Clinical overview
Cleft palate: ENT care must address airway safety, feeding, hearing and speech alongside the specialist cleft team's reconstructive, dental and developmental plan. A repaired palate does not end the need for otological or airway follow-up.
The incisive foramen separates primary palate anteriorly from secondary palate posteriorly. Describe the lip, alveolus, hard palate and soft palate separately, including side, completeness and any submucous defect.
Key concepts
Palatal muscles: Levator veli palatini forms the functional palatal sling for velopharyngeal closure; tensor veli palatini is central to active Eustachian tube opening. Abnormal muscle attachments help explain both speech and middle-ear problems.
Submucous cleft palate: A bifid uvula, zona pellucida and posterior hard-palate notch suggest submucous clefting, but symptoms and dynamic function determine its significance.
Adenoidectomy: The adenoid pad can contribute to velopharyngeal contact. Removing them can reveal or worsen velopharyngeal insufficiency; routine adjuvant adenoidectomy is inappropriate when palatal assessment is abnormal. NICE NG233
Hearing assessment: Confirm type, degree and functional impact, and keep surveillance for retraction and cholesteatoma after palate repair.
Airway obstruction after speech surgery: Assess sleep-disordered breathing before and after procedures that improve velopharyngeal closure. Pharyngeal narrowing may improve resonance while causing OSA.
1. Classification and mechanisms
Frequency and inheritance: Orofacial clefting occurs in approximately 1 in 700 births, with variation by population and cleft type. After one child with apparently nonsyndromic clefting, an approximate 2% to 5% recurrence estimate requires refinement by the pedigree and phenotype; a defined genetic diagnosis has its own inheritance pattern.
Facial development involves a frontonasal prominence and paired maxillary and mandibular prominences. Lip and primary-palate formation precede fusion of the secondary palatal shelves; failure of these stages produces different cleft patterns.
More detail
First-arch development begins around week 4. Lip formation occurs mainly during weeks 4 to 6; secondary-palate development starts around week 6 and fusion is completed over subsequent weeks, by approximately week 12.
Veau group | Extent |
|---|---|
I | Soft palate only |
II | Hard and soft palate, posterior to the incisive foramen |
III | Unilateral complete cleft involving the palate and alveolus, usually with the lip |
IV | Bilateral complete cleft |
Veau does not adequately describe isolated cleft lip. LAHSHAL records lip, alveolus, hard palate, soft palate, then the corresponding left-sided structures; document completeness using the centre's recording convention.
In cleft palate, the levator fibres can run longitudinally into the cleft margin rather than forming a transverse sling. Functional repair repositions the muscle and closes nasal and oral layers without excessive tension.
In submucous clefting, the muscle defect is covered by mucosa. Some children have no velopharyngeal symptoms and do not require palatal surgery; others present with hypernasality, nasal escape or regurgitation.
Robin sequence involves micrognathia, glossoptosis and resulting upper-airway obstruction; a cleft palate is commonly associated. Consider syndromic associations, especially Stickler syndrome, rather than treating the sequence as an isolated palatal finding.
2. History and examination
Airway and sleep: stridor/stertor, work of breathing, apnoea, cyanosis, sleep quality, snoring and previous airway support. Micrognathia and glossoptosis can cause immediate or evolving obstruction.
Feeding and growth: latch, feed duration, intake, nasal regurgitation, coughing/choking, chest infections and weight trajectory. Difficulty forming suction does not imply that swallowing is absent; assess both feeding efficiency and airway protection.
Hearing and ears: newborn screen, subsequent testing, fluctuating or persistent hearing difficulty, discharge, grommets and hearing devices. Ask about language access and listening at nursery/school.
Speech: hypernasality, audible nasal emission, weak pressure consonants, compensatory articulation and intelligibility. Establish developmental progress and the effect on participation, not simply whether the palate looks closed.
Palatal examination: With illumination and a tongue depressor as tolerated, inspect the lip, alveolus, hard and soft palate and uvula. Look for a fistula, bifid uvula, translucent midline or palatal tenting on phonation; gently palpate the posterior hard-palate margin for a notch. Assess symmetrical elevation while the child phonates. A normal surface does not exclude a muscular defect.
Craniofacial examination: Assess the jaw, nasal airflow and asymmetry, dentition and cranial nerve function. Inspect the pinnae and canals for microtia, pits or tags; examine both tympanic membranes for effusion, retraction pockets, perforation or discharge.
More detail
In a unilateral cleft lip/nose, the cleft-side alar base is often displaced laterally and inferiorly, with a flattened dome. The anterior septum and columella tend toward the non-cleft side, while posterior bowing can narrow the opposite nasal passage. Record the actual obstruction and deformity rather than inferring it from the cleft label.
Review family history and associated cardiac, ocular, skeletal, renal, neurological or immune findings. Lower-lip pits suggest Van der Woude syndrome; palatal dysfunction with cardiac or other characteristic features raises concern for 22q11.2 deletion. Assess for Treacher Collins, Goldenhar and CHARGE when the craniofacial or associated-system findings suggest them. Involve clinical genetics for a defined syndrome, multiple anomalies, familial disease or recurrence counselling.
Antenatal history: Ask about smoking, alcohol, maternal diabetes, nutrition and exposure to retinoids, anticonvulsants or other potentially teratogenic medicines. Thalidomide and folate deficiency are recognised historical associations; review an exposure with obstetric/genetics services rather than inferring causation in an individual child.