Upper Airway Obstruction in Performance Horses: Differential Diagnoses and Treatment

Respiratory Disease: Medicine and Surgery

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Upper Airway Obstruction in Performance Horses Differential Diagnoses and Treatment

Paul W. Dean, DVM, MS*

PHARYNGEAL LYMPHOID HYPERPLASIA

Horses younger than 3 years of age have a diffuse distribution of lymphoid tissue along the walls and roof of the nasopharynx, the epiglottis, and the pharyngeal recess. The concentration and size of the lymphoid tissue normally regress as horses age; the follicles rapidly regress in 3-yearolds and become sparsely distributed and small by the time the horse is 5 years old. Some horses, however, have persistent abnormal amounts of proliferative nasopharyngeal lymphoid tissue. Pharyngeal lymphoid hyperplasia (PLH) describes both the normal finding of increased lymphoid follicular activity in the nasopharynx in young horses and the disease that results in respiratory noise and exercise intolerance. Moderate lymphoid hyperplasia commonly is accompanied by lower airway disease. The significance of the mechanical obstruction caused by moderately enlarged follicles is questionable. In the author's clinical experience exercise intolerance more commonly is caused by small airway obstruction with mucus than by mechanical obstruction caused by lymphoid follicles. One study 1 showed that gas exchange was not impaired in horses with PLH unless the hyperplasia was severe. Chronic cough produced by the presence of severe pharyngeal lesions or small airway disease also may contribute to reduced performance. Air turbulence during training, viral respiratory disease, environmental pollutants, and allergens have been incriminated as causes of PLH. Diagnosis A diagnosis of PLH is made by using nasopharyngeal endoscopy. A grading scheme describes four degrees of severity on the basis of the *Diplomate , American College of Veterinary Surgeons; Private Practitioner, Equine Surgical Center, Aubrey, Texas Veterinary Clinics of North America: Equine Practice-Vol. 7, No. 1, April 1991

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endoscopic appearance of the follicles. Mild disease usually is subclinical and often is diagnosed during endoscopic screenings of yearlings. Various sizes and colors of follicles, ranging from small and white to pink and edematous, are seen on the dorsal pharyngeal wall in horses with mild disease. Moderate PLH is characterized by many large, pink follicles with a few areas of follicular accumulation forming polyplike structures. In severe disease, single follicles may not be discriminated because of their coalescence and surrounding tissue fluid. Lateral radiographic projection of the pharynx shows thickening of the roof of the pharynx. Serous or mucoid nasal discharge often accompanies the moderate and severe forms. External pressure on the pharynx may elicit a cough. The most important factor in making a diagnosis of PLH is eliminating other causes of reduced respiratory performance. For example, intermittent laryngopalatal dislocation commonly is associated with chronic PLH . Endoscopic examination of the trachea often reveals excessive mucus on the tracheal floor, which may indicate that small-airway disease accompanies the pharyngitis. Respiratory epithelium and relatively hypocellular mucus in large quantities are common tracheal wash results in these cases. These findings in conjunction with PLH may indicate a viral or irritant cause, which has both upper and lower respiratory tract consequences. Treatment

Mild-to-moderate PLH commonly is observed endoscopically in horses with vague histories of respiratory noise or coughing during training. These horses often are treated successfully without removing the horse from training by using daily nebulization or nasopharyngeal washes that contain antibiotics, dimethyl sulfoxide, and corticosteroid combinations. Alternatively, good results often are obtained by applying freon or component coolant to the follicles with a polyethylene tube passed through the biopsy channel of the endoscope for superficial freezing. Realistically, only about 50% of the surface area of the dorsal pharyngeal wall can be freeze-treated without endangering the arytenoid mucosa. Horses treated with mucosal freezing may resume training by the fourth day after therapy. Some horses with excessive lower airway mucus production and PLH may benefit from nebulization during training, but most require at least 6 weeks of rest in addition to local therapy. Horses with infectious bronchitis are treated using antibiotics and an appropriate rest period. The author's experience with PLH primarily has been with 3-year-old and 4-year-old racehorses that have not improved with prolonged rest or with systemic or conservative local treatments. If all other causes of respiratory noise, exercise intolerance, and lower respiratory disease are eliminated from the diagnosis, electrofulguration of the dorsal pharyngeal wall through a ventral laryngotomy is recommended. A ball-tipped electrocautery probe is swept over the follicles , taking care to avoid other pharyngeal or laryngeal structures . An assistant guides the surgeon by using

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a nasally introduced endoscope. Horses affected with PLH that require a laryngotomy for other surgical diseases also are treated with electrofulguration. A diphtheritic membrane forms , and the superficial tissue sloughs within 2 weeks. Horses are returned to training after an endoscopic examination at 6 weeks postoperatively.

PHARYNGEAL CYST

Pharyngeal cysts most commonly are located in the subepiglottic tissue . They are believed to arise from lack of closure of the embryologic thyroglossal duct. Rarely, cysts are found on the dorsal pharyngeal wall; they are remnants of the craniopharyngeal ducts . Subepiglottic cysts cause respiratory noise and exercise intolerance in performance horses and dysphagia with aspiration pneumonia in foals. Newborn foals may not be able to swallow milk at birth. 30 Older horses may experience dysphagia but rarely develop aspiration pneumonia. Subepiglottic cysts may be accompanied by intermittent or persistent entrapment of the epiglottis.

Diagnosis Diagnosis of a pharyngeal cyst is made by endoscopic visualization of the fluid-filled cyst (Fig. 1). Occasionally, visualization of the subepiglottic cyst is obscured by the caudal margin of the soft palate, which makes diagnosis more difficult. The cysts may come into view during swallowing. Subepiglottic cysts or masses that are not apparent on nasopharyngeal endoscopic examination often are suspected of causing an upright or tilted epiglottis. An alternative method of diagnosing a suspected cyst in horses

Figure 1. Endoscopic view of a large multiloculated subepiglottic cyst in a 2-year-old Quarter Horse filly racehorse that suffered respiratory noise and exercise intolerance.

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with an upright epiglottis is endoscopy or palpation of the subepiglottic area while the horse is under intravenous anesthesia. The operator must not mistake the oropharyngeal tonsilar tissue located on either side of the subepiglottic tissue for a cyst or tumor. Treatment

Subepiglottic cysts may be removed using a variety of approaches including standard ventral laryngotomy and pharyngotomy or by using a snare. There is no advantage of pharyngotomy over ventral laryngotomy. Multiloculated cysts should be removed surgically through a ventral laryngotomy, because snaring may remove excessive mucosa. Regardless of the method chosen, the entire cyst must be removed without rupturing to prevent recurrence. The author usually prefers using an orally introduced snare to avoid a ventral laryngotomy incision. The horse is under intravenous general anesthesia. Obstetric wire is doubled and inserted into a Chambers catheter to make a loop at one end. The loop is placed around the base of the cyst manually. In foals and horses with small heads, endoscopic visualization of the cyst aids in grasping the cystic mucosa using sponge forceps. The loop is introduced over the forceps and positioned for cyst removal. The endoscope then is passed into the nasopharynx to ensure that the epiglottis is not included in the snare. The cyst is removed by sawing with the ends of the obstetric wire. If an epiglottic entrapment accompanies a subepiglottic cyst, the entrapping tissue is divided longitudinally using a hooked bistoury before cyst removal. An intense inflammatory reaction is expected after surgery of the arytenoepiglottic tissues. Training is resumed after the acute inflammatory reaction is resolved. Horses with excessive granulation tissue may require further rest and nasopharyngeal washes after surgery.

