Evaluation of survival rate and athletic ability after nonsurgical or surgical treatment of cleft palate in horses: 55 cases (1986–2008)

Shannon J. Murray Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210.

Search for other papers by Shannon J. Murray in
Current site
Google Scholar
PubMed
Close
 DVM, MSc, DACVS
,
Yvonne A. Elce Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210.

Search for other papers by Yvonne A. Elce in
Current site
Google Scholar
PubMed
Close
 DVM, DACVS
,
J. Brett Woodie Rood and Riddle Equine Hospital, 2150 Georgetown Rd, Lexington, KY 40511.

Search for other papers by J. Brett Woodie in
Current site
Google Scholar
PubMed
Close
 DVM, MSc, DACVS
,
Rolf M. Embertson Rood and Riddle Equine Hospital, 2150 Georgetown Rd, Lexington, KY 40511.

Search for other papers by Rolf M. Embertson in
Current site
Google Scholar
PubMed
Close
 DVM, DACVS
,
James T. Robertson Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210.

Search for other papers by James T. Robertson in
Current site
Google Scholar
PubMed
Close
 DVM, DACVS
, and
Warren L. Beard Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210.

Search for other papers by Warren L. Beard in
Current site
Google Scholar
PubMed
Close
 DVM, MSc, DACVS

Click on author name to view affiliation information

Abstract

Objective—To determine survival rate and athletic ability after nonsurgical or surgical treatment of cleft palate in horses.

Design—Retrospective case series.

Animals—55 horses with cleft palate.

Procedures—13 of the 55 horses died or were euthanized without treatment and were not included in all analyses. Medical records were reviewed for signalment, history, method of diagnosis, soft or hard palate involvement, type of surgical procedure performed, postoperative complications, and survival to hospital discharge. Information on athletic ability was acquired from race records and follow-up conversations with owners, trainers, or referring veterinarians.

Results—The predominant reason for initial evaluation was milk or feed in the nostrils (60%). The diagnosis was confirmed by means of videoendoscopy of the upper portion of the airway in all cases. Most cases involved the soft palate only (92.7%). Twenty-six of the 55 (47.3%) horses underwent surgical repair, and 12 of these had dehiscence at the caudal edge of the soft palate. Among potential racehorses, 14 of 33 had surgery. Of these, 12 of 14 survived to discharge and 2 horses raced. Among potential racehorses, 10 of 33 were discharged without surgery and 2 of these raced. Among nonracehorses, 12 of 22 underwent surgery and 11 survived to discharge. All horses that were discharged and for which follow-up information was available survived to 2 years of age or older without ill thrift despite dehiscence at the caudal edge of the soft palate and continued mild nasal discharge.

Conclusions and Clinical Relevance—Horses with cleft palate had a higher survival rate than previously reported.

Abstract

Objective—To determine survival rate and athletic ability after nonsurgical or surgical treatment of cleft palate in horses.

Design—Retrospective case series.

Animals—55 horses with cleft palate.

Procedures—13 of the 55 horses died or were euthanized without treatment and were not included in all analyses. Medical records were reviewed for signalment, history, method of diagnosis, soft or hard palate involvement, type of surgical procedure performed, postoperative complications, and survival to hospital discharge. Information on athletic ability was acquired from race records and follow-up conversations with owners, trainers, or referring veterinarians.

Results—The predominant reason for initial evaluation was milk or feed in the nostrils (60%). The diagnosis was confirmed by means of videoendoscopy of the upper portion of the airway in all cases. Most cases involved the soft palate only (92.7%). Twenty-six of the 55 (47.3%) horses underwent surgical repair, and 12 of these had dehiscence at the caudal edge of the soft palate. Among potential racehorses, 14 of 33 had surgery. Of these, 12 of 14 survived to discharge and 2 horses raced. Among potential racehorses, 10 of 33 were discharged without surgery and 2 of these raced. Among nonracehorses, 12 of 22 underwent surgery and 11 survived to discharge. All horses that were discharged and for which follow-up information was available survived to 2 years of age or older without ill thrift despite dehiscence at the caudal edge of the soft palate and continued mild nasal discharge.

