- Cleft lip and cleft palate are congenital deformities caused by failure of facial structures to fuse properly during development in utero. - The document discusses the epidemiology, classifications, embryology, etiology, pathophysiology, associated conditions, timing of surgery, anesthetic concerns, and postoperative care for patients undergoing cleft lip and cleft palate repair surgery. - Key anesthetic considerations include the patient's young age, potential for a difficult airway, risk of multiple surgeries, shared airway with the surgeon, and potential for associated congenital anomalies.

1. ANESTHESIA FOR
CLEFT LIP
& CLEFT PALATE
- DR ABHISHEK SINGH

2. INTRODUCTION
• Definition : Unilateral or bilateral fissure in the upper lip and/or soft palate
(may extend into hard palate) due to failure of fusion of maxillary and
medial & lateral nasal processes
• MC type of craniofacial deformities worldwide

3. EPIDEMIOLOGY
• Incidence : 1 in 1000 live births forCleft lip (CL)
1 in 2500 LBs forCleft palate (CP)
• Isolated CL – 25%
• Isolated CP – 25%
• Combined CL+CP (CLP) – 50%
• CL & CLP is more common in males, while CP is more common in females

4. CLASSIFICATIONS
I. Veau’s classification
A) Cleft lip
Class I : U/L notching of vermillion border, not extending into the lip
Class II : cleft extending into the lip, but not including the floor of the nose
Class III: cleft extending into the floor of the nose
Class IV: any b/l cleft of the lip, whether incomplete or complete

5. B) Cleft palate
Class I : soft palate
Class II : soft/hard palate, extending no further than incisive foramen
Class III: complete unilateral cleft, extending from uvula to incisive foramen,
then deviating to one side
Class IV: two clefts extending forward from the incisive foramen into the
alveolus

6. II. Kernahan and Stark’s classification
1. Clefts of structures anterior to the incisive foramen
2. Clefts of structures posterior to the incisive foramen
3. Clefts affecting structures anterior and posterior to the incisive foramen
III. Nagpur classification
Group I – cleft lip only
Group Ia – cleft lip + cleft alveolus
Group II – cleft palate only
Group III – cleft lip + cleft alveolus + cleft palate

7. IV. LAHSHAL classification
LAHSHAL is a paraphrase of the anatomic areas affected by cleft
• L – lip
• A – alveolus
• H – hard palate
• S – soft palate
• H – hard palate
• A – alveolus
• L – lip

8. TYPES OF CLEFTS
A) CL
• U/L or B/L
• Complete (lip, nasal floor, alveolus) or
Incomplete (lip only)
B) CP
• U/L or B/L
• Primary/Prepalatal (anterior palate, alveolus, lip, nostril floor, alae nasi) or
Secondary/Postpalatal (posterior to incisive foramen)
• Complete or Incomplete

9. EMBRYOLOGY
• Development of facial structures starts @ end of 4th week
• 5 facial prominences around stomatodeum
Unpaired frontonasal process
Paired maxillary prominences
Paired mandibular prominences
• Frontonasal process gives rise to medial & lateral nasal processes

10. • In following 2-4 weeks:
- 2 Medial nasal processes fuse in midline – upper lip
- Mandibular processes fuse in midline – lower lip
- Frontonasal process – bridge of the nose
- Medial nasal process – tip of nose and philtrum of upper lip
- Lateral nasal process – ala of the nose
- Maxillary and medial nasal process fuse – primary palate
- 2 outgrowths from maxillary prominences c/as palatine shelves fuse –
secondary palate

11. ETIOLOGY
• Exact etiology unknown
• Multifactorial origin with genetic and environmental influences
• Familial: affected parents have a 3-5% chance of an affected child, and with
one affected child, sibling risk is 20-40%
• Monozygotic twins show the same defect in 40-50% of cases, but only 5% in
dizygotic twins.
• Some cases may result from mechanical obstruction by tongue position,
structural hypoplasia

12. • Environmental factors:
- Maternal smoking or tobacco exposure
-Viral infections (Rubella)
- Poor nutrition
• Teratogenic drugs - Steroids, Mercaptopurine, Mtx,Valium, Dilantin,
Anticonvulsants (phenytoin, BZD), Salicylates
• The risk increases with rising maternal and paternal age
• Folic acid 400 mcg/day has a role in preventing CLP

13. PATHOPHYSIOLOGICAL FEATURES
• Difficulty in
- Feeding since birth
- Suckling
- Swallowing
- Phonation
• Abnormal dentition
• Inadequate weight gain,
nutritional deficiencies, anemia
• Chronic URTI
• Regurgitation of fluid & food
predispose to LRTI and ear
infections

14. ASSOCIATED CONDITIONS
• 70% - isolated cleft defect, 30% - syndrome
• >200 syndromes/sequences associated
• Additional abnormalities are most likely a/w isolated CP and least likely with
isolated CL
• Craniofacial abnormalities are most common, f/b CNS abnormalities e.g.
mental retardation and seizures, congenital cardiac disease, renal and
abdominal defects

