytenoid cartilage (LA) in this horse has been "over-abducted" as a result of a left laryngoplasty.

Figure 37b. The arytenoid over-abduction has allowed for aspiration of feed material which is visible in the trachea.

In some of these horses, there will be improvement over time (months) following the laryngoplasty but in others, the cough is so persistent that they simply cannot perform. Removal of the laryngoplasty suture may be of some benefit, particularly in those horses with a great deal of abduction. It is preferable to wait until at least two months from the time of the laryngoplasty. This allows for maturation of the scar tissue around the prosthetic suture such that a significant degree of abduction will be maintained. The suture should be located and removed with minimal disruption of this scar tissue. The arytenoid cartilage will shift to a more "relaxed" position but some abduction will be maintained.

The prognosis for success following laryngoplasty is dependent on many variables and this is reflected in the wide range of success (or lack of it) in retrospective studies [61,62,64,67]. The most demanding test of a laryngoplasty is in the race horse, because of the high volume of airflow required to compete successfully. The horse that has demonstrated the ability to race successfully before acquiring laryngeal paralysis has the best prognosis. Approximately 65 - 70% of these horses can be expected to return following laryngoplasty and race productively. Unraced horses have a poorer prognosis. Laryngoplasty and sacculectomy can be successful in other types of performance horses, including Draft breeds. In most show horses, a successful laryngoplasty and sacculectomy will eliminate any objectionable respiratory noise. In some horses, a sacculectomy or ventriculocordectomy alone will alleviate the noise.

Failure of laryngoplasty can be the result of an inability to produce abduction at the time of surgery or a failure of the cartilage (usually the muscular process) to hold the suture. Fracture of the muscular process or cutting of the suture into the muscular process or the cricoid cartilage can cause postoperative "relaxation" of the suture and some loss of abduction. Most horses lose some degree of the abduction achieved at surgery. Those that lose most of the abduction or were never satisfactorily abducted in the first place are in the "failure" group. The surgery may have been successful in reducing or eliminating the abnormal respiratory noise, particularly if a sacculectomy or ventriculocordectomy was performed, but the exercise intolerance persists because of inadequate abduction. However, it should be noted that the degree of abduction achieved at surgery does not necessarily correlate with future performance or client satisfaction. Although most performance horses benefit from the arytenoid cartilage being in a well abducted position, some can perform satisfactorily with an arytenoid fixed in a less than desirable position. Performing a second laryngoplasty may be beneficial in horses where there has been a postoperative failure of laryngoplasty. A new laryngoplasty technique, utilizing steel cable and stress reducing washers, has been mechanically tested in vitro and shown to be less likely to fail than a conventional laryngoplasty [68]. Another technique has been recently described utilizing a nylon suture secured with a precision crimping device [69]. Two purported advantages of this technique are that the tension of the suture can be adjusted precisely before it is secured and using this particular type of suture may improve its retention in the laryngeal cartilages, minimizing the loss of arytenoid abduction in the postoperative period. To date, there have been no clinical reports of efficacy for either of these two new techniques.

C. Arytenoid Chondritis

Arytenoid chondritis is an inflammatory condition that can affect either one or both cartilages [35]. Horses can present with an acute, suppurative form of chondritis or with a more chronic form that is generally progressive but may be quiescent for long periods of time. An inflamed and thickened arytenoid cartilage has limited motion and produces laryngeal obstruction as a result of its space occupying effect. The disease usually involves the body of the arytenoid and may also cause deformity and thickening of the corniculate process as well as the muscular process. The degenerating and inflamed cartilage becomes thickened and in some cases cavitated (Fig. 38). Frequently there is a fistula that connects the diseased cartilage to the lumen of the larynx. The luminal opening to this fistula is often surrounded by granulation tissue, producing an intraluminal projection. The disease process may also produce inflammation or infection of the adjacent musculature or adjacent cartilages of the larynx. Arytenoid chondritis may be further complicated by inflammation and ulceration of adjacent soft tissues such as the aryepiglottic tissue or by other airway obstructive lesions such as nasopharyngeal cicatrix formation. Horses may also develop arytenoid chondritis following laryngeal surgery.

Figure 38. A cross-sectional portion of the body of the left arytenoid cartilage affected with chondritis. The cartilage is thickened and the central portion is undergoing degeneration.

Trauma and infection have been suggested as possible etiologies. The cartilage can be inoculated with bacteria from the lumen of the larynx following an injury to the mucosa that extends into the cartilage or the cartilage(s) can become secondarily infected as a result of perilaryngeal lymph node abscessation caused by an upper respiratory tract infection (Fig. 39).

Figure 39. A bacterial infection in this horse led to abscess formation (A) dorsal to the larynx and produced bilateral arytenoid chondritis. The epiglottis is denoted by an E.

The clinical signs of airway obstruction produced by arytenoid chondritis range from mild to severe. Usually the disease is discovered in its earliest stages in performance horses that have an endoscopic examination because they begin to make an abnormal respiratory noise or show decreased performance. Sedentary horses may develop advanced chondritis and serious airway obstruction before it is noticed. With the acute form of suppurative chondritis, which is usually bilateral, the onset of signs may be sudden and the obstruction severe, even necessitating a temporary tracheostomy.