Conclusions and Clinical Relevance—Horses with cleft palate had a higher survival rate than previously reported.

Cleft palate is an uncommon congenital disorder affecting approximately 0.1% to 0.2% of all foals1–3 and 4% of foals with congenital deformities.2,4 The cleft results from an interruption of the fusion of the palatal folds that occurs along the midline in a rostral to caudal direction. This fusion process is normally complete by day 47 of gestation.5 The length of the defect varies depending on the point of disruption in the fusion process.1,2,6 Clinical signs associated with a cleft palate are often evident shortly after initial nursing and include milk running from the nostrils, dysphagia that may predispose to aspiration pneumonia, and unthriftiness.4,7–9 Definitive diagnosis of a cleft palate is made by endoscopic examination of the upper portion of the airway.

Current treatment involves both surgical repair and medical management of associated complications. Surgical repair can be challenging because of the length and inaccessibility of the defect, poor visibility, and a postsurgical complication rate that has been reported to be as high as 7 of 8 horses.3,6,8 Complications following surgery include dehiscence of the surgical repair, oronasal fistula, suture dehiscence of the inferior lip, osteomyelitis, instability of the mandibular symphysis, and aspiration pneumonia.8 Current literature describes the high complication rate and poor survival rate3,6–8 of foals with cleft palate but consists of small numbers of cases, not exceeding 11 cases in any of the published reports. Serious complications can follow surgery, such as severe aspiration pneumonia. Euthanasia can result because of these complications despite a successful repair and contribute to the poor survival rates.8

One of the greater challenges of repair is surgical access, which may contribute to failure of the surgery.7 Mandibular symphysiotomy is the most common surgical approach and may provide the best exposure for surgical access.7,10,11 Other surgical approaches include the transoral approach, bilateral buccotomy, laryngotomy, and pharyngotomy.1,5,6,11,12 The most common repair failure is dehiscence of the caudal aspect of the soft palate, which has been reported in 90% of the surgical cases.7,8,11,13,14,a The prognosis for correction of the defect is better for the soft palate than for the hard palate; however, the prognosis for complete surgical correction remains poor in all situations.1,7 The objective of surgical correction is to create a complete repair, eliminating the nasal reflux of milk and other foods and the risk of aspiration, resulting in an athletic horse.

The purpose of the study reported here was to determine the survival rate, complications, and athletic ability in a large case series of horses treated conservatively or with surgery for cleft palate.

Materials and Methods

Criteria for selection of cases—Medical records for all horses examined at The Ohio State University and Rood and Riddle Equine Hospital between January 1986 and August 2008 were reviewed to identify horses with a cleft palate. Horses were eligible for inclusion in this study if cleft palate had been diagnosed by use of endoscopy.

Medical records review—Fifty-five horses met the inclusion criteria. Horses included were grouped into 4 populations: surgically treated racehorses, nonsurgically treated racehorses, surgically treated nonracehorses, and nonsurgically treated nonracehorses. The medical records were reviewed for breed, sex, weight, age at initial evaluation, clinical signs, soft or hard palate involvement, type of surgical procedure performed, postoperative complications, survival to discharge from the hospital, and follow-up examination. Long-term outcome was determined through telephone conversations with owners, trainers, or referring veterinarians. Where applicable, race records were obtained.b,c Information obtained included the number of starts and total lifetime earnings. A successful outcome was defined as survival to discharge from the hospital without signs of ill thrift or chronic disease, and a successful athletic outcome was defined as the horse being able to achieve its intended use.

Statistical analysis—Multivariable analysis was performed for age, surgery, rectal temperature > 38.6°C (101.5°F), racehorse versus nonracehorse, and pneumonia versus no pneumonia. Analysis was performed in a stepwise backward manner. Iterations were completed until only variables with significant (P < 0.05) associations with survival outcome remained. Softwared was used for all analyses.

