Chondrite septique abcédée de l’épiglotte chez 2 jeunes chevaux de course Thoroughbred. Une chondrite septique abcédée de l’épiglotte a été diagnostiquée chez 2 jeunes chevaux de course Thoroughbred. Le cartilage infecté a été enlevé par vidéo-endoscopie puis une antibiothérapie systémique a été instaurée. Le processus inflammatoire a été enrayé mais un déplacement dorsal permanent du palais mou (DDPM) causé par un cartilage de l’épiglotte raccourci et déformé s’est développé. La chirurgie du DDPM par sternothyroïdectomie partielle bilatérale ou avancement laryngée a échoué.

(Traduit par Docteur André Blouin)

On physical examination, no abnormalities of significance were noted. An upper airway videoendoscopic examination revealed focal swelling of the rostral third of the epiglottis, ulceration on the dorsal surface of the epiglottis, and loss of the scalloped edge of the epiglottic cartilage with the appearance of a concomitant aryepiglottic entrapment (Figure 1A). Indeed, loss of the scalloped edge of epiglottic cartilage and a mucous membrane that appeared to attach to the lateral aspect of the corniculate process gave the false impression of an aryepiglottic entrapment. However, a slightly more dorsal view (Figure 1B) showed a rather inflamed and enlarged mucous membrane of the epiglottic cartilage, not the aryepiglottic membrane. Intermittent dorsal displacement of the soft palate (DDSP) was observed during the examination. Finally, a white structure protruded for approximately 1 cm beyond the dorsal surface of the epiglottic cartilage through an ulcerated area of the epiglottis; this was presumed to be a necrotic section of cartilage surrounded by abscessation. A tentative diagnosis of septic chondritis of the epiglottic cartilage was made.

Figure 1 Videoendoscopic view of a 5-year-old Thoroughbred horse with chondritis and abscessation of the epiglottic cartilage. A) Note focal swelling on the rostral third and loss of the scalloped edge of epiglottic cartilage, suggestive of epiglottic entrapment. (more ...)

The animal was sedated with detomidine hydrochloride (Dormosedan; Pfizer, Exton, Pennsylvania, USA), 0.012 mg/kg body weight (BW), IV, and butorphanol tartrate (Torbugesic; Fort Dodge Animal Health, Iowa, USA), 0.008 mg/kg BW, IV, to facilitate further investigation of the epiglottic cartilage (1). Local anesthetic, 50 mL of 2% lidocaine hydrochloride solution (Lidocaine; Phoenix Scientific, St Joseph, Missouri, USA) was applied to the dorsal aspect of the epiglottic cartilage and nasopharynx through the videoendoscope biopsy channel. Under videoendoscopic visualization, approximately 1.25 × 0.75 cm of necrotic epiglottic cartilage protruding through the ulcerated area was removed with bronchoesophageal forceps (Richard Wolfe Medical Instrument Corp., Vernon Hills, Illinois, USA) inserted through the right nostril. The sample was submitted for histopathologic examination, culture, and sensitivity testing. A cranial pedunculated tag of epiglottic mucosa, measuring approximately 1.25 × 1.0 cm, was removed, using a diode laser and bronchoesophageal forceps. The tag’s removal enhanced exposure to the ulcerated area on the dorsal aspect of the epiglottic cartilage, allowing better local debridement and removal of smaller pieces of necrotic debris from the abscess with forceps. Polyethylene (PE) tubing was passed through the videoendoscope biopsy channel into the epiglottic cartilage defect, which was then lavaged with 250 mL of a solution of sterile physiological saline solution containing 1g of sodium ampicillin (Amicillin; American Pharmaceutical Partners, Schaumburg, Illinois, USA) per liter. Histopathological examination of the sample revealed sheets of degenerated cartilage that had undergone ischemic necrosis. Colonies of mixed bacterial rods and cocci covered and extended into the chondroid lacunae. Streptococcus pneumoniae, sensitive to ampicillin and enrofloxacin, was isolated from the aerobic culture.