The diagnosis of arytenoid chondritis is made on endoscopic examination. Subtle, unilateral arytenoid chondritis can be confused with arytenoid paralysis but it is possible to differentiate between the two diseases with careful endoscopic evaluation (Fig. 40). There is reduced mobility of the cartilage with both diseases but with chondritis there is usually some swelling or deformity of the corniculate process, an intraluminal projection and the palatopharyngeal arch is often visible on the affected side because of enlargement of the body of the arytenoid cartilage. If there is an intraluminal projection, there is usually a "kissing lesion" on the opposing surface of the opposite arytenoid (Fig. 41). The muscular process of the arytenoid cartilage may feel abnormal on digital palpation.

Figure 40. This horse has subtle left arytenoid chondritis (vs. left arytenoid paralysis). There is deformity of the left arytenoid cartilage (LA) with an intraluminal projection of tissue (arrow).

Figure 41. Left arytenoid chondritis (LA) with gross deformity of the corniculate process, a visible left palatopharyngeal arch (open arrow) and a "kissing lesion" on the luminal surface of the right arytenoid (solid arrow).

A lateral radiograph of the larynx may show a contour abnormality of the corniculate process of the affected cartilage(s), a diminished laryngeal saccule (the result of encroachment from the enlarged body of the arytenoid cartilage), arytenoid cavitation if there is an abscess and irregular cartilage or soft tissue densities or an abnormal area of dystrophic calcification within the arytenoid cartilage (Fig. 42) [70]. A soft tissue density situated dorsal to the larynx is suggestive of perilaryngeal abscessation. If there is a fistula from the abscess to the lumen of the larynx, there may be a visible gas density.

Figure 42. An abnormal area of arytenoid calcification is visible (arrow) on this lateral radiograph of the larynx of a horse with chondritis.

Treatment of Arytenoid Chondritis - The horse with an acute, suppurative form of arytenoid chondritis usually has a fever and may be in respiratory distress as a result of laryngeal obstruction. Frequently both arytenoid cartilages are involved. The horse is treated, initially, with antibiotics, non-steroidal anti-inflammatory drugs, rest and, if necessary, a temporary tracheostomy. The tracheostomy tube is removed when the laryngeal swelling subsides. It may take weeks for the infection to resolve, however, there is usually residual and permanent cartilage damage with some loss of arytenoid cartilage mobility (Fig. 43a and Fig. 43b). Even after apparently successful treatment, the chondritis can recur.

Figure 43a. Endoscopic view of the larynx of a horse with an acute suppurative form of arytenoid chondritis. Both arytenoid cartilages are involved.

Figure 43b. Following two weeks of treatment with antibiotics, anti-inflammatories, rest and a temporary tracheostomy there is reduced swelling and improved mobility of the arytenoids. Intraluminal projections and reduced mobility may be permanent changes.

Some performance horses that have mild, unilateral or even bilateral chondritis can continue to be useful without needing surgery or they may be retired without a need for surgery. However, the disease is often progressive and the affected cartilage(s) may enlarge over time, necessitating surgical treatment. Horses can successfully perform again after a unilateral arytenoidectomy providing the opposite arytenoid cartilage has normal function. Surgical options for the treatment of arytenoid chondritis include: arytenoidectomy; excision of intraluminal granulation tissue with focal curettage of the underlying arytenoid cartilage and permanent tracheostomy.

The easiest and most economical solution, particularly in horses with bilateral chondritis is a permanent tracheostomy (Fig. 44) [64]. This can be performed standing and is particularly useful in non performance horses such as pregnant broodmares.

Figure 44. Chronic, bilateral arytenoid chondritis in a pregnant Draft breed broodmare. The condition produced a severe obstruction and was successfully treated by performing a standing permanent tracheostomy.

Focal excision of intraluminal masses can be considered in those horses where there is still cartilage mobility but the intraluminal projection is determined to be obstructive. This can be done standing under endoscopic guidance using a diode or an ND:YAG laser or under general anesthesia with conventional resection of the mass and delicate curettage of the underlying bed of cartilage (Fig. 45a and Fig. 45b) [71,72]. These techniques should be minimally invasive because overzealous curettage or laser treatment can provoke further cartilage degeneration.

Figure 45a. Granulating mass on the arytenoid cartilage.

Figure 45b. Arytenoid cartilages following laser resection of the mass.

Unilateral arytenoidectomy is indicated with unilateral arytenoid disease when the thickened cartilage is obstructive and the owner wishes to maintain the horse as a performance horse or does not want the horse to have a tracheostomy. Unilateral arytenoidectomy may also be considered in a horse with bilateral chondritis if one side is minimally affected and still has an acceptable amount of residual arytenoid movement.

There are two arytenoidectomy techniques available: partial and subtotal [73]. Partial arytenoidectomy involves removing the body of the arytenoid as well as the corniculate process. The muscular process is preserved. With a subtotal arytenoidectomy, the corniculate process, as well as the muscular process is preserved. In addition, with either of these techniques, the saccule and vocal cord on the affected side can also be removed. Experimental data have shown that in regards to improving airway mechanics, the partial arytenoidectomy is superior to the subtotal technique and is preferable for use in performance horses [63,74].

