INTRODUCTION
Facial clefting is the most common congenital malformation
affecting the head and neck. Clefts can involve the
lip, the soft or hard palate, and can vary from a
minor notching of the lip or duplication of the uvula
to a complete defect that involves the entire lip
and palate. The lip is not only an important cosmetic
feature of the face, it also has functional significance
in accurate speech and feeding.
A facial cleft may be unilateral or bilateral,
with the more severe lesions tending to be bilateral
and the relatively minor anomalies unilateral. The
majority of clefts are isolated, but some, particularly
the large bilateral clefts are associated with underlying
causes, the most well recognised of which are the
lethal trisomies 13, and 18. Under such circumstances
however, the facial cleft may be less significant
than the accompanying abnormalities.
Isolated cleft lip and/or palate evolve from a
combination of genetic and environment influences.
There is an increased risk if a sibling or parent
is affected, implying a genetic influence in some
families. Teratogens such as alcohol, tobacco (which
may be increasingly relevant as the number of young
women smokers is on the increase), vitamin A and
certain drugs such as anti-epileptics are known to
be aetiological factors in a minority of facial clefts.
Cleft lip can occur with or without cleft palate
and has a different aetiology from an isolated cleft
palate as the embryological origin of the two facial
clefts are different. Abnormal development of the
primary palate leads to cleft lip but also may interfere
with the development of the palate leading to combined
cleft lip/palate. The development of cleft palate
occurs as a later event during formation of the secondary
palate and the lip does not become involved.
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ANTENATAL
Ultrasound imaging can be used to diagnose cleft
lip and to a more limited extent cleft palate as
the hard palate is difficult to visualise and so
diagnosis is uncertain. The prenatal diagnosis of
isolated lesions can be difficult and careful ultrasound
surveillance is required. In some series of apparently
isolated lesions, up to 20% are subsequently found
to have associated anomalies. The diagnosis of cleft
lip may be made by ultrasound by 13 weeks and of
cleft palate by 18 weeks but is usually made at 20
weeks at the mid trimester scan.
Identification of a cleft may prompt a karyotyping
procedure to exclude any underlying chromosome defect,
especially if a bilateral or midline cleft is seen.
In the majority of fetuses affected by a lethal trisomy
there will be additional structural abnormalities
that can be diagnosed on ultrasound then the survey
should include the heart, a search for intracranial
anomalies and for amniotic bands.
Although experimental, in-utero surgery
has been attempted for cleft lip and palate, the
only perceived advantage is the improved healing
and reduced scarring. The major disadvantage is the
risk of preterm labour and the associated perinatal
and maternal morbidity and mortality.
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POSTNATAL
Treatment of facial clefts has improved over recent
years, not only with advances in surgical care but
also with the development of a multidisciplinary
approach to ensure that continued care is provided
from infancy through to adult life. The initial care
of the neonate involves establishing satisfactory
feeding, and this depends upon the severity of the
lesion, the gestation at delivery and the wishes
of the parents. Most babies can be breast-fed, or
bottle fed with breast milk with minor adaptations
to normal methods. The premature baby can present
difficulties as the suckling reflexes are poorly
developed, and this may require tube feeding initially.
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WEST MIDLANDS
DATA
To be added
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