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Craniofacial - Pediatric > Cleft Palate > Flashcards

Cleft Palate Flashcards

1
Q

what is the epidemiolgy of CP?

A

CP is a separate epidemiological entity from CL and CLP (which are on a spectrum)

  • Overall CP is 1:2000, no race distinction
  • most common cleft is bifid uvula 2/100
  • this is in contrast to CL/P 1:1000 with race distinctions (higher in asian, less in africain)
  • CP more common in GIRLS 2:1
  • Opposite is true for CL/P
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2
Q

What is the timing + prominences involved in embryologic developement of CP

and pathogenesis of CP

  • for primary palate
  • for secondary palate
A

Palatogenesis week 4-12

  • Wk 4, MNP and LNP form from the FNP
  • Wk 4- 6; MxP and MNP and LNP FUSE to form the primary palate and lip - fusion from posterior to anterior
    • failure of fusion at wk 6 leads to cleft of 1’ palate+cleft lip/alveolus
  • Wk 6: MxP forms vertical shelves which lie adjacent to tongue = Lateral palatine Processes (LPP)
  • wk 7: as neck extends, tongue descends, mandible moves forward and LPP ELEVATE horizontally to be dorsal to tongue . R shelf before L shelf = ADHESION and CONTACT between the shelves
  • FUSION between shelves with apoptosis of epidermis and mesenchymal penetration - fusion from anterior to posterior
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3
Q

What is the arterial supply and nerve supply to the hard palate and soft palate

A

Hard Palate

Artery: Greater Palatine Artery

Nerve: Sensory - GPn via V2

Soft Palate

Artery: AScending Palatine (most important from facial), Lesser Palatine, Ascending pharyngeal, recurrent pharyngeal

Nerve: Motor: 9,10 (all velar muscles PP, PG, Mus.Uvalae, Sup. Constrictor, LVP) EXCEPT TVP by CV 5

Nerve Sensory: V2

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4
Q

What muscles are more important VeloPharyngeal competance

A

LVP

Superior constrictor

Musculus uvulae

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5
Q

Name the muscles of the soft palate and their function

A
  • LVP (9,10) - elevate velum superior and posterior, E tube dilatation
    • O: petrous bone, Etube
    • I: midline velum, at midpoint
  • TVP (5) - dilate Etube
    • O: Etube, Sphenoid, pterygoid process
    • I: paaltine aponeurosis, in anterior 1/3 of velum)
  • Musculus Uvulae (9,10) - elevates uvula
    • O: palatine aponeurosis
    • I: posteriro Connective tissue
  • Superior Pharyngeal constrictor (9,10) - move lateral pharyngeal walls medially
    • O: midline raphe
    • I: pteryogomandibular raphe
  • Palatoglossus (9,10) - elevate tongue
    • O: palatine aponeurosis
    • I: anterior tonsillar pillar and tongue
  • Palatopharyngeus (9,10)- depress velum, pull inferior pharynx upward
    • O: palatine aponeurosis
    • I: posterior tonisillar piallar, lateal/posterior pharyngeal wall
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6
Q

List the aberrant anatomic features of the cleft Palate (Bone, muscle, fascia)

A
  • Fascia
    • no palatine fascia on cleft side
  • Bone
    • Vomer: failed fusion with palatine shelves
      • Unilat CLP - Vomer atatched to non cleft palate shelf fro entire length
      • Bilat CLP - Vomer only attached aneriorly at premaxilla
      • Isolated CP - vomen atatched as far atnerio as is start of cleft
  • Muscle
    • LVP - orgin same, insertion - runs parallel and along medial margin of cleft (with PG, PP). Can be separated from tensor white fibers
    • TVP - origin same - runs along hamulus but no palatine aponeurosis - instead has tendon insertion lateral to LVP/PP/PG at posterior palatine shelf
    • PP - inserts with PG and LVP at posterior edge of hard palate
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7
Q

How do you classify CP?

A
  • By Anatomy
    • Veau
    • Kernahan and stark Y
    • LAHSHAL
  • By Etiology
    • non-syndromic
    • syndromic
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8
Q

Describe the veau classificaiton of CLP

A

SP = 1

SP/HP = 2

Unilat CLP = 3

Bilat CLP = 4

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9
Q

Describe the Kernahan stark y classification

A
  • Classified according to embryology
    • Y point is incisive foramen to separate 1’ and 2 palate
  • 1/4 = lip
  • 2/5 = alveolus
  • 3/6 = HP anterior to incisve foramen
  • 7/8 - ant/post half of HP
  • 9 = SP
  • Millard added triangel for nasal deformity
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10
Q

What are causes/etiologies of CP?