LARYNGEAL HEMIPLEGIA

Laryngeal hemiplegia is a distal axonopathy of the recurrent laryngeal nerve that results in neurogenic atrophy of the intrinsic laryngeal musculature. 4 The abductor muscles of the arytenoid generally follow the adductors in order of paralysis. The disease is left-sided in at least 95% of the cases; right-sided and bilateral paralysis occur infrequently. Abductor disease occurs in various forms, which has led to confusion regarding terminology. Laryngeal hemiplegia describes complete immobility or inability to fully abduct the cartilage, whereas laryngeal hemiparesis refers to any other functional abnormality of the abductor, including arytenoid tremors, asynchrony of abduction between arytenoids, or weakness (partial paralysis) of the affected arytenoid. There is no evidence that hemiparesis progresses to hemiplegia. The nerve degeneration is irreversible in the idiopathic form of the disease. Rarely, arytenoid function can be restored

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after known nerve damage resulting from trauma or surgery in the area of the recurrent laryngeal nerve. Reversal in these cases may occur from 2 weeks to several months after the traumatic incident. Respiratory noise produced while the horse is at work results from air turbulence caused by the axial position and lack of abduction of the arytenoid cartilage during inspiration in horses with laryngeal hemiplegia. Exercise tolerance is progressively or acutely reduced during fast work, because increasing negative pressure within the larynx causes dynamic collapse of the affected arytenoid into the laryngeal lumen during inspiration, which results in further luminal compromise. Respiratory noise usually is evident during fast work and is never present during rest in horses with unilateral abductor disease. Flexion of the neck during exercise often exaggerates the noise, probably as a result of superimposed functional compromise of the pharynx. Laryngeal paraplegia (bilateral paralysis) results in severe exercise intolerance and usually results in dyspnea at rest. Tracheostomy may be required for horses with paraplegia. Hemiparesis usually is diagnosed in affected horses undergoing endoscopic evaluation and laryngeal palpation for exercise intolerance or for prepurchase examination. These horses often have either a vague history or no history of respiratory noise or dyspnea while exercising. However, attentive listening during training often reveals an inspiratory noise consistent with laryngeal hemiplegia. Although the clinical relevance of hemiparesis is debatable, circumstantial evidence together with clinical deduction suggest a correlation between hemiparesis (diagnosed by laryngeal palpation) and exercise-induced pulmonary hemorrhage (EIPH) in Thoroughbreds. 5 The author has noticed a similar correlation (diagnosed endoscopically) among Quarter-type horses used for timed events, particularly barrelracing horses (Fig. 2).

Figure 2. Endoscopic view of the arytenoids in neutral position in a barrel-racing horse with exercise intolerance and respiratory noise. A diagnosis of left laryngeal hemiparesis is made because there is axial displacement of the left arytenoid and palpable prominence of the left muscular process. Arytenoid abduction was symmetric and complete. Endoscopy of the trachea revealed large amounts of blood-stained mucus.

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Diagnosis

A presumptive diagnosis of laryngeal hemiplegia or hemiparesis can be made after considering the history, palpating the larynx, and listening to the horse make the characteristic noise generally associated with the condition. Individuals experienced with laryngeal palpation may be able to detect subtle changes in left cricoarytenoideus muscle mass according to the relative prominence of the left muscular process, using the right side as the control. 5 Laryngeal palpation also reveals the resiliency of the laryngeal cartilages; squeezing the larynx may produce air turbulence and noise or a cough in horses with arytenoid chondropathy. Muscular process palpation is more difficult in Quarter-type horses than in Thoroughbreds, because their larger surrounding musculature limits precise identification of laryngeal prominences. Because many upper respiratory diseases produce signs indistinguishable from laryngeal hemiplegia and because laryngeal palpation does not accurately differentiate hemiplegia from hemiparesis, endoscopy remains the definitive diagnostic tool. Differentiating between hemiparesis and hemiplegia is practical in determining disease management. Diagnosis of laryngeal dysfunction is made by observing rima glottidis symmetry and arytenoid cartilage dynamics during arytenoid movement, rather than by estimating symmetry or degree of luminal compromise caused by arytenoid cartilages in the neutral (resting) position. Hemiplegia is diagnosed when the arytenoid cartilage is seen to be incapable of reaching maximal abduction producing perfect symmetry while using the opposite arytenoid as control (Fig. 3). The degree of axial deviation of the affected cartilage in the neutral position varies greatly among horses with hemiplegia; progressive axial

Figure 3. Laryngeal hemiplegia in a 4-year-old Thoroughbred gelding. Although medial displacement of the left cartilage is not severe, the cartilage is incapable of complete abduction.

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displacement of the arytenoid cartilage may be noticed with intermittent endoscopic examinations of horses with idiopathic laryngeal hemiplegia. Hemiparesis is diagnosed when the arytenoid cartilage is capable of attaining maximal abduction, there is supporting palpable evidence of excessive left-sided muscular process prominence, and one or more of the following accompanying conditions occurs: (I) arytenoid tremors at rest or during abduction; (2) axial deviation of the arytenoid in the resting or neutral position (asymmetry of the rima glottidis); (3) significant asynchronous movement or difference in speed of abduction between arytenoids. (Subtle discrepancies are considered normal.) Reproducing maximal arytenoid range of motion often is challenging for the endoscopist. Ideally, videoendoscopy is performed during highvelocity treadmill exercise. Endoscopy using only a twitch for restraint and nostril occlusion to simulate conditions that cause arytenoid abduction is effective in evaluating arytenoid function. 17 The disadvantages of using twitch restraint include the normally induced phenomenon of intermittent or persistent dorsal displacement of the soft palate and freezing of the arytenoids in intermediate abduction. Xylazine may be used to enhance restraint, but it is preferable to attempt endoscopy before its administration for comparison purposes because of its controversial effects on the pharynx and larynx. 10 Swallow inducement is useful in determining maximal arytenoid abduction in otherwise uncooperative horses. Endoscopy after longeing the horse is an important part of upper respiratory examination, but it is rarely of additional diagnostic b.enefit in differentiating hemiparesis from hemiplegia. Theoretically, a paretic abductor muscle that is able to abduct the cartilage completely during cursory endoscopic examination under simulated conditions may fatigue and ultimately fail to produce maximal abduction during strenuous exercise. In the author's experience, performing endoscopy immediately after mild, moderate, or strenuous exercise does not reproduce exactly the conditions during exercise, even with horses with seemingly severe left abductor paresis. Although it is unlikely that arytenoid fatigue from hemiparesis contributes to laryngeal obstruction during heavy exercise, endoscopy during high-speed treadmill exercise is necessary to be definitive. 22 Treatment

Laryngeal hemiplegia is treated optimally by using laryngoplasty combined with ventriculectomy. Prosthetic laryngoplasty usually is contraindicated, however, in horses diagnosed with hemiparesis that have a wide range of abductor ability of the affected arytenoid cartilage, because the combined activity of abduction and adduction may cause loosening of sutures. Laryngoplasty is a permanent surgical connection of the cricoid cartilage and the muscular process of the arytenoid cartilage in which heavy nonabsorbable suture is used. 20 Arytenoid abduction is attained by tightening the prosthesis, although some relaxation of the suture tension is to