Results

Fifty-five horses met the inclusion criteria. Of the 55 horses, 46 (83.6%) horses were initially evaluated when they were < 1 year of age (mean, 52 days; median, 16 days; range, 1 to 270 days) and 9 (16.4%) horses were evaluated when they were ≥ 1 year of age (mean, 5 years; median, 4.5 years; range, 2.5 to 14 years). The breed distribution included 27 Thoroughbreds, 7 Standardbreds, 8 Quarter Horses, 3 Miniature Horses, 2 warmbloods, 2 mixed breeds, 2 American Paints, and 1 each of Rocky Mountain Horse, Clydesdale, Appaloosa, and Tennessee Walking Horse. Thirty-three horses were intended for racing, and 22 horses were not intended for racing. The sex distribution was 23 females, 15 sexually intact males, and 4 geldings, and the sex was not recorded in 13 horses. Body weight was recorded in 21 foals (mean, 111 kg [244 lb]; median, 95 kg [209 lb]; range 13 kg to 272 kg [29 to 600 lb]) and 7 adults (mean, 418 kg [920 lb]; median, 482 kg [1,060 lb]; range, 418 to 536 kg [920 to 1,180 lb]).

Figure 1—
Figure 1—

Endoscopic images of a cleft soft palate in a yearling Thoroughbred colt that went on to race following conservative treatment (A), and a cleft soft palate extending to the nasal septum in a 7-month-old Standardbred colt that went on to race after surgical repair (B).

Citation: Journal of the American Veterinary Medical Association 243, 3; 10.2460/javma.243.3.406

The predominant reason for initial evaluation was milk or feed in the nostrils (33 [60%] horses), and other reasons for initial evaluation included pneumonia, fever, or both (4 [7.3%]); dysphagia, coughing, or both (4 [7.3%]); history of a cleft palate (4 [7.3%]); abnormal noise from the proximal portion of the airway during training (3 [5.5%]); multiple congenital abnormalities (2 [3.6%]) as well as history of choke (1 [2%]), colic (1 [2%]), not nursing (1 [2%]), and bilateral entropion (1 [2%]). The diagnosis of cleft palate was confirmed by videoendoscopic examination of the proximal portion of the airway (Figure 1). Symmetry of the cleft was recorded in 34 horses. In 29 (85.3%) of those horses, the cleft was symmetric along the midline.

The majority (92.7%) of the cases involved only the soft palate, with only 4 (7.3%) cases involving both the soft and hard palate. Four Thoroughbred foals had a defect that included the hard palate. Of these 4 foals, 2 were euthanized following the diagnosis and 2 underwent surgical repair. Surgical repair of the hard palate was successful; however, the caudal edge of the soft palate dehisced in both foals. One of these foals was euthanized following surgery because of severe aspiration pneumonia.

Twenty-three (41.8%) horses had pneumonia as a concomitant illness at initial evaluation. Pneumonia was diagnosed by use of auscultation, thoracic ultrasonography, and thoracic radiography and a transtracheal wash in 3 instances. All horses with pneumonia or undergoing cleft palate surgery received perioperative administration of broad-spectrum antimicrobials (most horses received gentamicin and potassium penicillin or procaine penicillin), and 22 of 26 horses treated with surgery received NSAIDs (flunixin meglumine, phenylbutazone, or ketoprofen) and opioids (morphine or fentanyl patches) as needed for analgesia. Additional findings on initial examination were fever (> 38.6°C [101.5°F]) in 17 of 42 (40.5%) horses for which temperature was recorded, high WBC count (≥ 12,000 cells/μL) in 16 of 36 (44.4%) horses, and high fibrinogen concentration (≥ 400 mg/dL) in 24 of 31 (77.4%) horses.