Partial Arytenoidectomy - In preparation for surgery, the horse is administered broad spectrum, intravenous antibiotics and a non-steroidal anti-inflammatory drug. The surgical site is clipped including the ventral cervical area in preparation for a tracheostomy. The author (JTR) prefers to perform a tracheostomy immediately after the horse receives the induction drugs and pass the endotracheal tube through the tracheostomy incision rather than trying to pass the tube orally and through the obstructed larynx [35,64]. The endotracheal tube is taken to one side of the neck so it is not laying over the laryngotomy site. A routine laryngotomy is performed and self retaining retractors are placed into the larynx. The lumen of the larynx can be inspected and if additional exposure is required for an arytenoidectomy, the cricoid cartilage and proximal portion of the cricotracheal ligament can be incised on ventral midline with a scalpel. The objective of a partial arytenoidectomy is to obtain a smooth laryngeal opening without any loose membrane that could collapse during inhalation during exercise. To achieve this goal one should preserve as much mucosa as possible to close over the dead space created by removing the body and corniculate process of the arytenoid cartilage. However, it is almost impossible to preserve mucosa where there is intraluminal granulation tissue formation. Experimental work has shown that it is not necessary to preserve mucosa in order to have the area heal satisfactorily but it is the author’s opinion that there is faster healing and less granulation tissue production, hence a better quality result if the mucosa is preserved and carefully sutured [75].

Using a Beaver blade, a three sided rectangular shaped incision is made through the mucosa overlying the axial surface of the arytenoid cartilage [64]. The initial vertical incision is made rostrally at the level of the juncture of the corniculate process and the body (or laminar) portion of the arytenoid. The incision is continued horizontally along the ventral margin and then vertically along the caudal margin of the arytenoid. Using a periosteal elevator, the mucosa is then separated from the underlying cartilage, creating a large, three-sided flap of mucosa with its base near the dorsal midline of the larynx. The mucosa overlying the corniculate process is also elevated and a curved elevator can be used to get around the front contour of that process. The abaxial muscle attachments are then sharply excised with scissors. The cartilage is grasped with forceps and traction is applied and the remaining attachments and the muscular process are severed with scissors. A pair of sharply curved, heavy duty or cartilage scissors are very useful for amputating the muscular process. A critical aspect to this procedure is to remove the entire corniculate process. The corniculate process tends to crumble or fragment when it is being removed and it is important to carefully remove all of the fragments of cartilage attached to the mucosa. Some surgeons recommend en bloc amputation of the corniculate process and its mucosa. This greatly simplifies the procedure. However, if a portion of the mucosa overlying the corniculate cartilage is preserved as a cuff of tissue, it may act as a physical barrier to aspiration during swallowing and provide support for the palatopharyngeal arch on that side. Two disadvantages of preserving this tissue are that the mucosal dissection over the corniculate process can be difficult and time consuming and in some horses this tissue will collapse into the airway during exercise. This phenomenon may only be observed during simultaneous exercise and videoendoscopy on a high speed treadmill (Fig. 46a and Fig. 46b).

Figure 46a. Larynx of a horse that had a unilateral, partial arytenoidectomy performed for treatment of left arytenoid chondritis. A portion of the mucosa overlying the corniculate process was preserved to form a cuff of tissue (arrow). The horse was presented following the second postsurgical race for poor performance and making an abnormal respiratory noise.

Figure 46b. Treadmill videoendoscopy showed that at high speed, there was dynamic collapse of this residual cuff of mucosa and the left aryepiglottic tissue (arrow). (Photo courtesy of Dr. E. Parente, University of Pennsylvania, New Bolton Center)

The incised margin of this mucosal cuff is tacked laterally to the remaining soft tissues with simple interrupted sutures of 3-0 synthetic absorbable suture material. The mucosal flap is then closed over the defect, leaving ventral gaps that allow drainage from the dead space. If only a portion of the mucosa could be salvaged, the resulting defect(s) can be left to heal by second intention. If possible, the suture knots should be buried and not exposed to the lumen. Protruding tags of mucosa should be excised because they can become swollen and produce obstruction in the early postoperative period. The saccule and vocal cord can then be removed. Kissing lesions on the opposite arytenoids cartilage should be left alone. If the cricoid was incised, the cut ends are tightly and securely apposed by suturing the adjacent soft tissues rather than the cartilage. Passing sutures through the cartilage can induce chondroma formation. The laryngotomy incision is left open to heal by second intention. The horse should be recovered with the endotracheal tube remaining in the trachea. Once the horse is fully recovered, the endotracheal tube is replaced with a self retaining tracheostomy tube. This tube is removed at the earliest possible time.

The amount of postoperative swelling at the arytenoidectomy site can vary greatly (Fig. 47a and Fig. 47b). In some horses, it may be necessary to maintain a tracheostomy for up to a week. In others the tube can be safely removed after 12 hours. A tracheostomy tube should be removed at the earliest possible time in order to reduce the chance of producing a tracheal ring deformity. Postoperative administration of non-steroidal anti-inflammatory drugs or even corticosteroids can help reduce swelling at the surgical site. If the mucosal sutures dehisce and mucosa protrudes into the airway, the postoperative obstruction may be prolonged.

Figure 47a. Severe swelling at the site of a partial left arytenoidectomy performed two days earlier for treatment of a unilateral chondritis. The mucosa overlying the arytenoid, including the corniculate process, had been preserved and became excessively swollen. The horse was treated with a non-steroidal anti-inflammatory drug, low doses of dexamethasone and the temporary tracheostomy tube that was placed at the time of surgery was maintained for an additional three days.

Figure 47b. Ten days following surgery, the swelling at the arytenoidectomy site was resolving satisfactorily and the horse was discharged from the hospital.