A diagnosis of septic chondritis of the epiglottic cartilage with abscessation was made and the following treatment was instituted: nonsteroidal antiinflammatory medication, phenylbutazone (Vedco; St Joseph, Missouri, USA), 2.2 mg/kg BW, PO, q12h for 10 d postoperatively, and enrofloxacin (Baytril; Bayer Animal Health, Shawnee, Kansas, USA), 7.5 mg/kg BW, PO, q24h for 21 d. A 20-mL “throat spray” consisting of 250 mL glycerin (Humco; Texarkana, Texas, USA), 250 mL dimethyl sulfoxide 90% (DMSO; Butler Company, Columbus, Ohio, USA), 500 mL furacin (nitrofurazone powder USP; PCCA, Houston, Texas, USA), 50 mL dexamethasone sodium phosphate (25 mg/mL) (American Regent, Shirley, New York, USA), and ticarcillin and clavulonate (Timentin; SmithKline Beecham, Philadelphia, Pennsylvania, USA), 3 g, was applied to the nasopharynx through a flexible, soft rubber, 10 French catheter via the ventral nasal meatus twice daily for 14 d. The horse was confined to a stall with daily hand walking as exercise until being reevaluated 2 mo later.

At the approximately 2-month postoperative, reevaluation physical examination, all vital signs were within normal limits. Videoendoscopy of the larynx revealed that the soft palate was persistently positioned dorsal to the epiglottic cartilage. After sedation and administration of local anesthetic, as described previously, further examination with the aid of bronchoesophageal forceps revealed a shortened and deformed epiglottic cartilage and an aryepiglottic entrapment. The aryepiglottic folds were edematous and thick, with prominent margins, and they covered 1/3 of the short, edematous, misshapen, and discolored epiglottis, which was approximately half its normal length, presumably as a result of its previous infection. A grave prognosis for return to racing was given, and the horse was prepared for surgery to correct the epiglottic entrapment and DDSP.

Because of the very thick aryepiglottic folds and deformed epiglottic cartilage, removing a section of aryepiglottic membrane by laryngotomy was judged to be less likely to cause injury to the remaining deformed epiglottic cartilage and to have less likelihood of recurrence of the epiglottic entrapment than making a linear incision of the membrane with a hook blade or laser. The DDSP treatment planned was a partial Llewellyn procedure (2), because a tie-forward procedure cannot be done at the same time as a laryngotomy (3). The horse was placed in dorsal recumbency, a 2-cm section of the sternothyroideus tendon and associated muscle was removed bilaterally, and the entrapping aryepiglottic membrane was resected through a laryngotomy. Recovery from anesthesia was uneventful.

The colt also received nonsteroidal antiinflammatory medication, phenylbutazone (Vedco), 2 mg/kg BW, PO, q12h for 5 d, and the “throat spray” described above for 14 d. In addition, the following treatment was recommended: trimethoprim/sulfamethoxazole (Tribissen; Teva Pharmaceuticals, Sellersville, Pennsylvania, USA), 30 mg/kg BW, PO, q12h for 10 d, and a period of rest with controlled exercise/walking for 2 wk. Endoscopic examination 5 mo later revealed a persistent DDPS. The horse returned to racing, but he was unable to compete successfully in 2 starts and was retired from racing.

Results from a complete physical and visual examination, palpation of the colt’s head and neck, and auscultation of the upper and lower respiratory tract and cardiovascular system were within normal limits. The horse was comfortable and no abnormal upper respiratory noise could be heard at rest. Videoendoscopic examination of the upper respiratory tract, performed with the use of a lip chain for restraint, showed that the dorsal aspect of the epiglottis was swollen and ulcerated (Figure 2). In addition, the soft palate was noted to displace frequently during the examination, and multiple swallowing episodes were needed to replace it to its correct anatomical position. The scalloped edge of the epiglottic cartilage could still be seen. A lateral radiograph of the laryngeal area with the horse standing revealed a thick epiglottis, a blunted rostral third of the epiglottic cartilage, and the caudal free edge of the soft palate in the normal subepiglottic position. The horse was restrained in stocks, sedated, and had local anesthetic applied to the nasopharyngeal structures, as described for Case 1. The ulcer on the dorsal aspect of the epiglottic cartilage was explored with bronchoesophageal forceps. Purulent exudate found deep within the ulcer was submitted for bacterial culture. Further exploration revealed that the tip of the epiglottic cartilage was loose from the main cartilage; it was removed with the bronchoesophageal forceps. The remaining purulent exudate was lavaged, as described in Case 1. A diagnosis of septic chondritis of the epiglottic cartilage with abscessation was made. It was expected that shortening of the epiglottic cartilage as a result of the chondritis would lead to persistent DDSP. Therefore, surgical advancement of the larynx (laryngeal tie-forward) with partial sternothyroideus muscle tenectomy was performed under general anesthesia (2,3). The animal recovered uneventfully from anesthesia.