Horses treated with surgery—Twenty-six of the 55 (47.3%) horses had surgical repair (23 foals; 3 adults), 16 were discharged without surgery, 12 were euthanized after initial evaluation, and 1 foal died prior to surgery from severe aspiration pneumonia. Horses were more likely to be euthanized after initial evaluation if severe aspiration pneumonia, a hard palate defect, a large soft palate defect, or multiple congenital anomalies were present. Of the 26 horses that had cleft palate repair, a tracheotomy was performed for delivery of anesthetic in 24. The method of delivery of anesthesia for the remaining 2 horses could not be determined from the medical records. Mandibular symphysiotomy and ventral laryngotomy with primary suture repair were performed in 24 of 26 horses as described.7,14,15 In most surgeries for which the surgical report was available, the soft palate cleft was closed by use of a 3-layer technique; dorsal (nasal mucosa) and ventral flaps (oral mucosa) were created and closed with 1 suture layer in the oral mucosa, a second suture layer was placed over the everted oral mucosa, and a third suture layer was placed in the nasal mucosa. Tension-relieving sutures were often included at the caudal portion of the soft palate to add further strength to the repair. The suture materials used were braided lactomer 9-1, polyglactin 910, and silk. All 3 suture types ranged in size from 0 to 3-0. Releasing incisions made parallel to the suture line were used as needed to aid in the release of tension. Stabilization of the mandibular symphysis was accomplished by figure-8 wiring between 2 screws (1 placed on either side of the mandibular symphysis). In the remaining 2 horses, the palate defect was repaired via a modified laryngotomy. In 2 of the 26 horses, 2 surgeries were performed to repair the cleft.

Two foals and 1 adult were euthanized in the immediate postoperative period because of complete dehiscence of the repair or severe pneumonia. Postoperative care included the continued administration of broad-spectrum antimicrobials, NSAIDs, and opioids for analgesia. Ten of 26 horses were fed through a nasogastric feeding tube. Postoperative findings prior to discharge from the hospital or euthanasia included milk from nostrils in 13 of 26 (50%) horses, skin suture dehiscence in 2 (7.7%), and broken wire at the mandibular symphysiotomy site in 1 (3.8%). Recheck endoscopy was performed in all 23 horses that survived to discharge. The surgical repairs were checked as early as 8 days and up to 1 year after surgery. If the examination was initially performed when the foal was < 1 month of age, the procedure was repeated 4 weeks after surgery. Twelve of 23 (52%) horses had dehiscence of the repair at the caudal edge of the soft palate, whereas 9 (39%) had intact repairs. In 2 horses, an oronasal fistula was detected under the epiglottis.

Horses treated without surgery—Among the 16 horses that were not treated with surgery and were discharged from the hospital, 2 were euthanized within days after discharge, 9 were lost to follow-up, and 5 lived to ≥ 2 years of age (of which 2 raced).

Racehorses—Among the 33 racehorses, 14 (42.4%) had surgery, 10 (30.3%) were discharged from the hospital without surgery, and 9 (27.3%) were euthanized. Of the 14 horses that had surgery, 12 survived to discharge, 6 were registered through either the Jockey Club (n = 5) or the United States Trotting Association (1), and only 2 raced. Tw of the 4 horses that were registered but did not race survived to be at least 2 years old (one was used as a broodmare, and the other was sold with the intention to enter race training); the other 2 horses were lost to follow-up. Of the 6 that were not registered with a racing association, 4 were lost to follow-up and 2 survived to be at least 2 years old (one horse was sold to enter race training, and the other was turned out to pasture as a pet).

Of the 10 horses that were discharged without surgery, 2 were euthanized at their home farm within days after discharge. Two were registered and raced. Of the 6 horses that were not registered, 5 were lost to follow-up and 1 survived to be at least 2 years of age and was given away at that time. Twenty-two of 33 racehorses treated surgically and nonsurgically initially survived, and follow-up was available for 11, all of which lived to be at least 2 years of age with no clinical signs of chronic pneumonia (coughing or ill thrift).

Nonracehorses—Of the 22 nonracehorses, 3 were euthanized after initial evaluation, 1 died prior to surgery, 12 had surgery, and 6 did not have surgery. Of the 12 horses that had surgery, 1 was euthanized prior to discharge because of severe aspiration pneumonia and 11 survived to discharge from the hospital. Follow-up information was unavailable for 6 of the 11 horses; the remaining 5 horses survived to be 2 years of age or older. The owners considered all 5 horses to have had a successful outcome. Two became athletic (used for pleasure riding and barrel racing), 1 was a Miniature Horse that served as a companion animal to other horses, 1 was anticipated to begin dressage training, and 1 was still a weanling at the time of the study. Of the 6 horses that did not have surgery and were discharged, 4 were lost to follow-up. The remaining 2 horses survived to be 2 years of age or older. One of the horses was a Miniature Horse that was a pet, and the second horse participated in barrel racing and was euthanized as an adult for an unrelated sinonasal mass.