Postoperatively, the horse is confined to a stall and can be handwalked for exercise. The surgical site can be assessed endoscopically at 30, 45 and 60 days in order to decide when training can be resumed. Residual inflammation and, particularly, buds of intraluminal granulation tissue are indicators that the horse requires more rest before resuming exercise. Some surgeons remove these intraluminal masses with a laser.
Arytenoidectomy is a salvage procedure and the prognosis for a horse to resume racing successfully following a partial arytenoidectomy for unilateral chondritis is likely to be 50% or less [76]. Horses that do resume a racing career usually do at a much lower level of competition than initially intended.

Complications associated with unilateral partial arytenoidectomy include aspiration of food material and persistent airway obstruction in performance horses. A few horses develop significant aspiration with a food tinged nasal discharge and a chronic cough. Postoperatively, exercise limiting laryngeal obstruction may be the result of a failure of the partial arytenoidectomy to create an adequate luminal diameter or may be the result of dynamic collapse of the remaining soft tissues on the side of the arytenoidectomy. If the opposite arytenoid cartilage does not function normally, it is unlikely that the horse will be a successful athlete. The prognosis for successful postoperative performance seems to be better in horses treated for unilateral chondritis than those treated for failure of laryngoplasty. This may be because a normal cricoarytenoideus dorsalis muscle is attached to the muscular process at the surgical site and may help to prevent against soft tissue collapse. Horses that have nasopharyngeal cicatrices as well as arytenoid chondritis respond poorly to arytenoidectomy [77]. With bilateral arytenoidectomy there is a possibility of laryngeal web formation.

D. Fourth Branchial Arch Defects (4-BAD) [36]

This uncommon condition involves defects of laryngeal structures derived from the fourth branchial arch during abnormal embryological development [35,36]. The prevalence in Thoroughbreds is no less than 2 in 1000 horses foaled [36]. The condition occurs in other breeds including Hanoverian, Warmblood, Haflinger and Standardbred. The condition can be bilateral or unilateral but it appears that the right unilateral form occurs most frequently, at least in Thoroughbreds. This condition has also been referred to as cricopharyngeal-laryngeal dysplasia and, historically, as rostral displacement of the palatopharyngeal arch (RDPA) [35,78]. Although RDPA is frequently an endoscopic observation with this syndrome, that nomenclature was unsatisfactory because the syndrome represented a much more complex disorder, involving abnormalities of the thyroid cartilage, an absence of the cricopharyngeus muscles and hypoplasia of other intrinsic laryngeal muscles. Besides, RDPA is not a consistent finding. Because of the cartilaginous abnormalities, the function of the cricoarytenoideus dorsalis muscle is compromised and as a result there is reduced arytenoid cartilage abduction.

The clinical signs produced by 4-BAD are variable and reflect the degree of abnormality present. Horses that are severely affected have very limited movement of both arytenoids and as a result, serious laryngeal obstruction and also have rostral displacement of the palatopharyngeal arch that produces dysphagia and aerophagia. Air swallowing can lead to repeated episodes of colic. Less affected horses may only make an abnormal airway noise at exercise, a noise that is the result of air turbulence associated with laryngopalalatal instability and sounding similar to that produced by intermittent dorsal displacement of the soft palate.

A definitive diagnosis of 4-BAD can be made endoscopically if there is a rostral displacement of the palatopharyngeal arch over the apical area of the corniculate cartilages (Fig. 48). The degree of RDPA can be variable between horses and in some horses there is some retraction of the palatopharyngeal arch when the arytenoid cartilages abduct. This condition (4-BAD) should always be considered as a differential diagnosis when there is an apparent right laryngeal paralysis, particularly in a young horse. RDPA may not always be evident. As with the clinical signs, the endoscopic findings are reflective of the severity of the condition.

Figure 48. Rostral displacement of the palatopharyngeal arch (arrows) over the apices of the corniculate processes in a horse with a fourth branchial arch defect.

Additional aids to diagnosis include digital palpation of the larynx and a lateral radiograph of the pharynx and larynx. Computed tomography (CT) of the larynx can also be used to further define the deformity. If the wing of the thyroid cartilage is malformed and angles dorsally instead of horizontally, it is difficult to palpate the muscular process of the arytenoid cartilage. In unilateral cases, there is clearly a palpable asymmetry. On a lateral radiograph, RDPA is seen cranial to the corniculate processes and there is usually air filling the proximal esophagus (Fig. 49).

Figure 49. On this lateral radiograph of a horse with a fourth branchial arch defect, the palatopharyngeal arch (arrow) is displaced rostral to the arytenoid cartilages. The proximal esophagus (E) is filled with air.

At the time of this writing, there is no effective treatment for 4-BAD. If there is serious airway obstruction and dysphagia, the horse may be euthanized. Horses that are less affected may show only signs of airway obstruction with exercise. The author has encountered two Thoroughbred racehorses that had mild RDPA that were able to race successfully but at a level of competition that disappointed the owners. Resection of the palatopharyngeal arch is of little benefit to these horses with RDPA. In unilateral cases, laryngoplasty is of little use because of the anatomical malformations; instead partial arytenoidectomy is indicated if arytenoid cartilage abduction is minimal. The most innocuous surgical treatment that might be considered in horses that have mild 4-BAD is sternothyroid myectomy/tenectomy but a poor prognosis should be given for improvement. The author would reserve this surgery for those cases that are less seriously affected by the condition. Simultaneous videoendoscopy and exercise on a high speed treadmill can be useful to rule out any other coexisting and possibly treatable condition such as axial deviation of the aryepiglottic folds that might be contributing to an abnormal noise and airway obstruction.