A
  • Environmental
    • Meds (isotretinoin, diazepa, valproate/phynitoin, steroids
    • Smoking
    • Maternal infection (toxo rub CMV)
    • Nutrition (vit b6,a)
    • Alcohol
  • Non-syndromic (geenticcs+environmental)
  • Chromosomal
    • trisomy 21, 13
    • microdeletion 22q11 (digeorge, VCF, Conotruncal anomaly face syndrome)
  • Syndromic (VolkSWagon GT catching Pierre Klip Ed)
    • Van der woude
    • Stickler
    • Waardenberg
    • Goldenhar
    • Treacher collins
    • VCF CATCH - most common submucous cleft
    • EED - ectrodactyly, ectrodermal dysplasia clefting
    • Klippel Feil
    • PRS
      *
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11
Q

What is Velocardio facial syndrome

A
  • due to microdletion of 22q11
  • Clinical features
    • C- cardiac anomalie
    • A- abnormal facies
    • T- thymic aplasia
    • C-Cleft palate
    • H- hypocalcemia
  • Most common clefting syndrome
  • has medialized carotids

CARDIAC= VSD, TOF

Abn FACIES= long face w VME. flat zygoma, small alae, long lip and philtrum, retrognathia

Thymic aplasia = 10% of VCF have digeroge (3/4 BA devlopmental issue w thymic aplasia, hypoPTH, conotruncal anomalie)

CLEFT PALATE - most common submucous cleft (triad of bifid uvula, rdige notch in poseriro palate, decussation/diastasis of velar musculature

Hypocalcemia = low PTH

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12
Q

What percentage of CLP vs CP are syndromic and no syndromic?

A
  • CP is more likley syndromic
    • 40% of CP are syndromic
    • 15% of CLP are syndromic
  • CLP is more likely non-syndromic
    • 85% of CLP are non-syndromic
    • 60% of CP are non-syndormic
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13
Q

What is Klippel Fell syndrome

A

cogenital fusion of Cspine & CP

scoliosis, spina bifida

heart, renal, deformities

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14
Q

What are issues to address with parents once child with CP is born

A
  • Feeding
    • Haberman
  • Airway
    • mainly for PRS
  • Middle Ear disease
    • myringotomy+silastic/grommet tubes
  • Etiology (syndromic vs non-syndromic)
    • syndromic in 40% CP and 15% CLP
    • full Hx/PE, investigation heart/skeletal, renal
  • Sequelae of unrepaired CP
    • poor speech, facial growth disturbance
  • Treatment plan
    • prenatal - counseling, geentic/prenatal
    • birth-4wks - diagnosis, w/u for other abN, feednig, airway, orthodontics
    • 3-6month - 1’ lip
    • 9mth - prepalate ENT consult
    • 9-14 mths - 1’ palate
    • 2.5yo - Speech
    • 5-6yo - VPI/secondary lip/nose
    • 9-11 alveolar BG
    • Orthognathic/rhino - F 16 M 18
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15
Q

What is the predicted recurrence of another child with CLP/CP

A

Cleft Palate

  • 1child 2%
  • 1 parent 7%
  • 1 child and parent 15%

CLP

  • 1child 4%
  • 1 parent 4%
  • 1 child and parent 15%
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16
Q

What are 2 factors to consider in CP surgery

A
  • Speech
  • Facial growth
    • note; CP/CLP differ on affect of maxillary growth
      • alveolus repair restricts max growth but isolated palate repair doesnt
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17
Q

What are the goals of CP surgery

A
  • close cleft
  • recreate VP sphincter (for speech and feeding)
  • Improve Etube fux
  • minimize effect on facial growth and dentoalveolar growth
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18
Q

What are the adv/disad of performing the palate repair early (3-9mths) versus late

A

EARLY 3-9MTHS

  • Adv: less speech problem, less pharyngoplasty
  • DisAdv: technically harder b/c smaller, high rate A/W problems

MIDRANGE 9-14MTHS * AT HSC

  • adv/disadv of both

LATE (SP only ay 6-12mth + obturator) then HP at 6-14yr

  • Adv: less facial growth impedance
  • DisAdv: more problems with speech, hearing, chronic ear infection
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19
Q