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be expected in over 50% of horses within 6 weeks of laryngoplasty. Prosthetic laryngoplasty is an efficient biomechanical method of stabilizing the arytenoid cartilage and preventing its collapse into the airway during high inspiratory flow rates, often regardless of the amount of abduction maintained. 9 • 26• 32 Because some degree of arytenoid relaxation commonly occurs after laryngoplasty, ventriculectomy is performed to reduce air turbulence at the rima glottidis by smoothing its asymmetric contour. Thyro-arytenoid adhesion resulting from ventriculectomy may also help to stabilize the arytenoid cartilage. The key to surgical exposure of the dorsolateral-aspect of the larynx is positioning the horse for laryngoplasty in right ventral recumbency with its head fully extended. The incision is made ventral to the linguofacial vein; a plane of dissection is established between the vein and the omohyoideus muscle. The perilaryngeal fascia is separated digitally to expose the dorsal larynx, and the linguofacial vein is retracted dorsally and laterally using a wide, malleable retractor. The prosthesis, made of doubled No. 2 or single No. 5 braided polyester, is passed using a one-half circle trocar-point needle. Accurate prosthesis placement for optimal arytenoid stabilization requires appreciation of the anatomy and function of the cartilaginous larynx and surrounding musculature. Of primary importance is obtaining proper position, orientation, and amount of purchase of the prosthesis in the cricoid cartilage while avoiding penetration of the laryngeal lumen. The prosthesis is positioned just lateral to the dorsal midline of the cricoid cartilage; the needle is placed within an indentation or notch, which usually is located just lateral to the dorsal midline. 19• 20 Exaggerated effort is made to direct the point of the needle axially so that it exits as close to the median crest of the cricoid cartilage as possible. The resultant vector representing the retraction of the muscular process for optimal abduction and stabilization points at or near the caudal midline of the cricoid cartilage. The length of cricoid cartilage purchase is at least 1 cm and preferably 1.5 cm. This measurement is comparable to the width of the index finger. The cricopharyngeus and thyropharyngeus muscles then are separated along the septum that joins them, and both arms of the prosthesis are passed under the cricopharyngeus, taking precautions to prevent crossover of the leading and trailing arms. The leading arm of the suture is passed through the muscular process from caudomedial to craniolateral, and the prosthesis is tightened by means of a single throw and secured with five additional square throws. The amount of tension to place on the first halfhitch is subjective. Some surgeons use the videoendoscope to evaluate the degree of abduction while performing surgery. Generally, the prosthesis is made as tight as is reasonable. This method is unlikely to cause abrupt mechanical cartilage failure or overabduction and provides a correctly placed prosthesis in normal cartilage. 8 Laryngeal cartilage has a high intrinsic strength to retain prostheses, and the first throw offers a significant amount of friction that causes resistance to tension.

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Surgical closure consists of reapposition of the cricopharyngeus and the thyropharyngeus in a continuous pattern and apposition of the omohyoideus to the fascia surrounding the linguofacial vein with interrupted absorbable suture, which is followed by skin closure. The horse then is rolled into dorsal recumbency. The approach for ventriculectomy is a standard laryngotomy through the cricothyroid space. On entering the lumen, the surgeon examines the dorsal laryngeal mucosa for mucosa} laceration or exposed prosthetic material. M ucosal laceration without prosthetic exposure is managed medically using systemic antibiotics. Luminal protrusion of the prosthesis indicates need for its immediate removal, because massive contamination probably will result in infection of the prosthesis regardless of medical or surgical preventive measures. Ventriculectomy is performed using a burr to seize the ventricular mucosa and evert it for removal. Once everted in the axial direction, the mucosa is grasped at the mouth of the saccule with Kelly hemostatic forceps for further retraction, and the mucosa is cut adjacent to the forceps. The laryngotomy site is left to heal by second intention. A laryngotomy is not required for sacculectomy using a Nd:Yag laser under endoscopic visualization. 28 Endoscopy is performed upon recovery of the patient. The maximal degree of abduction achieved by the prostheses is observed at this time (Fig. 4). Some arytenoid relaxation is expected during a 10- to 14-day hospital stay. In vitro testing of laryngoplasty prostheses suggests that incomplete muscular process cartilage failure accounts for the varied degrees of arytenoid relaxation noticed in postoperative horses. 8 Aftercare consists of routine wound management with stall rest until laryngotomy healing is complete, which takes 3 weeks. The horse can then be turned out in a small paddock or hand-walked for an additional 3 weeks and then can return

Figure 4. Endoscopy immediately after standing upon recovery from laryngoplasty and ventriculectomy. Maximal abduction is observed at this time. Laryngopalatal dislocation is also apparent as a result of incomplete recovery from effects of the anesthetics.

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to normal activity. Improvement in respiratory capacity and reduction of inspiratory noise is expected after successful laryngoplasty and ventriculectomy. Results of the combined procedures, however, are not predicted from endoscopic examination before returning the horse to athletic endeavors, because varying degrees of cartilage relaxation are expected in a high percentage of horses. Some resultant abduction is preferred. Many performance horses experience complete recovery or significant improvement in signs if the cartilage relaxes to near its preoperative position. Although horses that race long distances that have this amount of postoperative arytenoid relaxation often are surgical failures, many Quarter-type racehorses are able to compete without noise or dyspnea. Complications of laryngoplasty include prosthesis infection, poor clinical results from improper placement, or sustained overabduction. Infection of the prosthesis is a devastating complication that necessitates its removal in most cases. The leading cause of failed laryngoplasty is technical error in prosthesis placement or inadequate cricoid cartilage purchase. These complications result from poor surgical exposure and from inexperience of the operator. Although muscular process failure occurs in vitro during progressive tensile loading of prostheses, cartilage failure in surgical patients is more likely to result from inadequate incorporation of cricoid cartilage. Another common error that leads to failed laryngoplasty is positioning the prosthesis too lateral on the cricoid cartilage, which results in elevation but not abduction of the arytenoid. Maintenance of the arytenoid in an overabducted position may lead to dysphagia and chronic cough. Sustained overabduction may result in aspiration or a chronic cough. Failed laryngoplasty is managed by using either total arytenoidectomy or laryngoplasty revision, although the results of either procedure generally are less rewarding than laryngoplasty. 2 • 3 1• 36 Risk Factors

Right-sided laryngeal hemiplegia is a risk factor, because the surgeon is compelled to perform the procedure in reverse direction. Patient age may also affect laryngoplasty results. Two-year-old horses are suspected of having poorer results than those of older horses as a result of their soft laryngeal cartilage, and aged horses may have mineralized cartilage that can preclude prosthesis insertion or cartilage abduction. 16 • 21 Healthy 2year-old horses have biomechanical cartilage properties similar to 3- and 4year-old horses, but the effects of atrophied muscle on the health and maturation of adjacent cartilage and cricoarytenoid articulation are not known. 8 Currently, there appears to be no reason to delay laryngoplasty in 2-year-old horses. Aged horses suspected of having advanced laryngeal mineralization are identified by using laryngeal radiography. Other agerelated risk factors include horses with concurrent pulmonary disease. Thoroughbred or Standardbred racehorses may suffer from laryngeal hemiplegia and EIPH. Laryngeal hemiplegia in middle-aged show horses may

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be complicated by mild or moderate chronic obstructive pulmonary disease. Of particular concern is a history of coughing in horses that are known to have laryngeal hemiplegia. Coughing is not a clinical sign produced by hemiplegia alone. Chronic obstructive pulmonary disease is identified by results of pulmonary auscultation, tracheal endoscopy, and tracheal wash or bronchoalveolar lavage.

ARYTENOID CHONDROPATHY Of all performance horses, Thoroughbreds are most commonly affected with arytenoid chondropathy; the disease is fairly uncommon among working horses of any other breed. Older (>6 years), sedentary, or retired Thoroughbreds represent a small proportion of affected nonworking horses when compared with other breeds. Arytenoid chondropathy results in obstructive laryngeal disease through progressive thickening and structural distortion of the arytenoid cartilage or swelling of periarytenoid tissues. Any comb.ination of thickened cartilages, axially projected proliferative mucosal lesions, or periarytenoid edema reduces the diameter of a cross section of the laryngeal lumen. Lack of arytenoid movement contributes to laryngeal obstruction, because the thyroid cartilage, which is located laterally, prevents abduction of thickened arytenoid cartilages. Histopathologic findings vary but often include central necrosis or lamination of the cartilage with fibrous connective tissue, cartilage disease characterized by disruption or loss of hyaline cartilage, and acute or chronic inflammation of the periarytenoid tissues. Acute inflammatory chondropathy, chronic inflammatory chondropathy, and chronic noninflammatory chondropathy are the different forms of the disease that are observed in both performance and sedentary horses. Each pathologic type of disease produces different clinical circumstances. Chronic inflammatory chondropathy, the most common form, is characterized by inflammation and infection of the cartilage and surrounding tissues alternating with disease quiescence. This form is likened to osteomyelitis because of the recurring nature of the septic process. 14 Performance horses with chronic inflammatory chondropathy generally have progressive clinical signs; exercise tolerance may be reduced over several weeks to 1 year. The character of the noise and tolerance to exercise may improve or worsen according to the degree of inflammation and infection of the tissues . In horses with active inflammatory disease, response to empiric antiinflammatory, antibiotic, and local throat sprays is temporary; respiratory signs recur soon after withdrawal of treatment. Horses with chronic inflammatory disease progressively become incapable of maximal exercise, make respiratory noises, and may eventually become dyspneic at rest. 14 Chronic noninflammatory chondropathy, otherwise known as chondroma, is characterized by a slow progression of cartilage thickening,