E. Laryngeal Cyst

Laryngeal cyst formation is rare. A paralaryngeal accessory bronchial cyst has been reported as a cause of laryngeal hemiplegia in a horse [37]. The diagnosis was made at the time of laryngoplasty surgery where a large cyst was discovered medial to the thyroid cartilage and lateral to the cricoid and arytenoid cartilages. There were associated cartilage deformities. A CT scan or MRI could be useful for assessing the position of a laryngeal cyst and the degree of cartilaginous deformity.

The cyst was thought to have been a congenital anomaly, originating from the respiratory tract rather than being retained branchial remnants. It is likely that as the cyst developed and enlarged, it put pressure on the surrounding cartilages of the larynx producing deformity and signs consistent with laryngeal hemiplegia. As with most congenital cysts in this region, the only effective treatment is surgical removal. If there is a permanent loss of arytenoid abduction, a laryngoplasty may be necessary. Accurate placement of the laryngoplasty suture may be difficult if the laryngeal cartilage anatomy is distorted and a partial arytenoidectomy might be a better alternative.

F. Hyperkalemic Periodic Paralysis (HPP)

Hyperkalemic periodic paralysis is a heritable disease of horses (primarily heavily muscled Quarter Horses) that produces episodes of muscle weakness and tremors that can culminate in recumbency, paralysis or even death. Most horses that are homozygous for HPP have a history of making abnormal respiratory tract noises, sometimes in association with a generalized abnormality of muscle activity, sometimes not. Endoscopic observations in a number of these horses during these episodes of respiratory stridor revealed upper airway obstruction produced by pharyngeal collapse and laryngeal spasm [38,39]. Other endoscopic observations included pharyngeal edema, dorsal displacement of the soft palate and eversion of the laryngeal ventricle. These episodes of airway obstruction are usually acute in onset, induced by some form of stress and can lead to asphyxiation. In many of these horses, the signs of pharyngeal and laryngeal collapse are apparent from the time of birth. Heavily muscled Quarter Horses that are having episodes of respiratory stridor should be genetically tested for HPP. Electromyographic identification of abnormal muscle activity (laryngeal muscles included) helps to confirm the diagnosis.

Although HPP can be managed medically with dietary modifications and the administration of acetazolamide, some of these horses that have episodes of severe airway obstruction may require emergency tracheostomy as a life saving measure. Although unilateral, partial arytenoidectomy has been reported as a treatment option, the prognosis is poor.

G. Epiglottic Abnormalities

Abnormalities of the epiglottis, including hypoplasia, deformity, flaccidity and inflammation are associated with dorsal displacement of the soft palate (DDSP), either at rest or during exercise [35]. Unless the soft palate is persistently displaced, the epiglottis is visible on endoscopic examination and a subjective assessment of the size, shape and the consistency of the epiglottis can be made during a resting examination. Inflammation of the epiglottic cartilage or the associated aryepiglottic tissues can also be seen endoscopically. The response of the epiglottis to nasal occlusion may give some indication of how it responds to increased (negative) nasopharyngeal pressures but epiglottic function is probably best assessed with simultaneous videoendoscopy and exercise on a high speed treadmill. The role that the epiglottis plays in predisposing to intermittent DDSP is controversial, however, the author (JTR) feels that the epiglottis must have sufficient length and be rigid enough to resist the tendency of the soft palate to displace when nasopharyngeal pressures are increased (become more negative). Further assessment of the epiglottis, including a measurement of thyroepiglottic length, can be made with lateral radiographs of the laryngeal region.

By strictest definition, a hypoplastic epiglottis is shorter than normal (thyroepiglottic length <7 cm) and predisposes to intermittent DDSP [16,35]. The term hypoplastic has also been used in a broader sense (and probably incorrectly) to describe an epiglottic flaccidity, regardless of length. Flaccid is a descriptive term that is applied if the epiglottis changes shape or bends, easily, in response to nasal occlusion or direct contact with the endoscope (as happens with passing the endoscope into the trachea) (Fig. 50). It should be noted that many young horses, particularly yearlings, show some degree of epiglottic flaccidity and displace their soft palate easily during endoscopic examination at rest but only a small percentage of them go on to develop intermittent DDSP during exercise [18]. Epiglottic flaccidity may be a reflection of immaturity in the young horse and in many, the epiglottis "matures": as the horse ages (at least until the horse is 3 years of age, after which, there is likely to be little change). Furthermore, an epiglottis that appears flaccid at rest, may appear normal during exercise. There appears to be a physiologic response of the epiglottis and its associated soft tissue structures to exercise.

Figure 50. In response to nasal occlusion, the epiglottis (E) of this young horse becomes flaccid. Bilaterally, aryepiglottic tissue (dark arrows) forms a "border" along the lateral margin of the epiglottis. There is a separation of the aryepiglottic fold (dark arrow) from the lateral pillar of the soft palate (white arrow) as air leaks from the oropharynx into the nasopharynx.