What are surgical options for Repair of the Cleft Hard Palate

A
  • Von Lagenbeck
  • Veau-Wardill-Kilner “puch back”
  • Hybrid (Clarke)
  • Two-flap (Bardach)
  • No palatal insicions (Sommerlad)
20
Q

Describe briefly the technique and use of each HP cleft repair

A
  • Von lagenbeck
    • bipedicled mucoperiosteal flaps
    • Use: Complete CP
    • No lengthening, requires relaxing incisions ???higher VPI rate/poor speech
  • Veau WardillKIlner push back
    • axila MC flaps based on greater palatine artery
    • Use: Incomplete CP only
    • Lengthening achieved, high Max growth restriction b/c scarring of denuded bone ???hgihger fistula
  • Hybrid (Clarke)
    • bipedicled MC flap on noncleft isde and axial unipedicled VWK flap on cleft side
    • Use: Complete unilat
    • Lengthens cleft side
  • Two flap Bardach
    • similar to VWK unilat flaps except no puchback
  • Sommerlad
    • Superioyly based vomerine flap - single layer closure of hard palate
    • Use: complete unilat CP
21
Q

Describe technique of both options for repair of a cleft SP

A
  • Furlow Double opposing Zplasty
    • used for :
      • submous cleft
      • to lengthen palate
      • to correct VPI
    • Adv: restores normal anatomy
    • Disadv: difficul in wide clefts
  • Intravelar velopalsty
    • Used for any SP cleft
    • Used in conjunciton with HP repair
      • divide TVP and LVP muscle insertion at HP and recreate sling
22
Q

What are your treatemtn otions for a incomplete cleft of the SP

A
  • furlow
  • IVV
23
Q

What are your treatment options for an incomplete cleft of hard and soft palate

A
  • Von lagenbeck with med/lat relaxing incisions
  • Veau Wardill Kilner
  • Two flap Bardach

+ IVV or furlow

24
Q

What are your treatment options for a complete cleft palate that is unilateral and bialteral

A

Unilateral

  • Hybrid = Veau+VLb + Vomer + IVV
  • 2 flap bardach
  • Sommerlad
  • All with IVV

Bilateral

  • Veau= bilateral Veau, bilateral vomerine flaps, anterior V flap of 1’ HP AND IVV or furlow
25
Q

What are complications following cleft palate repair

A

EARLY

  • Hemorrhage (especially VWK)
  • Airway obstruction (tongue stitch, NP tube)
  • dehiscence
  • INfection
  • mortality

LATE

  • Palatal fistula
  • Poor speech outcome (1/3 have good speech, 1/3 need SLP, 1/3 need SLP + VPI OR)
  • Sleep apnea
  • disrupted facial growth
26
Q

Where are palatal fistulas located, how do they present and what is the etiology

A
  • Most commonly immediate post-alveolar or in HP
  • Most commonly assocaited w severity of cleft BCLP>UCLP>CP
  • Present w nasal crusting, nasal emissions, nasal regurg
  • Etiology
    • post- op - trauma, infection, hematoma, techqnieu
    • not yet repaired
27
Q

what options for treatment of Palatal alveolar fistula

A
  • Non-surgical - obturator
  • Surgical
    • two layer closure w
      • palatal ucoperiosteal flap
      • tongue flap
      • buccal flap
      • free flap RFF
28
Q

What is required for proper speech

A
  • airstream
  • functional VP sphincter
  • lip/tongue movement
  • normal occlusal/skeletal relations
  • normal hearing/intelligence
29
Q

What are features of a Cleft palate speech

A
  • Hypernasality
  • Difficulty with pressure consonants (fricative/plosive) and compensating for this
  • error in tongue and lip placement
  • Nasal emissions dugin consonants
30
Q

What are fricative and plosive consonents

A

Fricative

Th, V, F, S, Z, Sh

Plosive

P B K D T G

31
Q

How would you manage a patient presenting with VPI

A

History

  • FHx clefting/VPI
  • Nasal regurg/emission
  • ObSA (daytime sleepiness, snoring)
  • exercise intolerance, mouth breathing
  • Difficulty with hearnig, speaking
  • ear infections
  • Hx of SLP
  • PMHx, surgery, adenoidectomy/tonsillectomy

Exam

  • fistula, SMC, bifid uvula, tonsil/adenoid, denttiion

Nasoendoscoy

Radiography

32
Q

What is VPI?