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resulting in an insidious onset of clinical signs. This form is rare and occurs most commonly in older (>5 years), nonracing performance horses. Of particular significance are its clinical and endoscopic similarities to laryngeal hemiplegia. Lack of involvement of the periarytenoid tissues differentiates this form of chondropathy from the inflammatory forms. Acute inflammatory chondropathy results in rapid progression of respiratory signs in a few hours to a few days. Horses commonly are presented for dyspnea at rest. Periarytenoid interstitial edema and inflammatory exudates primarily obstruct the laryngeal lumen; cartilage deformity or thickening is usually present but is of minor significance. Clinical and laboratory features of acute inflammatory disease may include depression, respiratory noise at rest, profuse serous nasal discharge, fever, and leukocytosis. Diagnosis

Diagnosis of arytenoid chondropathy is made on the basis of compatible historical facts, together with results of physical examination, laryngeal endoscopy and radiography, and digital (surgical) examination of the affected cartilage. Laryngeal palpation abnormalities include increased hardness or loss of cartilage elasticity; squeezing the larynx induces a cough or respiratory noise from airway constriction. Lateral radiographic projection of the laryngeal cartilages may show abnormalities consistent with arytenoid chondropathy. Xeroradiographic or good quality standard radiographic evidence of chondropathy includes abnormal patterns of mineralization, increased density of the cartilages, abnormal contour or size of the corniculate process, obliteration of the laryngeal ventricle, and laryngeal masses. 23 The degree of mineralization must be evaluated carefully in aged horses and those that have had previous laryngeal surgery; both conditions can result in increased mineralization. 7• 36 Upper airway endoscopy provides the definitive diagnosis for arytenoid chondropathy. Features of the rima glottidis that are consistent with chondropathy include reduced luminal size, abnormal contour or thickness of the arytenoid, immobility of the arytenoid, mucosa} lesions, and generalized laryngitis. No other infectious disease is known to produce laryngitis in horses. A wrinkled-appearing corniculate process often is the first endoscopic abnormality observed. Further examination may reveal an abnormal contour or convexity of the cartilage body. Mucosa} lesions, usually observed on the body, may be ulcerative, proliferative granulating masses that protrude into the lumen or may be scarring from healed ulcers. Observation of mucosa} integrity is extremely important in differe ntiating laryngeal hemiplegia and chondropathy with minimal cartilage distortion during disease quiescence, because in both cases the cartilage is displaced toward the midline. Similarly, with chronic noninflammatory chondropathy, the absence of any mucosa} lesion makes the disease particularly difficult to distinguish from hemiplegia.

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Arytenoid function is assessed during endoscopic examination because the degree of cartilage mobility may be of diagnostic or prognostic significance, particularly in distinguishing unilateral from bilateral disease. If one cartilage is obviously affected and mucosa} lesions are present on the opposite cartilage, determining the degree of mobility may be of diagnostic help in distinguishing mucosa} trauma inflicted by the diseased cartilage from chondrosis of the opposite cartilage. Because periarytenoid inflammation limits arytenoid movement, endoscopy should be repeated to reevaluate arytenoid function after inflammation is controlled by antibiotics and antiinflammatory medication. Digital examination of the cartilage is performed routinely during laryngotomy for arytenoidectomy. Rarely, a definitive diagnosis of chondropathy may require digital examination, which may be performed orally in anesthetized horses. 13 · 14 Regardless of the approach, the index finger is inserted into the ventricle and the thumb placed axially on the body. The cartilage thickness and contour are then estimated. Treatment

The decision for medical or surgical management of arytenoid chondropathy depends on the pathologic type or stage of disease. With acute inflammatory chondropathy, initial treatment consists of rest, broad-spectrum systemic antibiotics, and antiinflammatory drugs. Temporary tracheostomy relieves laryngeal edema by reducing air turbulence in patients that have respiratory noise at rest. Endoscopy performed after 5 to 10 days of medical management often reveals minimal cartilage thickening or deformity. Depending on the amount of luminal compromise caused by cartilage thickening, the use of the horse, and the treatment expectations of the owner, surgical removal of the affected cartilage may be advisable because of the progressive nature of the disease. Medical therapy produces a complete but temporary respiratory recovery in some nonracing performance horses. After resolution of the inflammatory process, however, acute inflammatory disease often recurs in the form of chronic inflammatory chondropathy. Arytenoidectomy is the definitive treatment for chondropathy in performance horses. Laryngoplasty is contraindicated because the thickened cartilage is unable to abduct; if minimal abduction is achieved, the progressive nature of the disease precludes any long-term benefits of laryngoplasty. Partial and total arytenoidectomy are the recommended procedures for performance horses, because both removal of the entire corniculate cartilage and ventriculocordectomy are crucial toward improving respiratory capacity. The corniculate cartilage and the vocal cord are left intact using the subtotal arytenoidectomy procedure. Other principles of successful arytenoidectomy include rigorous patient preparation, mucosa! apposition, and first intention healing. Candidates for arytenoidectomy are prepared by medically resolving any inflammatory

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process with rest, antimicrobial and nonsteroidal anti-inflammatory drugs , and, if necessary, a temporary tracheostomy. Improvement in the endoscopic appearance of the airway is expected after several days ; however, arytenoidectomy should be delayed until the inflammatory component is minimal. Persistent inflammation of the periarytenoid tissues may be observed histopathologically despite 10 days of medical treatment and endoscopic evidence of improvement; this inflammation is known to adversely affect arytenoidectomy results. To optimize surgical results, arytenoidectomy should be delayed 30 days or longer in patients with endoscopic evidence of periarytenoid infection or inflammation. Partial arytenoidectomy is the technique of choice for mucosal salvage and removal of the corniculate cartilage because of the rostral location of the incision. 40 The approach is made through a standard laryngotomy incision in the cricothyroid space. Splitting of the thyroid cartilage should be avoided but may be necessary in Quarter-type horses, which have a small cricothyroid space. The incision encircles the ventricle and follows the contour parallel and caudal to the corniculate cartilage. Careful submucosal dissection proceeds in both rostral and caudal directions , salvaging all mucosa. The body of the cartilage is retracted and removed using Mayo scissors. Rongeurs are used to retrieve pieces of cartilage and to trim the remnants of any protruding muscular process. The corniculate mucosa is retracted into the lumen and sutured using continuous absorbable stitches after any excessive mucosa is trimmed. To prevent postoperative aspiration, some surgeons prefer to tack redundant mucosa laterally rather than excising it and retracting the corniculate mucosa for suturing. This leaves a fold or rim of corniculate mucosa at the opening of the larynx that simulates a piriform trough through which food can enter the esophagus easily without contaminating the larynx. Although second-intention healing of laryngeal defects is efficient and acceptable, prolonged temporary tracheostomy intubation often is a complication of second-intention healing in clinical cases. 7• 37 Care should be taken to avoid cutting the interarytenoid ligament to assist in mucosal apposition, because aspiration of food is known to result from interarytenoid ligament transection. 29 Postoperative care consists of antimicrobial and anti-inflammatory agents and routine tracheostomy care. Two possible surgical treatments for bilateral chondropathy include removing both cartilages in the same procedure or removing only the cartilage with the worse disease or the least mobility. Because chondropathies are progressive in nature and because most horses undergoing unilateral arytenoidectomies for bilateral disease require a second arytenoidectomy, bilateral arytenoidectomy is favored over staged unilateral arytenoidectomy. Dorsal glottic stenosis may result from bilateral arytenoidectomy but this complication is rare. 12 Preserving the dorsal commissure mucosa may prevent this complication. Permanent tracheostomy is a useful salvage procedure for horses with severe chondrosis or after failed arytenoidectomy, but it is not recommended for performance horses. 6 • 27