Epiglottic augmentation has been recommended for those horses where the epiglottis appears to lack the rigidity required to hold the soft palate in a subepiglottic position [29,79,80]. Polytetrafluoroethylene paste is injected into the subepiglottic and aryepiglottic tissues via a laryngotomy in an effort to increase epiglottic bulk and induce subepiglottic fibrosis that increases epiglottic rigidity [81]. The augmentation procedure is usually done in combination with a sternothyroid tenectomy/myectomy and a staphylectomy [64]. The procedure is costly and the horse may require as long as six weeks of rest following surgery. There can be some significant short term and long term complications. In the initial postoperative period, many of these horses are febrile and some are dysphagic for a few days. Long term complications include persistent dorsal displacement of the soft palate, chronic granulomatous reactions in the subepiglottic tissues and entrapment of the epiglottis.

There have been some rather spectacular results from this surgery but it is difficult to measure the specific contribution of the augmentation when it is combined with other procedures. The augmentation procedure does appear to offer some improvement in prognosis over the simpler procedures alone, providing the diagnosis is correct and there are some scientific criteria for selecting the appropriate surgical candidates. There is likely to be little benefit from an augmentation if it is performed in horses without much regard for epiglottic assessment. Horses with a history of previous epiglottic surgery are not candidates for epiglottic augmentation because subepiglottic fibrosis does not allow for an even distribution of the polytetrafluoroethylene paste.

Trauma to the epiglottis, particularly that associated with epiglottic surgery can produce an inflammation of the epiglottic cartilage that results in chondritis and deformity. This can contribute to an intermittent or even, persistent dorsal displacement of the soft palate. When performing surgery around the epiglottis, every effort should be made to minimize direct trauma to the epiglottic cartilage. The epiglottic cartilage should never be directly grasped with an instrument or incised during the resection of aryepiglottic tissue. Once the epiglottis becomes deformed, there is no type of surgery that will correct the problem (Fig. 51a, Fig. 51b).

Figure 51a. The apex of the epiglottis in this horse appears blunted. This deformity was associated with intermittent dorsal displacement of the soft palate which was documented with treadmill videoendoscopy. Previous epiglottic surgery was suspected.

Figure 51b. Deformed epiglottic cartilage. Unknown cause.

Epiglottitis can occur spontaneously and cause airway obstruction, coughing and possibly, dysphasia [82]. The entire epiglottis and surrounding soft tissues appear swollen, inflamed and frequently the aryepiglottic tissues are ulcerated (Fig. 52a). Possible etiologic factors include bacterial infection and trauma, even if it is not part of the history. Horses with epiglottitis are frequently misdiagnosed as having epiglottic entrapment. On close endoscopic inspection, the apex and dorsal surface of the epiglottis will be visible. There may be obvious necrosis of cartilage at the tip of the apex of the epiglottis. In most horses, the condition will successfully resolve with rest, antibiotic and anti-inflammatory therapy. A lateral radiograph of the larynx can be taken as a precaution in order to help rule out the presence of a radiopaque foreign body. Surgical resection of the inflamed tissues should be avoided as this may contribute to the development of a more severe epiglottic deformity and the likelihood of a persistent dorsal displacement of the soft palate. Some of these horses, interestingly, will represent after the epiglottitis has apparently resolved, with an entrapment of the epiglottis (Fig. 52b). Dorsal epiglottic abscesses are rarely encountered and can be drained transendoscopically using a laser or per os using a long instrument with the horse under anesthesia [83]. Producing an epiglottic deformity is a risk of this type of epiglottic surgery.

Figure 52a. Acute epiglottitis in a 2 year old Standardbred racehorse. The entire epiglottis and particularly the subepiglottic tissue, is swollen, inflamed and ulcerated. The apex, lateral borders and the dorsal surface of the epiglottis were visible, differentiating this condition from an aryepiglottic fold entrapment. The condition was successfully treated medically and the horse resumed racing.

Figure 52b. Approximately one year later, the same horse presented with an entrapment of the epiglottis. The mucosal surface of the entrapment is ulcerated on the right side.

Epiglottic Entrapment - Epiglottic entrapment [84,85] is a common abnormality, with a prevalence range in racehorses from 0.74% to 8% (Fig. 53a). The cause of this disease is unknown, but is associated with hypoplastic epiglottis in some horses. Endoscopic/videoendoscopic examination during exercise reveals that during inspiration the arytenoepiglottic fold is taut ventrally, causing virtually no upper airway obstruction. During expiration, air raises the arytenoepiglottic fold causing an expiratory obstruction. This causes exercise intolerance and abnormal respiratory noise. The respiratory noise is created by aryepiglottic membrane vibration induced during expiration. Many horses develop ulceration of the entrapped membrane (Fig. 53b) as well as the caudal edge of the soft palate (Fig. 13). Both epiglottic entrapment and dorsal displacement of soft palate can occur concomitantly.

Figure 53a. Aryepiglottic fold entrapment. Note the outline of the epiglottic cartilage is visible.

Figure 53b. Aryepiglottic fold entrapment with ulceration.

Diagnosis - The diagnosis of epiglottic entrapment is made based on a history of upper respiratory noise and/or exercise intolerance, which directs the clinician to an endoscopic/videoendoscopic examination of the upper airway. On endoscopy, one can observe that the rostral end of the epiglottis is no longer visible. Unlike dorsal displacement of the soft palate (Fig. 13), the contour of the epiglottis is visible with epiglottic entrapment (Fig. 53a and Fig. 53b). The diagnosis of epiglottic entrapment can be difficult to make if the entrapment is intermittent. With intermittent entrapment, repeated endoscopic/videoendoscopic examinations after (or during) exercise may be required to diagnose the epiglottic entrapment. In long-standing cases, ulceration can be seen on the entrapping membrane. Once the diagnosis is made, one should evaluate the epiglottic cartilage. Although the size and strength of the epiglottic cartilage can be estimated during endoscopy, radiographic examination of the larynx is helpful for an accurate determination of the length of the epiglottis.

