Cleft Palate

Also known as:

Congenital oronasal fistula Palatoschisis

A congenital cleft palate defect (Courtesy of Alun Williams (RVC))

Description

An abnormal communication between the nasal and oral cavities involving the soft palate , hard palate, premaxilla and or lip . Abnormalities arise during foetal development where there is incomplete closure of the primary palate, secondary palate or both. The primary palate develops into the premaxilla and lip. If closure is not complete this will result in a primary palate or cleft lip(harelip). The secondary palate forms the hard and soft palate and incomplete closure of either of these results in a secondary palate or cleft palate.

Signalment

Dogs are more commonly affected than cats. In particular brachycephalic breeds are more commonly affected. Other at risk breeds include, Boston terriers, Pekingese, minature schnauzers, beagles and cocker spaniels. Siamese are the most commonly affected cat breed. Present at birth but not always noticed straight away. In large animals, cleft palate has been reported in foals, calves, lambs and kids. The primary cause of this condition is often hereditary but maternal nutritional deficiencies, toxins and viral exposure have also been implemented.

History and Clinical Signs

Failure to thrive with signs such as nasal discharge, nasal milk regurgitation, gagging, coughing or sneezing during nursing, and respiratory infection due to aspiration pneumonia or rhinitis.

Diagnosis is made on physical exam. A cleft lip can be easily identified however a full oral examination is needed to diagnose incomplete closure of the premaxilla, hard and soft palate. In some instances anaesthesia may be required to diagnose a soft palate problem. If a primary palate problem is recognised always check for a secondary problem. Increased noise over lung fields may be heard if aspiration pneumonia is present. Affected animals often have other concurrent congenital abnormalities and hence a thorough physical exam should be undertaken.

Laboratory Tests

Often normal unless aspiration pneumonia is present.

Radiography

Radiographs of the skull are unnecessary however thoracic radiographs are useful to check for the presence of aspiration pneumonia.

Treatment

A large proportion of animals with primary or secondary palate defects die or are euthanased. In some cases however the defects can be managed medically until the patient is old enough for surgery.

Affected animals should fed via a feeding tube to avoid aspiration pneumonia until surgery can be undertaken. Aspiration pneumonia should also be treated with appropriate antibiotics, expectorants and oxygen. Surgery should be delayed until the animal is 12-14 weeks old or longer if possible in order to get the best possible post surgical outcome. More mature tissue is less friable and holds suture better. Surgical correction is normally only carried out if the defect is small and owners must be warned that more severly affected animals may need multiple procedures.

Hard palate defects

Three procedures have been described the Lagenbeck or sliding pedicle technique whereby longitudinal strips of mucosa are released from the hard palate and slid together at the midline. Hard palate bone is exposed laterally however granulation and epithelisation occur quickly. The second technique is the Sandwich or overlapping flap technique where by a donor bed is created by releasing strips of mucosa from the opposite thirdly a combination technique can be applied where both of the above tecniques are used to produce a double layer of mucosa over the cleft.

Prognosis

• The commonest structural defect is probably the various forms of cleft palate due to:
  • failure of fusion and the ingrowths of the palatine shelves or
  • frontonasal and maxillary processes.

Also known as Palatoschisis

- aspiration pneumonia is a common sequel