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Risk Factors

Factors that are suspected of or are known to complicate arytenoidectomy for chondropathy and have a deleterious effect on the prognosis of working horses include bilateral disease, excessive mineralization of the laryngeal cartilages, left-sided involvement, and previous laryngeal surgery. 36 Bilateral arytenoidectomy generally is considered a salvage procedure ; nonracehorses may be able to resume their former level of performance, but it is unusual for racehorses to compete successfully after this procedure. Persistent inflammation of the periarytenoid tissues results in poor arytenoidectomy results, because surgery aggravates the inflammatory component. Paralyses of the opposite cartilage and pharyngeal cicatrices are known to have a deleterious effect on the prognosis after arytenoidectomy, but these occur mostly in aged, sedentary horses. 7

LARYNGOPALATAL DISLOCATION

Because horses are obligate nose breathers, the caudal margin of the soft palate normally rests ventral to the epiglottis at all times except during swallowing. Laryngopalatal dislocation (LD), a term synonymous with dorsal displacement of the soft palate, refers to shifting of the caudal free edge of the soft palate dorsal to the epiglottis. LD specifically refers to the analogous "unbuttoning" of the laryngeal cartilages from the intrapharyngeal ostium, which forms a buttonhole that encircles and grips the cartilages. 6 Performance horses experience respiratory noise and exercise intolerance as a result of the abnormal laryngopalatal relationship, which becomes normal during rest and immediately after swallowing or strenuous exercise in intermittent LD. Conversely, with persistent LD, the caudal edge of the soft palate remains displaced at all times. Respiratory noise is a result of vibration of the soft palate and mouth breathing, which produces a loud, gurgling, guttural noise during both phases of respiration. Rapid loss of respiratory capacity occurs during heavy exercise as a result of obstruction of the larynx by the caudal edge of the palate. Nonracing performance horses usually do not suffer exercise intolerance but often are presented for respiratory noise. There appear to be multiple causes of LD. Dynamic collapse of the pharynx may occur from negative pressure secondary to any obstruction cranial to the rima glottidis, such as pharyngeal lymphoid hyperplasia. Soft palate paresis, hyperflexion of the neck, caudal retraction of the larynx, ventral deviation of the epiglottis caused by excessive contraction of the sternothyrohyoideus muscles, and epiglottic abnormalities including hypoplasia and entrapment by arytenoepiglottic folds are known to cause or have a circumstantial relationship to LD. 6 There also is a congenital form of the disease that is believed to result from an anatomic abnormality. 25 Clinical experience and surgical trial and error suggest that a hypoplastic

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or flaccid epiglottis and contraction of the sternothyrohyodeus (STH) muscles during exercise are primary causes of LD in performance horses. Hypoplastic epiglottis is discussed in a separate section. Diagnosis

Diagnosis of intermittent LD is made on the basis of compatible historical facts and endoscopic observation of the horse exercising on a treadmill, observation of the horse during training while making a characteristic noise, or endoscopy performed immediately after strenuous training that simulates race conditions. Because of the intermittent nature of the disease, endoscopy in the resting horse often is of little diagnostic aid except in identifying accompanying lesions. Of particular historical significance is the character of the noise and the effect of a tongue-tie on respiratory performance. Tying the tongue should be attempted before any surgical correction on racehorses with a compatible history and an otherwise normal upper airway. Tongue-ties are not practical in nonracing performance horses. Pulling the tongue forward and securing it to the mandible helps counteract caudal retraction of the larynx from excessive STH contraction. Tongue retraction also may prevent displacement by positioning or rotating the larynx rostrally for a more complementary laryngopalatal relationship. Endoscopic findings in horses with intermittent LD usually are equivocal unless accompanying pathology or predisposing factors are identified. Horses twitched for endoscopy often displace the soft palate initially; eventually, a single swallow should replace the palate easily. Many unsuccessful swallowing attempts are an inconclusive finding suggestive of LD. Another suggestive finding is billowing of the palate and displacement during nostril occlusion with difficulty replacing the palate. LD is differentiated from an entrapped epiglottis by observation of the epiglottis. With an entrapped epiglottis, the entire outline of the epiglottis is visible; with LD, the epiglottis is not apparent on nasopharyngeal endoscopy. Of particular endoscopic importance are the anatomy, size, function, and position of the epiglottis. Epiglottic abnormalities predispose to LD, and their recognition is central in formulating a treatment regimen for an individual horse. Oropharyngeal endoscopy by a mouth speculum may be required to diagnose epiglottic abnormalities in horses with persistent LD. The entrapped epiglottis also may be noted below a displaced palate on lateral radiographic projection. Epiglottic size also may be evaluated radiographically when obscured from endoscopic view by the palate, epiglottic entrapment, or both. Treatment

Surgical treatment of LD consists of any combination of STH muscle resection, staphylectomy, and epiglottic augmentation, although results are inconsistent. In racing horses, surgical correction of LD is not necessary if a tongue-tie is an effective management tool.

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STH muscle resection is the first treatment of choice in horses with an otherwise normal upper airway in which a tongue-tie is ineffective. 11 In addition to epiglottic abnormalities, accompanying lesions that may predispose to LD and complicate surgical treatment include a congenitally narrow nasopharynx or nasal cavity and pharyngeal lymphoid hyperplasia. Advantages of STH muscle resection are because it has relatively few complications compared with other procedures and because it can be performed in the standing horse using tranquilization and a local anesthetic. The procedure is performed with the horse's head stretched straight out; a 5-cm longitudinal incision is made through the skin and cutaneous colli muscle on the ventral midline at the junction of the middle and cranial thirds of the neck. The paired muscles are identified and dissected from surrounding connective tissue, and 5 to 6 cm of these muscles are elevated from the trachea. Approximately 4 cm of muscle belly are removed using Mayo scissors or a scalpel. Closure consists of continuous absorbable suture in the cutaneous muscle and interrupted skin sutures. A neck bandage is applied for 3 days to prevent hematoma or seroma formation. Alternatively, a Penrose drain is placed deep into the cutaneous muscle, and is removed after drainage is reduced significantly, which usually takes 2 to 4 days postoperatively. Training is resumed within 7 days of surgery. Staphylectomy often is successful in horses that do not respond to STH muscle resection alone. The author recommends staphylectomy only in horses in which the epiglottis is of normal length and rigidity or the epiglottis is only mildly hypoplastic. Staphylectomy is performed through a standard ventral laryngotomy in the cricothyroid space. A 1- to 2-cm width of the caudal edge of the soft palate is removed using Mayo scissors while stabilizing the tissue using Allis tissue forceps. The cut is made in a crescent shape, removing 0.5 cm at the margin and approximately 1.5 cm at the midline. The tissue, including the laryngotomy site, is left to heal by second intention, and the horse resumes training after the laryngotomy incision produces an airtight seal. Clinical experience with LD and hypoplasia or flaccidity of the epiglottis suggests that epiglottic augmentation combined with staphylectomy and STH muscle resection may produce optimal results in race horses. Polytetrafluoroethylene (Teflon) is injected submucosally on the ventral or lateral epiglottic surface through a ventral laryngotomy. An inflammatory response is expected for up to 30 days, causing marked changes in the contour and thickness of the epiglottis. By 60 days postoperatively, epiglottic thickening persists as a result of submucosal distention from fibrosis and foreign body inflammatory response. Although the early postoperative endoscopic appearance of the epiglottis is striking, no complications or discomfort are known to result from Teflon injection. 35 Risk Factors

Factors that are known to complicate the surgical procedures used for treatment of LD or that cause poor surgical results generally are suspected

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of being congenital. These include but are not limited to hypoplastic epiglottis and narrow nasal passages or nasopharynx. Other predisposing lesions, such as severe pharyngeal lymphoid hyperplasia, are treated before any surgical intervention. Persistent displacement of the soft palate also is considered a risk factor, because surgical results generally are poorer than in horses with intermittent LD. Complications associated with sternothyrohyoideus muscle resection usually are limited to seroma formation at the surgical site. Swelling and inflammation in the area potentially could interfere with recurrent laryngeal nerve function, as could overzealous use of local anesthetic in the area. Dysphagia, a devastating complication of staphylectomy, results from trimming the caudal palate too short. Staphylectomy is contraindicated in horses with significant epiglottic hypoplasia because of the increased risk of dysphagia.