Treatment - The treatment alternatives for epiglottic entrapment consist either of two surgical approaches: a) Removal of a wedge of arytenoepiglottic fold at the rostral ends of the epiglottic cartilage. b) Axial division of the arytenoepiglottic fold at the rostral ends of the epiglottic cartilage.

The improved success following axial division (82%) compared to wedge resection (27%) makes axial division of the arytenoepiglottic fold the technique of choice. Thus, laryngotomy and wedge resection should be reserved for treatment of intermittent entrapment or when the entrapment adheres to the epiglottic cartilage.

Multiple surgical procedures (hooked bistoury, electrocautery, or Neodymium: yttrium aluminum garnet or Diode laser) can be used to achieve axial division. This can be done transnasally under endoscopic/videoendoscopic control with the animal standing. The horse is sedated with xylazine or detomidine hydrochloride, and 35 ml of 2% lidocaine hydrochloride is applied to the arytenoepiglottic fold. Alternatively, the horse can be anesthetized, a mouth gag placed, and the same procedures performed transorally. One can also use an embryotomy knife using the transoral approach. Finally, a ventral midline laryngotomy can be done, and the epiglottic cartilage inverted into the larynx to expose the arytenoepiglottic folds.

We do not recommend the use of the hooked bistouries passed transnasally with the horse standing because of the possibility of inadvertent injury to the epiglottis, soft palate and nasal passage. Inadvertent transection of the soft palate leads to chronic coughing and sometimes to dorsal displacement of the soft palate.

The presence of an ulcer on the aryepiglottic fold does not change the treatment unless the ulcer results in adhesions of the aryepiglottic fold to the epiglottic cartilage. In those cases, if the adhesion cannot be broken down with gentle transoral or transnasal manipulation, a midline ventral laryngotomy may be required to allow more precise dissection. There is no need to resect the ulcer as its resolution occurs once the entrapment is released. The pathophysiology of the ulcer is unknown.

Postoperatively, the horse should receive non steroidal anti-inflammatory drugs and a throat spray (250 ml glycerin, 500 ml nitrofurazone, 250 ml DMSO and 50 mg dexamethasone 2 mg/ml, 20 cc BID for 10 days). The horse can return to training in two to six weeks, depending on the inflammation present and the surgical technique employed.

Complications following treatment of epiglottic entrapment include recurrence, dysphagia and dorsal displacement of the soft palate. Recurrence of the epiglottic entrapment occurs in approximately 10% of horses. Excessive swelling of the subepiglottic tissue may result in DDSP and requires a long delay (up to 2 months) for resolution. Dysphagia and dorsal displacement of the soft palate are consequences of subepiglottic masses. Apparently, scarring of the ventral surface of the epiglottis can interfere with swallowing and lead to dorsal displacement of the soft palate. These complications are rare.

Prognosis following treatment of epiglottic entrapment is good providing there are no coexisting abnormalities such as epiglottic hypoplasia or dorsal displacement of the soft palate. Some of the chronic entrapment results in deformation or fracture of the tip of the epiglottic cartilage.

Axial Displacement of the Aryepiglottic Membrane - Axial collapse of the aryepiglottic folds occurs during inhalation and therefore, is a source of inspiratory noise and obstruction [86]. The noise can be similar to that of horses with laryngeal hemiplegia. This disease affects mainly racehorses (Thoroughbreds, Standardbreds and racing Arabians), and the pathophysiology of this disease is poorly understood. It is typical of horses with rostral displacement of the palatopharyngeal arch, and is seen in horses with suboptimal tension on the aryepiglottic folds in horses with laryngeal hemiplegia or after partial arytenoidectomy. However, it is also seen in horses with normal full abduction of the arytenoid cartilage and on the contralateral side of horses with laryngeal hemiplegia. In those latter cases, it is thought to be due to alteration of flow pattern due to a primary obstruction.

The diagnosis can only be made during treadmill videoendoscopy and the degree of axial collapse is not proportional to the degree of respiratory noise. Often additional airway obstruction is seen and the axial collapse of the aryepiglottic folds is secondary to the flow pattern alteration. The treatment consists of resection of the axial component of the aryepiglottic folds usually done during standing endoscopy with the aid of a surgical laser (Fig. 54).

Figure 54. Resection of aryepiglottic fold using a laser.

H. Subepiglottic Cyst

A subepiglottic cyst forms as the result of cystic development of remnants of the thyroglossal duct [35,87]. These cysts can develop at variable rates and can become quite large, even in foals. Often, they do not become apparent until the horse is two or three years of age, when the cyst becomes large enough that it interferes with breathing and swallowing. Foals with relatively large subepiglottic cysts are often presented for coughing and aspiration pneumonia whereas older horses are usually presented for signs of airway obstruction and poor performance [87]. The endoscopic appearance of a subepiglottic cyst can vary, depending on the size of the cyst and the length of the stalk. In foals with a very large cyst, the epiglottis may be deviated dorsally and obscured from view (Fig. 55). More typically, the cyst is located predominantly to one side, under the epiglottis (Fig. 56). If the stalk is long enough, the cyst can be situated in the oropharynx and not visible on initial endoscopic examination. However, it can usually be brought into view by stimulating swallowing and changing its position. Occasionally a subepiglottic cyst will be seen in conjunction with an entrapment of the epiglottis.