A

Dysfunction of the velopharyngeal sphinter to close during speech/eating and open for nasal emissions

33
Q

How is VPI diagnosed?

A

Dx is made based on history (hypernasality, nasal regurg, compensatory articulations

Invstigations (abnormal closure pattern on nasoendoscopy or videofluoroscopy

34
Q

What is the etiology or DDX of VPI

A

STRUCTURAL

  • Palatopharyngeal mismatch (repaired cleft, tonil/adenoid removed, submucous clef)
  • abN Levator (submucous cleft)
  • oronasal fistula
  • adenoid/tonisl hypertrophy
  • tumor

FUNCTIONAL

  • developmental delay, hearing D
  • CNS paresis (infection mningitis/encephalitis), CP
35
Q

What investigations are done for VPI

A
  • nasometry
  • Nasoendoscopy
  • Video flurometry
  • Oral nasal acoustis radio
36
Q

What closure patterns are seen on nasoendosopy

A
  • coronal - velum closing
  • sagittal - lateral pharyngeal walls closig
  • circular - velum and lat pharyngeal wall
  • circular _ passavant ridge = all velum, lat wall and posteriro pharyngal wall
37
Q

What are options for management of VPI?

A

ALL OPTIONS REQUIRE SLP

Non-operative

  • obturator
  • paaltal lift

Operative

  • Lengthen/reconstruct soft palate
    • furlow
    • IVV
    • V-Y pusch back
  • VP narrowing procedure
    • pharyngeal flap
    • sphincter pharyngoplasty
    • posterior pharyngela wall augmentation
38
Q

How will you manage the VPI patient and based on what

A

Cloure rating and patterm dictate management**

Timing age 5-6

  • 2’ Furlow Palatoplasty - for closure rate >0.9 and small central defects
    • double opposing z plasty - to lengthen velum
  • Pharyngeal flap - for noncoronal closure patterns
    • superior based pharyngeal wall w superior pharyngeal constrictors are raised and secured to velum -
  • Sphicter pharyngoplasty - for coronal closure pattesm
39
Q

What are options for management of an alveolar bone cleft?

A
  • Presurgical orthotics (NAM) and gingivoperiosteoplasty
  • Alveolar bone grafting
    • primary age 0-2
    • secondary age 7-12
  • LeFort osteotomy 2piece
  • Distraction osteogenesis of palate (interdental)
  • Dental rehab (bridge/Osseointegrated implants)
40
Q

What are the pros/cons of NAM+GPP, ABG early vs late

A
  • NAM GPP- arches aligned until muscosa abutting. GPP stuulates bone growth
    • pro - reduced rate of needing 2’ ABG
    • con - may constrict arch w molding, GPP-stimulated bone of lesser quality, potential risk of tooth buds
  • primary ABG early ag 0-2 - after CL and before CP
    • pro - early closure of fistula, less time needed w orthotics
  • secondary ABG late 6-12 for mixed dentition and lat incisor eruption or 11-22 for canine eruption. Use ABG. Good for tooth movement, tooth eruption
41
Q

What is a submuous cleft

A

due to failure of fusion of velar musculature post palatal shelf fusion

42
Q

Classic triad of SMCP

A
  • bific uvula
  • notched hard palate
  • diastasis of velar musculature (zona pellucida
43
Q

What is the presentation and treatment of SMCP

A

50% have VPI,

Treatment - investigate for VPI and treatment as VPI

  • SLP and
  • non-op vs
  • op: furlow, push back V-Y, pharyngeal flap, sphincter pharyngoplasty
44
Q

What secondary deforities are CLP pateints at risk for

A
  • maxillary hypoplasia (Vertical hegith restriction and max arch constriction)
  • midface retrusion
  • class 2,3 malocclusion
  • lower face increased height
  • residual Oronasal fistula
  • nasal defomrities
45
Q

What are orthognathic options for correction of secondary CLP deformities

A
  • LeFort 1 (1 or 2,3 pieces) to correct malocclusion, midface/max hypoplasia/retrusion, close ORF, stbailize arches
  • Lefort 2/3
  • BSSO, genioplasty
46
Q
A

Craniofacial - Pediatric (4 decks)

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