ENTRAPPED EPIGLOTTIS

Epiglottic entrapment is the dorsal reflection of the subepiglottic tissue and arytenoepiglottic folds surrounding and obscuring the apex, lateral margins, and a portion of the dorsal surface of the epiglottis. 3 Clinical signs are extremely variable and range from subclinical and unobserved to exercise intolerance or respiratory noise and cough. A variety of respiratory noises may be noticed during either or both phases of respiration. As with LD, the disease may be intermittent or persistent; the intermittent form is difficult to diagnose. Intermittent entrapment may be observed during swallowing or by the use of videoendoscopy during highspeed treadmill exercise. The practitioner who deals primarily with nonracing performance horses most often observes entrapped epiglottis as an incidental finding in horses endoscoped for prepurchase examination or other reasons. Entrapment of the epiglottis can occur alone or may accompany other upper airway abnormalities including laryngeal hemiplegia, subepiglottic cyst, cleft palate, and laryngopalatal dislocation. 15 Possibly, any disease that interrupts the seal produced by contact of the soft palate with the subepiglottic tissue may result in the arytenoepiglottic fold being rolled dorsally over the epiglottis during swallowing or strong negative pressure within the pharynx. Entrapment of the epiglottis has been associated with hypoplasia of the epiglottis. Every entrapment in a young horse should arouse the suspicion of hypoplasia of the epiglottis. Diagnosis

A diagnosis of epiglottic entrapment is made by nasopharyngeal endoscopy. The outline of the epiglottis is visible, but the serrated edges and the arcuate vessels of the epiglottis are obscured by the arytenoepiglottic

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fold, and the epiglottis is commonly tipped dorsally, ventrally, or to either side (Fig. 5). Ulceration of the arytenoepiglottic fold at the tip of the epiglottis may occur, or the apex of the epiglottis may protrude through the fold. Because the epiglottic hypoplasia is of prognostic significance, its size may be estimated endoscopically with the entrapment in place or the length can be measured on lateral radiographs of the pharynx. Although epiglottic width and function are estimated best by endoscopy, a radiographic measurement of epiglottic length 7.5 cm or less (measured from the apex to the body of the thyroid cartilage) is considered abnormal. 18 Good quality lateral radiographic projection of the pharynx clearly shows the arytenoepiglottic folds surrounding the epiglottis and the position of the soft palate. The entire epiglottis can be examined briefly by manual reduction of the entrapment using a nasally inserted stiff wire with a small blunt hook at one end. The hook is not bent sharply, so the arytenoepiglottic fold is easily disengaged from the instrument. The horse is sedated, and local anesthetic is administered topically on the fold through an 8F polypropylene urinary catheter inserted nasally. The arytenoepiglottic fold is hooked and retracted rostrally until the entrapment is reduced; the tissue is held for examination of the epiglottis, because re-entrapment will occur during subsequent swallowing. Treatment

Horses with epiglottic entrapment that have no clinical signs referable to the disease or have no impedance to performance require no treatment. Horses with respiratory signs are treated surgically by a number of methods, including axial division or resection of the arytenoepiglottic fold through a ventral laryngotomy or pharyngotomy; transnasal axial division in standing

Figure 5. Entrapment of the epiglottis by the arytenoepiglottic fold with an accompanying subepiglottic cyst. The outline of the epiglottis is visible, but the serrated edges and vasculature are obliterated. This horse had no respiratory signs.

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sedated or anesthetized horses using a hooked bistoury, Nd:YAG laser, or electrosurgery; and axial division using a bistoury through the mouth. Resection of a crescent-shaped portion of tissue through a ventral laryngotomy commonly is complicated by subsequent laryngopalatal dislocation, making this method least desirable. 15 Axial division using any of the described methods is preferred to avoid this complication. Regardless of the method used, the incision in the arytenoepiglottic tissue must extend to the apex of epiglottis to prevent re-entrapment. A hooked bistoury inserted orally in the anesthetized horse is the safest and most economical method, because laceration of the soft palate or other vital structures is avoided and the amount of tissue to be severed is monitored digitally. Anesthesia is maintained using intravenous anesthetics. One hand is inserted orally to stabilize the epiglottis; the bistoury is inserted and positioned for axial division of the fold. To ensure that adequate subepiglottic tissue is engaged by the point of the instrument, the subepiglottic tissue is digitally manipulated over the point and engaged. During rostral traction for division, the point of the bistoury is guarded with the operator's hand to prevent laceration of the tongue. The nasal approach using a bistoury in the standing horse introduces a significant risk of lacerating the soft palate and therefore should not be attempted unless the operator has exceptional experience and confidence in the procedure. The Nd:YAG laser instrumentation provides advantages that promote rapid convalescence in addition to avoiding general anesthesia. 34 Depending on individual experiences with results after surgical resection of epiglottic entrapment, the surgeon may elect to prevent laryngopalatal dislocation using sternothyrohyoid myectomy in the standing horse or staphylectomy and myectomy concurrently with axial division or resection of the fold through a ventral laryngotomy. The additional procedure is indicated in horses with mild epiglottic hypoplasia or epiglottic entrapment accompanied by LD or in horses in which LD develops following correction of an entrapment. Horses are monitored endoscopically for wound complications ; significant swelling and prolonged granulating are expected postoperatively. Local antimicrobial and anti-inflammatory agents are administered as needed by nebulizer or nasally inserted catheter. Horses usually are returned to work 7 to 14 days after surgery or after 30 days postoperatively if a laryngotomy approach was used. Using axial division of the arytenoepiglottic fold, a high success rate is expected if no accompanying lesions complicate treatment. Risk Factors Lesions that often accompany epiglottic entrapment and adversely affect the prognosis expected from its surgical treatment include laryngeal hemiplegia, LD , and hypoplastic epiglottis. Surgical treatment of an incidentally diagnosed entrapment introduces an additional risk factor because LD could result, potentially disabling an otherwise useful horse.

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HYPOPLASTIC EPIGLOTTIS

In exercising horses, the epiglottis serves to maintain intimate contact with the soft palate, providing a competent laryngopalatal seal. This relationship is of the utmost importance in preventing laryngopalatal subluxation during high-volume ventilatory work. The effectiveness of the epiglottis in maintaining laryngopalatal competency is considered to be a function of its size and rigidity. Hypoplastic epiglottis refers to the reduced size of the epiglottis resulting in loss of its function or rigidity. Any or all epiglottic dimensions, including the length, width, and thickness, may be affected. The clinical signs of hypoplastic epiglottis are those referable to laryngopalatal subluxation and entrapped epiglottis that occur secondarily. Currently, the pathogenesis (i.e., congenital, inherited, or acquired deformity) of hypoplastic epiglottis remains speculative. Diagnosis