Overall survival rate—The overall survival rate to hospital discharge was 67% (37/55). Among all 4 categories (surgically and nonsurgically treated racehorses and surgically and nonsurgically treated nonracehorses) for which the long-term follow-up information was available, horses survived to be 2 years of age or older if they were not euthanized immediately after diagnosis (n = 12) or prior to discharge because of severe aspiration pneumonia (1). Survival-to-discharge rate was 88.7% (23/26) for the combined surgical categories (racehorses and nonracehorses). The only significant (P = 0.002) association with survival to discharge as determined via multivariate analysis was surgery; 13 of 26 horses that did not have surgery died, compared with 3 of 26 that had surgery. However, this comparison includes 12 horses that were euthanized in the hospital immediately after diagnosis. Of 29 horses that did not have surgery, 16 survived to discharge, and of those horses that survived to discharge, 5 of 7 horses with long-term follow-up lived past 2 years of age. Importantly, all horses had continued mild intermittent nasal discharge and were in good body condition. Food was withheld from athletic horses 1 hour prior to and 1 hour following exercise. There were no observed clinical signs consistent with chronic aspiration pneumonia in these horses (coughing, weight loss, or exercise intolerance).

Discussion

In the present study, all surviving horses for which follow-up information was available lived to 2 years of age or older. Long-term data were difficult to obtain for many horses; however, the long-term survival for those with follow-up information was encouraging. Overall survival-to-discharge rate was 67%, compared with a previous report8 indicating a successful outcome in 6 of 11 horses.

The primary reason for initial evaluation and complications following surgery in the present study were similar to those reported in other studies.1,2,4,7,8,16 The overall complication rate (65%) following surgery (nasal discharge, suture discharge, wire breakage at the mandibular symphysis, and suture dehiscence of the lip) was less than rates of up to 10 of 11 horses with complications reported in a previous study.8 Incomplete healing occurred in 65% of the horses in the present study, primarily at the caudal edge of the soft palate under the epiglottis; oronasal fistulas and complete repair breakdown also occurred. This prevalence was slightly greater than that reported as 4 of 8 horses with incomplete healing when various surgical approaches3,7 were used, but less than that reported as 11 of 11 horses with incomplete healing when mandibular symphysiotomy was performed.8 Such a variation in morbidity rate is likely a result of the number of cases, number of surgeries per horse, and type of surgery performed in each study.

Similar to 3 previous studies,3,7,8 failure of the repair at the caudal edge of the soft palate was the most common complication. Explanations for breakdown of the repair at the caudal edge of the soft palate include lack of adequate exposure of the surgical site; lack of sufficient palatal tissue, resulting in high tension on the suture line; or the caudal portion of the palate under more tension than the cranial portion in a clinically normal horse. An equal amount of palatal tissue was present on both sides in 85% of the 34 horses for which this information was available in the present study. This finding indicated that sufficient tissue was present along the suture line, suggesting that either lack of adequate visualization or increased tension at the caudal edge of the soft palate, compared with the cranial portion of the palate, may have played a greater role in breakdown of the repair.

Additional complications reported with mandibular symphysiotomy include osteomyelitis, infection, or both around the implant site. Only one horse of the present study had radiographic evidence of osteomyelitis, and another was suspected to have an infection at the implant site, resulting in a complication rate of 9.5%, compared with a higher rate of osteomyelitis in 6 of 11 horses with palate repairs by use of mandibular symphysiotomy in a previous study.8 The primary difference between that study8 and the present study was the use of Steinmann pins (1 or 2), 1 screw combined with wiring, or both in the previous study, whereas in the present study, pins were not used and stabilization of the mandibular symphysis involved primarily placement of 2 screws with wire in a figure-8 pattern.