Figure 2 Videoendoscopic view of a 3-year-old Thoroughbred horse with chondritis and abscessation of the epiglottic cartilage. Note subepiglottic granulation tissue and thickening combined with an ulcer on the dorsal aspect of the epiglottic cartilage. The scalloped (more ...)

Aerobic bacterial culture of the epiglottic cartilage revealed a moderate number of Actinobacillus spp. In response to the results from culturing and sensitivity testing, the colt was treated initially with ampicillin (Ampicillin Na; American Pharmaceutical Partners), 15 mg/kg BW, IV, q8h, and gentamicin sulfate (GentaVed, Vedco), 6.6 mg/kg BW, IV, q24h for 10 d, followed by oral enrofloxacin (Baytril; Bayer Animal Health), 7.5 mg/kg BW, PO, q24h for 10 d. Postoperative treatment also included “throat spray” and phenylbutazone, as described in Case 1.

The horse was kept in a box stall with daily hand walking for 3 mo postsurgery. Endoscopic evaluation at 3 and 6 mo revealed an almost persistent DDPS without dysphagia. The epiglottic cartilage was observed to be blunt and reduced in size by approximately 50%. The horse made 3 unsuccessful starts 6 mo after presentation.

Septic chondritis of the laryngeal cartilages usually affects 1 or both arytenoid cartilages. The cause of arytenoid chondritis is not well understood; however, inhalation of debris and concussion of the paired arytenoid cartilages, resulting in mucosal damage and subsequent infection, have been suggested as causes (4,5). The condition is commonly overrepresented in Thoroughbred and standardbred racehorses, and it may be related to their level of athletic activity (4–6). An ulcerated mucosal lesion is presumed to lead to secondary bacterial invasion and destruction of the affected arytenoid cartilage (4–6). The mucosal ulceration is usually seen in horses at the rostral margin of the vocal process of the arytenoid cartilage. In 1 study, the ulceration progressed until it resulted in chondritis of the arytenoid cartilage in 5% to 10% of yearling Thoroughbred racehorses (6).

Septic chondritis of the epiglottic cartilage is a less common and understood process. We hypothesize that secondary bacterial invasion of the epiglottic cartilage followed either epiglottitis, an epiglottic abscess, or epiglottic mucosal ulceration. We feel that it is important to differentiate these 3 conditions from septic chondritis of the epiglottic cartilage with abscessation or to identify any concomitant disease present to achieve appropriate management and an accurate prognosis. Classically, epiglottitis is recognized endoscopically by signs of edema, reddening, and thickening of the epiglottis and aryepiglottic membranes and, occasionally, exposed cartilage at the tip of the epiglottis (7,8). No causal organism has been reported, but cultures are generally not attempted (7). Epiglottitis is a disease that requires local and systemic medical treatment (7,8). Following resolution of epiglottitis, various degrees of epiglottic deformity can be seen, as reported in 5 out of 16 horses with epiglottitis (7). These epiglottic deformities are usually mild, and a reasonable prognosis is expected (7,8). Epiglottic abscessation without chondritis has been reported to have the endoscopic feature of smooth round swelling at the dorsal surface of the epiglottic cartilage. Surgical drainage of the abscess appears to be important (1). In the absence of cartilage involvement, epiglottic abscessation does not lead to epiglottic deformation, and a good prognosis is expected (1). Presumably, epiglottic ulceration, like an arytenoid ulceration, has the potential to lead to epiglottic chondritis and, at least, should be monitored closely (6).

The differentiating endoscopic features in these 2 cases of septic chondritis of the epiglottic cartilage included an ulcer on the dorsal surface of the epiglottic cartilage (not ventrally or at the tip of the epiglottis). In addition, a white necrotic cartilage was protruding at the ulcer site. The optimal treatment cannot be identified in this report, as debridement and local and systemic antimicrobials successfully eliminated the infectious process, but the disease reduced the length of the epiglottic cartilage by approximately 50%. In this condition, the potential for severe shortening of the epiglottic cartilage exists, which could result in permanent DDSP. At this time, a poor prognosis appears to be indicated if significant epiglottic cartilage loss occurs. CVJ