The diagnosis of hypoplastic epiglottis is made on the basis of endoscopic and radiographic evaluation. The diagnosis of hypoplastic epiglottis made by nasopharyngeal endoscopy is subjective and is determined by the size of the epiglottis relative to other nasopharyngeal structures and its stiffness. The epiglottic length is an important dimension that is easily measured on lateral pharyngeal radiographs. 18 Hypoplastic epiglottis is documented radiographically in Thoroughbreds with reduced epiglottic length, but clinical data suggest that true epiglottic shortening may not be the most common form of the disease. Epiglottic thickness also can be measured on lateral pharyngeal radiographs, but the clinical significance of these measurements is unknown. The epiglottic width, thickness, and inherent rigidity are estimated during routine endoscopic maneuvers. The epiglottis should be of sufficient size and resiliency to resist the pressures associated with soft palate billowing and to prevent laryngopalatal subluxation while negative airway pressure is created by nostril occlusion. In horses with hypoplastic epiglottis, the soft palate often elevates considerably so as to obstruct view of the larynx during inspiration, quickly followed by laryngopalatal subluxation. Rather than resisting elevation of the palate, the hypoplastic epiglottis appears passive or flaccid and tends to fold. Treatment

Historically, treatment of hypoplastic epiglottis has been directed toward management of the laryngopalatal and entrapped epiglottis sequelae. Clinical experience with mild hypoplasia of the epiglottis and laryngopalatal subluxation suggests that the best results are obtained by combining staphylectomy and sternothyrohyoideus myectomy, although results are inconsistent. With entrapped epiglottis and epiglottic hypoplasia, division

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of the arytenoepiglottic fold axially is performed in conjunction with staphylectomy and myectomy to prevent the likely subsequent complication of laryngopalatal subluxation. Primary treatment of hypoplastic epiglottis consists of epiglottic augmentation using a polytetrafluoroethylene emulsion or bovine collagen, which is injected into the subepiglottic or lateral epiglottic tissues using a hypodermic needle. A foreign body inflammatory response ensues, and submucosal thickening persists for at least 60 days. 35 This procedure, performed through a ventral laryngotomy, is used to improve results of staphylectomy and myectomy for moderate-to-severe epiglottic hypoplasia and concurrent LD. Although little is known regarding using augmentation alone, preliminary results of the combined procedures are encouraging. (J. T. Robertson, personal communication, 1990.)

NASAL SEPTAL DISEASE

Deviation, cystic lesions, or diseases that cause thickening of the nasal septum result in obstruction of the nasal cavity. Respiratory noises and exercise intolerance resulting from nasal septal disease most commonly occur in young performance horses; nasal septal abnormalities may be congenital, may result from trauma, or may be sequelae to severe respiratory infection. Respiratory noise is evident on both phases of respiration but is loudest on inspiration. Cystic nasal septal lesions are congenital and may cause partial bilateral obstruction. Clinical signs often are not apparent until the horse is in training and is asked to perform strenuous exercise. Although congenital cystic lesions generally are considered to be the most common form of nasal septal disease, those caused by thickening and mineralization of the septum resulting from trauma (usually fracture) to the nasal bones across the midline are the most common type in the author's practice. Deviations of the septum are rare in performance horses and usually occur in foals with congenital deviation of the nasal bones and premaxilla and in nonworking horses with chronic sinusitis or another space-occupying lesion, which results in septal deviation from an adjacent advancing lesion. Diagnosis

A diagnosis of nasal septal disease should be suspected during physical examination when digital palpation of the septum reveals thickening in the rostral one third of the septum or when the amount of airflow through one nostril is reduced. Exercise testing may be beneficial, because noises emanating from the nasal cavity generally have a different sound from the more guttural noises produced in the larynx and pharynx. Air turbulence due to nasal obstruction is likened to a low-pitched snore. Endoscopic examination may support a diagnosis of nasal septal thickening through

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observation of contour changes or inability to advance the endoscope the entire length of the ventral meatus. Dorsoventral and lateral radiographic projections are diagnostic in most cases. Of particular diagnostic aid is the dorsoventral projection, which must be taken with precision to center the septum perfectly between the horizontal rami of the mandible. The cartilaginous septum is apparent on radiographic examination in this view partly as a result of the contribution of the vomer bone ventrally. The septum is not visible in the lateral projection unless focal septal mineralization has occurred. In horses with septal mineralization and thickening from a traumatic incident, the external appearance of the facial bones may be distorted. Mineralization usually is noted on lateral radiographic projection in the dorsal half of the septum adjacent to nasal bones that are often thickened secondary to fracture. Treatment

Nasal septum resection is performed to improve tolerance to exercise or, rarely, to stop progression of rapidly advancing lesions. The procedure is not efficient in eliminating respiratory noise, because the resultant anatomic changes still result in air turbulence. 38 Therefore, horses with respiratory noise caused by septal abnormalities that are capable of maximal exercise have a guarded prognosis for improvement of noise after nasal septum resection. Horses with congenitally narrowed nasal passages, which usually are intolerant to exercise, do not respond favorably to nasal septum resection, because removal of the normal septum does not substantially increase the diameter of th~ nasal cavity. The surgical principles of nasal septum resection include removal of a maximal amount caudally to maximize the distance between the remaining stump and the turbinates, leaving a portion intact rostrally to support the alar cartilages. With the horse in lateral recumbency, an 18-mm hole is trephined at the point of divergence of the nasal bones on the midline of the face. A Doyen intestinal forcep is placed on the septum at a 60-degree angle directed caudally to serve as a guide for the caudal cut and to stop the blind dorsal and ventral cuts. The rostral incision is made in a curved fashion facing rostrally, just caudal to the alar cartilages. A guarded chisel is engaged in the septum separately at the dorsal and ventral borders and is forced caudally until it contacts the Doyen forcep. The caudal incision is made using a chisel or meniscal knife along the rostral border of the Doyen forcep. The septum is removed using Vulsellum forceps . An alternative method of making the dorsal and ventral cut involves passing obstetric wire within a !OF-polypropylene catheter separately up both ventral and dorsal meati to the pharynx and to the trephine hole respectively; the wires are retrieved manually and tied together for sawing. Hemorrhage is profuse throughout the procedure and is controlled on completion of the procedure by using gauze packing. Because hemorrhage is expected, preparation of the patient includes cross-matching blood to

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potential donors and having a donor or 4 to 8 L of blood readily available. Temporary tracheostomy is performed, either before the procedure for administration of inhalation anesthetics or before recovery, to relieve airway occlusion caused by the nasal packing. Systemic antibiotics and phenylbutazone are administered for a period determined by clinical response and comfort of the patient. The gauze is removed 48 to 72 hours postoperatively, and routine wound care of the trephine hole is begun, in addition to flushing the nasal cavity with antimicrobial solutions. Excessive granulation tissue and infection of the stump are the most common complications of nasal septum resection. These are treated by using local flushes and systemic antibiotics. Risk Factors

Foals under 6 months of age have some degree of nasal bone collapse after nasal septum resection. The procedure should be delayed as long as possible in these horses to prevent this complication. Congenital narrowing of the nasal cavity noticed in Quarter-type horses has clinical signs similar to nasal septal abnormalities, but resection of a normal nasal septum in these horses is unlikely to increase their respiratory capacity significantly.