The only other study8 that attempted to evaluate the athletic performance of horses with a repaired cleft palate found that none of the horses achieved athletic status after surgery. Of the racehorses treated surgically and discharged from the hospital in the present study, only 2 of 12 raced and 2 of the 10 conservatively treated racehorses discharged raced. Horses of the present study were more likely to be euthanized on admission if they had severe pneumonia or severe defects in the hard palate or soft palate. Although information was not available in all of the medical records used in the present study, it appeared that horses that reached their athletic potential without surgical intervention had small defects at the caudal edge of the soft palate, which was the most common site of surgical repair breakdown in the present study and affected 52% of the surgically treated horses. Horses in which surgery was performed had larger defects of the palate. The length of the cleft influences whether surgery should be recommended. Results of the present study suggest that small defects of the caudal edge of the soft palate may not need to be surgically repaired in foals intended to become racehorses.

Of the 11 nonracehorses treated surgically, long-term follow-up was available for only 5 horses. Of those 5 horses, 4 progressed to achieve their intended use and the fifth was a Miniature Horse used as a companion animal. Of the 6 horses discharged without surgery, long-term follow-up was available for only 2 horses, of which 1 was considered to have athletic ability. Because of the low numbers of horses with follow-up in the surgically and conservatively treated groups, it is difficult to draw conclusions, although surgery appeared beneficial for nonracehorses to achieve their intended use. The authors suspect this was influenced by the length of the cleft palate, with surgery benefitting those horses with longer cleft palates. However, medical records for the nonracehorses indicated the length of the cleft palate in only a few instances, so it is unclear whether the length of the palate influenced either the decision to do surgery or the outcome. In the present study, it was difficult to determine the athletic ability for racehorses and nonracehorses because of difficulty in obtaining complete follow-up information. Results indicated that some horses became athletic; however, a larger case series with improved follow-up is needed to make a strong statement regarding athleticism. In addition, the findings of this study indicated that complete repair of a cleft palate was not essential to achieve an athletic outcome for either racehorses or nonracehorses. This was supported by the 9 (16%) athletic horses in this study, in which cleft palate was diagnosed as yearlings and older (mean age, 5 years; range, 1 to 14 years); the most common clinical sign at initial evaluation was abnormal sounds originating from the proximal portion of the airway. The cleft in these horses was at the caudal edge of the soft palate under the epiglottis, similar to the most common site of surgical repair failure. This suggests that a small cleft defect may allow horses to perform athletically without surgical repair.

Body condition for horses with cleft palate has been reported to be stunted.7,11 Horses of the present study for which follow-up was available were not considered stunted or underweight at ≥ 2 years of age, compared with unaffected horses. However, poor body condition may have been a reason several horses were not available for follow-up. There was no history of chronic pneumonia in all horses with follow-up information. This is important, particularly because many horses had partial dehiscence of the cleft palate repair and many had chronic nasal discharge. Results indicated that horses can successfully live and perform at some level of athleticism with small cleft palate defects. However, it is important to discuss with the owner the likelihood of persistent nasal discharge throughout the life of their horse.

Although this study included a greater number of cases than previous studies, there were important limitations. The retrospective nature of the study limited the information that was available from the records. Additional data that could have improved the study included the exact length and symmetry of the clefts before and after surgery and complete follow-up information. There was some bias in the selection of cases for surgery related to the severity of concurrent disease conditions such as pneumonia and economic factors or expectations of the owners. These limitations made it difficult to draw clear conclusions from the data relating to case selection and prognosis. The low number of cases with long-term follow-up made it difficult to determine significant associations between outcomes and the factors that affect both survival and athletic ability.

Horses with cleft palate in the present study had a higher survival rate to discharge from the hospital, longer term survival after discharge when follow-up was available, and a lower complication rate than previously indicated. Furthermore, results suggested that in some cases, surgery may not be required to obtain either an athletic horse or an outcome that is perceived as successful by the owner. The importance of the findings and their role in the decision to manage a case surgically versus conservatively warrants further investigation. A prospective study with improved information on the length of the cleft palate at admission, length of the cleft following dehiscence, and follow-up information on the athletic outcome would contribute greatly to our understanding of this condition.

a.