16. WHENTO UNDERGO SURGERY
• CL – ASAP (usually 3 months)
• Soft palate – 12-15 months
• Hard palate – 4-5 yrs
• No active infection
• No decompensated heart disease
• Rule of 10 : Hb >10
TLC <10000
>10 lbs for CL, >10 kgs forCP
• NOTE : Lip is repaired first as it decreases the width of palate defect

17. • CLP patients are likely to require further surgery either for plastic
improvements or for associated abnormalities. Around 20% will require
pharyngoplasty for velopharyngeal dysfunction at around 4-6 years
• Primary palatoplasty disrupts normal palate growth and despite orthodontic
treatment, some will require significant maxillofacial surgery in their teens
to correct midface hypoplasia and maxillary retrusion

18. ANESTHETIC CONCERNS
1. Young age
2. Difficult airway
3. Repeated surgeries
4. Shared airway
5. Associated congenital anomalies

19. PREOPERATIVE ASSESSMENT
• HISTORY:
General - Birth history, developmental milestones, vaccination status
Symptomatic - Recurrent infections, associated congenital heart defects,
breathing/feeding difficulties
• EXAMINATION:
General, identify associated congenital defects
Airway evaluation, location & size of defect
• INVESTIGATIONS:
CBC, Urine (R/M), CXR, X-ray mandible, Echo, As per associated anomalies

20. COPUR INDEX

21. PREOPERATIVE PREPARATION
• Blood typing & cross matching
• Antibiotic prophylaxis
• Avoid sedative premedication if difficult airway anticipated
• Oral atropine (0.02 mg/kg) – 45 minutes prior to induction
• Difficult airway cart
• Standard ASA NPO guidelines

22. INDUCTION
• ASA monitors
• Propofol + Fentanyl + MR
• Anticipated difficult airway – Sevoflurane + N2O
• In patients with hypoplastic mandibles or wide cleft palate , tongue can prolapse
into nasopharynx leading to airway obstruction during the induction of anaesthesia
• During laryngoscopy, place lubricated dental roll/gauze in the cleft to prevent
trauma to underlying tissue
• RAE (South pole) tube, Oxford tube, Armored tube
• Coventional laryngoscopy fails –Video LS, FOI, Lightwand
• Throat pack
• Check ET tube position after positioning, following insertion & opening of mouth
gag

23. MAINTENANCE
• Iso/Sevo + N2O + Fenta +Vec/Atra
• Fluid – RL, Holliday-Segar formula
• Normothermia, normocapnia, homeostasis
• Surgeons use Adrenaline – ensure dose/concentration (1 ml/kg of 1:200000)
• Remove throat pack at the end & examine oral cavity for edema or bleeding
• At the end of the surgery, the pharynx and the oral cavity s/b gently
suctioned, if possible under vision using the laryngoscope
• Do not exert pressure on the suture line
• Avoid insertion of OPA/NPA

24. EXTUBATION
• AWAKE
• Postpone if any evidence of swelling of tongue/uvula
• Nurse in lateral or prone position
• Head should be kept in dependent position, turned to the side and extended
• In this position, the blood or mucus will be drained out without any risk of
aspiration

25. POSTOPERATIVE PERIOD
COMPLICATIONS
i. Airway obstruction – 6% overall, 25% if any congenital anomaly +nt
ii. Bleeding
iii. Hypothermia
iv. Tongue edema
v. Flap edema
vi. Subglottic edema
vii.Mucosal swelling of hypopharynx

26. Causes ofTongue Edema:
 Venous stasis
 Hematoma formation
 Ischemia
 Necrosis
To reduce the incidence of tongue swelling during surgery , the gag s/b
released every 60-90 min to allow for tongue perfusion .

27. POST-OP ANALGESIA
A) SYSTEMIC:
• Paracetamol – 15 mg/kg PO as a premedication
30 mg/kg PR post induction
• Opioids - Morphine (0.1 mg/kg - 0.2mg/kg iv), Meperidine, Fentanyl
• Diclofenac suppository 1 mg/kg, 12 hourly
• NSAIDS – Ketorolac, Ibuprofen (avoided for 12 h post-operatively)
B) LOCAL infiltration

28. C)REGIONAL:
• CL -
1. Infra-orbital nerve block (post induction or post repair)
2. External nasal nerve block
• CP -
1. Greater palatine nerve block
2. Lesser palatine nerve block
3. Nasopalatine nerve block
4. B/L maxillary nerve block

29. IN PROGRESS
• The timing and the type of surgery have been hugely debated over the
recent years
• The advantages of fetal wound healing are being explored with
experimental evidence, suggesting in-utero surgery for cleft lip and palate
repair provides superior wound healing without scarring

30. THANKYOU…!!!