Figure 55. An extremely large subepiglottic cyst in a weanling foal. The epiglottis and larynx are obscured from view because the cyst is so large.

Figure 56. A more typical subepiglottic cyst, visible on the right side of the epiglottis.

Once identified, it is usually recommended that a subepiglottic cyst be removed [64]. This can be accomplished in a number of ways and the technique is somewhat dependent on the size of the horse. If the horse’s head is large enough to pass a hand through the mouth into the oropharynx, a snare can be placed around the cyst and it can be amputated (Fig. 57a, Fig. 57b, Fig. 57c and Fig. 57d). Alternatively, the snare can be introduced per os and with endoscopic guidance, placed around the cyst. The advantage of snare removal of a subepiglottic cyst per os is that it is simple and can be done under intravenous anesthesia. The disadvantage is that a larger mucosal defect is created and the resulting subepiglottic fibrosis may predispose to either an intermittent or a persistent dorsal displacement of the soft palate. The cyst can also be resected through either a laryngotomy or a pharyngotomy incision [64]. Resection of the cyst allows for preservation of the mucosa covering the cyst. Cyst removal may also be aided with transendoscopic use of a laser [88]. In some foals with a very large cyst, there may be permanent epiglottic deformity that could predispose to palate displacement following cyst removal. Most subepiglottic cysts have multiple loculations and are filled with relatively viscous, creamy colored fluid (Fig. 58). If the cyst is removed entirely, it will not recur.

Figure 57a. Snare formed with obstetrical wire passed through a plastic pipette.

Figure 57b. Subepiglottic cyst, removed intact, in the surgeon’s hand.

Figure 57c. A close up view of the cut surface of the subepiglottic cyst. Many of these cysts are multiloculated.

Figure 57d. The mucosa covering the cyst is also removed using the snare technique. A mucosal defect is created and the resulting subepiglottic fibrosis may predispose to dorsal displacement of the soft palate.

Figure 58. The content of this subepiglottic cyst was typical, a viscous, creamy colored fluid.

I. Neoplasia of the Nasopharynx and Larynx

Tumors in this area are rarely encountered. Squamous cell carcinoma, lymphosarcoma, fibrosarcoma, mast cell tumor and melanoma have all been reported to occur in the pharyngeal area [89]. Melanomas, are seen frequently in gray horses and tend to be relatively slow growing and benign until they become large enough to become obstructive. The clinical signs associated with nasopharyngeal or laryngeal neoplasia are dependent on their size and location and the extent of the associated tissue destruction. Larger masses will produce airway obstruction and could also produce dysphagia and nasal discharge. Regional lymph nodes may be enlarged. Tumor masses involving the nasopharynx and larynx can be identified endoscopically (Fig. 59). Guttural pouch endoscopy will allow visualization of retropharyngeal masses (Fig. 60). Differential diagnoses for neoplasia include retropharyngeal abscessation and foreign body penetration of the pharynx. Neoplasia of the larynx that infiltrates the cartilages and adjacent soft tissue involvement must be differentiated from arytenoid chondritis. Radiographs of the head are useful for assessing the size and specific location of the tumor. A computed tomography (CT) scan reveals even more information regarding the tumor location and tissue involvement. A definitive diagnosis is made following a biopsy of a tumor mass. Any enlarged regional lymph node(s) should also be biopsied. With melanoma, the diagnosis is usually self evident based on the colour and appearance of the masses and a biopsy is not required. The exception would be an amelanotic melanoma [89].

Figure 59. Squamous cell carcinoma (SCC) infiltrating the tissues on the right side of the larynx. A definitive diagnosis was made from a biopsy obtained via endoscopy.

Figure 60. A large retropharyngeal melanoma (M) fills the floor of the medial compartment of the left guttural pouch in this horse. The left stylohyoid bone (LSH) is visible.

It may be possible to obtain a diagnostic surface biopsy of the tumor through an endoscope. Frequently, however, those biopsies are not deep enough to get into the tumor mass and may show only chronic inflammation. It may be possible to biopsy the tumor mass(es) using an ultrasound guided biopsy needle (retropharyngeal or perilaryngeal location) or it may be necessary to perform a laryngotomy under intravenous anesthesia in order to get a diagnostic sampling that is then submitted for histopathologic examination.

If the tumor mass is localized and can be accessed, surgical debulking and possibly local injection of chemotherapeutic drugs may provide some temporary relief. This approach should only be contemplated when the tumor is of a more benign type or is also amenable to some form of systemic therapy (such as lymphosarcoma). Radiation therapy is also a possibility providing the tumor is radiosensitive [90,91]. The radiation treatment plan is based on the histopathological nature of the tumor and on the size of the tumor. A CT scan is used to delineate the limits and calculate the size of the tumor. Depending on the tumor type, radiation therapy may be palliative or effect a cure. Horses with lymphoma involving the nasopharynx or larynx are good candidates for megavoltage radiation treatment, however, the cost of repeated radiation treatments under general anesthesia may be prohibitive. A tracheostomy, either temporary or permanent is recommended in those horses where the tumor is obstructive and euthanasia is not elected at that time. Euthanasia is usually recommended in horses with an aggressive, destructive tumor.