Robertson JT, Ducharme NG. Dorsal displacement of the soft palate (oral presentation). Equine Upper Airway Symp, Lexington, Ky, 2008.

b.

Bloodstock Research Information Service [database online]. Lexington, Ky: Equibase Co LLC, 2008. Available at: www.brisnet.com/secure-bin/brisclub/pedigree/sbs.cgi. Accessed Dec 10, 2008.

c.

USTA PATHWAY [database online]. Columbus, Ohio: United States Trotting Association, 2008. Available at: pathway.ustrotting.com/online-reports/horse/bp_detail.cfm?horse_id=40863. Accessed Dec 9, 2008.

d.

JMP, version 9.0, SAS Institute Inc, Cary, NC.

References

  • 1. Gaughan EM, Debowes RM. Congenital diseases of the equine head. Vet Clin North Am Equine Pract 1993; 9: 93110.

  • 2. Jones RS, Maisels DO & De Geus JJ, et al. Surgical repair of cleft palate in the horse. Equine Vet J 1975; 7: 8690.

  • 3. Semevolos SA, Ducharme N. Congenital cleft palate in horses. Available at: www.aaep.org/health_articles_view.php?id=56. Accessed Nov 13, 2007.

    • Search Google Scholar
    • Export Citation
  • 4. Platt H. Etiological aspects of perinatal mortality in the Thoroughbred. Equine Vet J 1973; 5: 116120.

  • 5. Mason TA, Spiers VC & Maclean AA, et al. Surgical repair of cleft soft palate in the horse. Vet Rec 1977; 100: 68.

  • 6. Semevolos SA, Ducharme N. Surgical repair of congenital cleft palate in horses: eight cases (1979–1997), in Proceedings. 42nd Annu Meet Am Assoc Equine Pract 1998;267268.

    • Search Google Scholar
    • Export Citation
  • 7. Kirkham LE, Vasey JR. Surgical cleft soft palate repair in a foal. Aust Vet J 2002; 80: 143146.

  • 8. Bowman K, Tate L & Evans L, et al. Complications of cleft palate repair in large animals. J Am Vet Med Assoc 1982; 180: 652657.

  • 9. Sullivan EK, Parente EJ. Disorders of the pharynx. Vet Clin North Am Equine Pract 2003; 19: 159167.

  • 10. Nelson AW, Curley BM, Kainer RA. Mandibular symphysiotomy to provide adequate exposure for intra oral surgery in the horse. J Am Vet Med Assoc 1971; 159: 10251031.

    • Search Google Scholar
    • Export Citation
  • 11. Ducharme NG. Pharynx. In: Auer JA, Stick JA, eds. Equine surgery. 3rd ed. Philadelphia: WB Saunders Co, 2006;560564.

  • 12. Crowe MW, Swerczek TW. Equine congenital defects. Am J Vet Res 1985; 46: 353358.

  • 13. Bowman KF. Cleft palate. In: Robinson N, ed. Current therapy in equine medicine 2. Philadelphia: WB Saunders Co, 1987;13.

  • 14. Bowman KF, Lloyd PT, Robertson JY. Cleft palate. In: White N, Moore J, eds. Current practice of equine surgery. Philadelphia: Lippincott, 1990;277280.

    • Search Google Scholar
    • Export Citation
  • 15. Nelson AW, Curley BM, Kainer RA. Mandibular symphysiotomy to provide adequate exposure for intraoral surgery in the horse. J Am Vet Med Assoc 1971; 159: 10251031.

    • Search Google Scholar
    • Export Citation
  • 16. Haynes PF, Qualls CW Jr. Cleft soft palate, nasal septal deviation, and epiglottic entrapment in a Thoroughbred filly. J Am Vet Med Assoc 1981; 179: 910913.

    • Search Google Scholar
    • Export Citation
All Time Past Year Past 30 Days
Abstract Views 187 0 0
Full Text Views 728 598 241
PDF Downloads 1137 248 30
Advertisement