TRACHEAL STRICTURE

Small decreases in the internal diameter of the trachea cause significant obstruction through exponential increase in resistance to airflow and cause secondary air turbulence. Focal stricture of the trachea in performance horses most commonly occurs secondary to previous tracheal surgery or trauma. Iatrogenic causes of tracheal stricture include tracheal ring transection during tracheostomy, extended periods of temporary tracheostomy intubation, intratracheal injections, or transtracheal wash. Luminal compromise results because healing commonly is accompanied by chondritis and distortion of the cartilaginous rings. Submucosal granuloma formation may result from repeated intratracheal injections. Diagnosis

The degree of luminal compromise is estimated using endoscopy. Severe tracheal ring abnormalities are palpable externally. Lateral radiographic projection of the affected part of the trachea is useful in determining compromised tracheal diameter if the luminal protrusion originates on the tracheal floor. Tracheal narrowing from side to side is not appreciated on the lateral projection. Treatment

Performance horses with tracheal ring distortion causing exercise intolerance have a guarded prognosis for recovery. Discrete luminal pro-

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jections within the trachea that are not accompanied by significant distortion of the ring are excised optimally by using the contact Nd:YAG laser with endoscopic guidance. Successful tracheal reconstruction is possible in horses with tracheal ring distortion using a polypropylene prosthesis made of a syringe case drilled with multiple holes. The semicircular prosthesis is placed over the ventral trachea and secured to the normal tracheal rings adjacent to the distorted ring using preplaced polypropylene suture, taking care not to penetrate the tracheal mucosa. Similarly, preplaced sutures in the collapsed rings are secured to the prosthesis and tightened to expand the ring. Partial thickness chondrotomy incisions may be necessary to make the diseased rings conform to the prosthesis. 24 Tracheal resection and endto-end anastomosis may be attempted for salvaging performance horses with severe stricture that is not amenable to less invasive reconstruction. 33

REFERENCES 1. Bayly WM, Grant BD, Breeze RC: Arterial blood gas tension and acid base balance during exercise in horses with pharyngeal lymphoid hyperplasia. Equine Vet J 16:45, 1984 2. Belknap J, Derksen FJ, Nickels FA: Evaluation of subtotal arytenoidectomy as a surgical treatment for left laryngeal hemiplegia in the horse. Abstract Vet Surg 18:57, 1989 3. Boles CL: Epiglottic entrapment by aryepiglottic folds in the horse. J Am Vet Med Assoc 172:338, 1978 4. Cahill JI, Goulden BE: Equine laryngeal hemiplegia: Part II. An electron microscopic study of peripheral nerve. New Zealand Veterinary Journal 34:170, 1986 5. Cook WR: Recent observations on recurrent laryngeal neuropathy in the horse: Applications to practice. Proceedings 34th Annual AAEP 1988, p 427 6. Cook WR: Some observations on form and function of the equine upper airway in health and disease: I. The pharynx. Proceedings 27th Annual AAEP 1981, p 355 7. Dean PW, Cohen ND: Arytenoidectomy for advanced arytenoid chondropathy with accompanying lesions. Vet Surg 19:364-370, 1990 8. Dean PW, Nelson JK, Schumacher J: Effects of age and prosthesis material on in vitro cartilage retention of laryngoplasty prostheses in horses. Am J Vet Res 51:114-117, 1990 9. Derksen FJ, Stick JA, Scott EA, et al: Effect of laryngeal hemiplegia and laryngoplasty on airway flow mechanics in exercising horses. Am J Vet Res 47:16, 1986 10. Ducharme NG, Hackett RP, Fubini SL: Influence of sedation, side of endoscopy, and time of evaluation on subjective and objective evaluation of endoscopic examination in assessment of laryngeal function in racehorses. Vet Surg 18:63, 1989 11. Harrison IW, Raker CW: Sternothyrohyoideus myectomy in horses: 17 cases (1984-1985). J Am Vet Med Assoc 193:1299, 1988 12. Harrison IW, Raker CW: Dorsal glottic stenosis after bilateral arytenoidectomy in two horses. J Am Vet Med Assoc 192:202-204, 1988 13. Haynes PF, McClure JR, Watters JW: Subtotal arytenoidectomy in the horse: An update. Proceedings 30th Annual AAEP 1984, p 21-33 14. Haynes PF, Snider TC, McClure JR, et al: Chronic chondritis of the arytenoid cartilage. J Am Vet Med Assoc 177:1135-1142, 1980 15. Haynes PF: Dorsal displacement of the soft palate and epiglottic entrapment: Diagnosis, management, and interrelationship. Compend Contin Educ Pract Vet 5:S379-389, 1983 16. Johnson JH: Laryngeal surgery techniques and results. Proc Am Coll Vet Surg Form [Eq Resp Surg] 13:60, 1985 17. Lindsay WA, Duncan ID, Archer RMA: Endoscopic examination of the equine larynx: A comparison of stress testing techniques. Vet Surg 18:65, 1989

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18. Linford RL, O'Brien TR, Wheat JD, et al: Radiographic assessment of epiglottic length and pharyngeal and laryngeal diameters in the Thoroughbred. Am J Vet Res 44:16601666, 1983 19. Marks D, MacKay-Smith MP, Cushing LS, et al: Observations on laryngeal hemiplegia in the horse and treatment by abductor muscle prosthesis. Equine Vet J 2:158-166, 1970 20. Marks D , MacKay-Smith MP, Cushing LS, et al: Use of a prosthetic device for surgical correction of laryngeal hemiplegia in horses. J Am Vet Med Assoc 157:157-163, 1970 21. McAllister ES: Obstructive respiratory disease. In Mansmann RR, McAllister ES (eds): Equine Medicine and Surgery, ed 3, vol 2. Santa Barbara, CA, American Veterinary publications, 1982, p 738-770 22. Morris EA, Seeherman HJ: Evaluation of upper respiratory tract function during strenuous exercise in racehorses. J Am Vet Med Assoc 196:431, 1990 23. Orsini PG, Raker CW, Reid CF, et al: Xeroradiographic evaluation of the equine larynx. Am J Vet Res 50:845-849, 1989 24. Robertson JT, Spurlock CH: Tracheal reconstruction in a foal. J Am Vet Med Assoc 189:313, 1986 25. Shappell KK, Caron JP, Stick JA, et al: Staphylectomy for treatment of dorsal displacement of the soft palate in two foals. J Am Vet Med Assoc 195:1395, 1989 26. Shappell KK, Derksen FJ, Stick JA: Effects of ventriculectomy, prosthetic laryngoplasty, and exercise on upper airway function in horses with induced left laryngeal hemiplegia. Am J Vet Res 49:1760-1765, 1988 27. Shappell KK, Stick JA, Derksen FJ, et al: Permanent tracheostomy in equidae: 47 cases (1981-1986). J Am Vet Med Assoc 192:939-942, 1988 28. Shires GMH, Adair HS, Patton CS: Preliminary study of laryngeal sacculectomy, using a neodymium:yttrium aluminum garnet laser technique. Am J Vet Res 51:1247, 1990 29. Speirs VC: Partial arytenoidectomy in horses. Vet Surg 15:316-320, 1986 30. Stick JA, Boles CL: Subepiglottic cyst in three foals. J Am Vet Med Assoc 77:62, 1980 31. Stick JA, Derksen FJ: Use of videoendoscopy during exercise for determination of appropriate surgical treatment of laryngeal hemiplegia in a colt. J Am Vet Med Assoc 195:619-623, 1989 32. Tate LP, Corbett WP, Bishop B: Investigation of physiologic effect oflaryngeal hemiplegia followed by laryngoplasty in the exercising Thoroughbred [abstract]. Vet Surg 19:78, 1990 33. Tate LP, Koch DB, Sembrat RF, et al: Tracheal reconstruction by resection and end-toend anastomosis in the horse. J Am Vet Med Assoc 178:253, 1981 34. Tulleners EP: Transendoscopic contact neodymium:yttrium aluminum garnet laser correction of epiglottic entrapment in standing horses. J Am Vet Med Assoc 196:1971, 1990 35. Tulleners EP, Hamir A: Epiglottic augmentation in the horse: A pilot study [abstract]. Vet Surg 19:79, 1990 36. Tulleners EP, Harrison IW, Raker CW: Management of arytenoid chondropathy and failed laryngoplasty in horses: 75 cases (1979-1985): J Am Vet Med Assoc 192:670-675, 1988 37. Tulleners EP, Harrison IW, Mann P, et al: Partial arytenoidectomy in the horse with and without mucosa) closure. Vet Surg 17:252-257, 1988 38. Tulleners EP, Raker CW: Nasal septum resection in the horse. Vet Surg 12:41-57, 1983 39. White NA, Blackwell RB: Partial arytenoidectomy in the horse. Vet Surg 9:5-12, 1980

Address reprint requests to Paul W. Dean, DVM, MS Equine Surgical Center Route 1, Box 153 Aubrey, TX 76277