Cleft palate

Cleft palate is a condition in which, for genetic and/or environmental reasons, the hard surface of the roof of the mouth and the softer palate behind it fail to close completely. The first sign something is wrong (if you don't examine your pups immediately after delivery) is usually milk bubbling out the nose when the newborn attempts to nurse. In addition to strictly genetic cause, there are numerous other cases of environmentally-mediated cleft palate. It is a frequent defect found in offspring of diabetics. It has been produced experimentally by vitamin A imbalance whether too much or too little, and is often a result of poisons and steroids taken or produced by bitches in the first three weeks of gestation. Such corticosteroid production increase frequently can be associated with unsound character and/or a severe scare (fright). In canines, a deficiency of vitamin B-12 has also been identified as a cause. Antihistamines given early in pregnancy, at least in some doses, are also suspect. Viral infections at that stage, or certain other chemicals have also been determined to cause cleft palate. It is  believed that natural or synthetic hormones and steroids are potentially very dangerous if given to bitches during pregnancy; most of the time, cleft palate is a steroid caused birth defect. Cortisone and similar steroids can also facilitate spontaneous bleeding, which is more perilous during whelping and surgical convalescence than at other times.
 

Description
Cleft palate is commonly seen by veterinarians in dogs. Unfortunately many neonates with this disorder die early or are destroyed by the breeder so accurate statistics on the true incidence of the disease are not available. 

Defects (clefts) in the hard palate that forms the roof of the mouth, or the soft palate which lies caudally  and separates the oropharynx from the nasopharynx may be congenital or acquired. The cleft can involve the soft palate alone, the hard palate alone or both. The defect can be bilateral (ie involve tissues lying both sides of the midline) or unilateral. The latter are usually seen in the soft palate.

Congenital cleft palate is an abnormality which is thought to occur during fusion of the maxillary process with the medial nasal process, when the mesodermal fusion develops across the fused epithelial surfaces. If the epithelial barrier does not degenerate or if the mesodermal connective tissue is deficient cleft palate results. 

Acquired clefts are due to trauma - usually road traffic accidents or falls from a height.

Cause
There are several possible causes for congenital cleft palate:

a) Genetic cause

An hereditary basis for the disease is suspected for congenital clefts but the mechanism has not yet been determined. Any such genetic trait  is thought to be multifactorial recessive, polygenic and dominant with partial penetration. Assuming the trait is polygenic it means  it does not have a single-gene mode of inheritance.

b) Excess vitamin A intake during pregnancy

In 1967 Wiersig and Swenson reported that 125,000 IU of Vitamin A per kilogram body weight given to Beagle bitches on days 17-22 of gestation resulted in cleft palate developing in their puppies.

Vitamin A is an essential nutrient for normal growth and defects in bone growth are seen with insufficient as well as excessive dietary intake.  Vitamin A has a controlling influence over both the osteoblasts and osteoclasts in epithelial cartilage and so there is a rational explanation as to why excessive vitamin A intake might result in cleft palate.

In addition, commercially prepared complete pet foods contain more than sufficient available vitamin A yet breeders and owners frequently supplement their pet's ration with vitamin supplements. High vitamin A content is also a feature of many natural food sources including liver and fish oils. Cod liver oil is a very popular nutritional supplement with pet owners and it contains 18000mg per 100ml (4000 IU per gram). Some vitamin injections contain as much as 500,000 IU of vitamin A per ml.

c) Cortisone 

Administration of cortisone during pregnancy can lead to the development of cleft palate in the fetus.

d) Hydroxyurea

Administration of the cytotoxic drug hydroxyurea (hydroxycarbamide) is reported to cause cleft palate.

Acquired cleft palate is common following falls from a height, and less commonly following road traffic accidents.

Breed Occurrence
The following breeds of dog have been reported to have cleft palates : mixed and small terrier breeds, Beagle,  Bernese Mountain Dog, Boston Terrier, Bullmastiff, Bull Terrier, Chihuahua, Cocker Spaniel, Collie, Dachshund, English Bulldog, German Shepherd Dog, Golden Retriever, Miniature Schnauzer, Norwegian Elkhound, Pekingese, Shih Tzu, Staffordshire Bull Terrier, Toy Poodle Wire-haired Fox Terrier, 

Brachycephalic breeds are reported to have about 30% risk, whereas German Shepherd Dogs have the lowest risk.

Signs
There is a visible split in the roof of the mouth or the soft palate. This results in food material (particularly fluids) passing into the nasal cavity and the following signs :

Bronchopneumonia accounts for 30% of deaths due to cleft palate.

Cleft palate is sometimes associated with congenital deformities in other body systems.

Complications
Inhalation of foods leading to aspiration pneumonia - and death

Diagnosis
Diagnosis is based on the clinical signs and careful visual examination of the oral cavity. Fine-line fissures sometimes occur in the hard palate in the midline of the roof of the mouth following trauma such as road traffic accidents or falls from a height. These can be difficult to detect unless a careful examination is made.

Consider excess dietary vitamin A intake as a possible cause for congenital cleft palate when it occurs and review the mothers nutritional history

 

Treatment

Prevention
For the prevention of congenital cleft there  are the following  recommendations :

The most important factor would appear to be looking very carefully at the pedigrees of pups born with cleft palate. Obviously the parents should not be bred with each other again, nor with any other mate that has a history of cleft palate in its background. Also, as far as possible, avoid breeding dogs that have common ancestors in the last few generations. Breeding close relatives will greatly increase the risk of any heritable condition occurring in the offspring.

 

Treatment
Surgical repair of acquired lesions, and closure of congenital defects is recommended. In all cases surgery should be performed as soon as possible before secondary complications occur.  

Severe defects may be very difficult or even impossible to repair and in severely affected neonates euthanasia should be considered. Mild openings in the mouth roof can be surgically corrected.

If both the hard palate and soft palate are involved the hard palate should be closed first, followed by the soft palate. If necessary two separate procedures should be performed.

Most techniques involve the use of a flap taken by undermining the tissue on one or both sides of the defect and suturing them together. Techniques using artificial prostheses to close large defects have also been described in the literature, but these are not readily available and rejection is a common problem.

It is important to :

Prognosis
Good for minor defects. Guarded to poor for severe defects. Poor once secondary complication of inhalation pneumonia has developed

Long term problems
Respiratory infections