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364
Manipal Manual of Surgery
Table 35.2 Reconstruction following resection of oral malignancy. Ca—carcinoma
Anatomic site of cancer Surgery Reconstruction
1. Ca lip (<2 cm) V or W excision Direct closure
2. Ca lip (large lesion) Wide excision Bernard rotational flap: Advancement flap
3. Advanced Ca lip Total excision of lip (chin also) Total lip reconstruction by using forearm flap
4. Small lesions lateral tongue Partial glossectomy Primary closure or secondary healing
5. Large defect tongue (>2 cm) Partial glossectomy Reconstruction by radial forearm flap
6. Advanced lesions tongue Total glossectomy Reconstruction by using rectus abdominus flap
7. Floor of mouth T1 or T2 Wide excision Radial artery forearm flap
8. Floor of mouth T3 or T4 Wide excision with removal of anterior Fibula flap or iliac crest graft—deep circumflex
mandible iliac artery (DCIA) is used
9. Buccal mucosa Wide excision with removal of underlying Direct closure or radial artery forearm flap
buccinator muscle also
10. Lower alveolus Wide excision with segmental resection Primary reconstruction with fibula flap for enentof mandible ulous mandible and DCIA for dentate mandible
LIP RECONSTRUCTION PICTURES (Figs 35.36 to 35.41)
Fig. 35.36: Karapandzic flap—used for defect up to
2/3rd of lip size
and texture match
Figs 35.39 to 35.41: Wide excision of lip followed by reconstruction using nasolabial flap [Courtesy: Dr Biswas, Dr JK Jha, Dr SP
Nayak, Chittaranjan National Cancer Institute (CNCI), Kolkata]
Section II • General Surgery
. Good functional result, good colour
Fig. 35.37: Estlander flap. Used
for lateral lip defects up to
1/3rd size. Good functional
result
Fig. 35.38: Abbe’s flap. Used for up
to 1/3rd lip defect. Can be modified
for both upper and lower lips. Produces
good functional and cosmetic result
Oral Cavity, Odontomes, Lip and Palate
365
CARCINOMA MAXILLARY ANTRUM (Key Box 35.16)
It is rare in Western countries but common in Asia. The
workers in furniture industries, chromic and nickel
industries are more prone for the development of
carcinoma maxillary antrum.
Ohngren’s Line
• Antral carcinoma can be divided by a line joining
medial canthus of eye to the angle of mandible. This
line is called Ohngren’s line.
• The region above the plane is suprastructure and one
below is termed infrastructure.
• Poor prognosis in suprastructure because of proximity
to skull base and pterygoid region.
• These suprastructure lesions as usually inaccessible
and unresectable.
Key Box 35.16
Carcinoma Maxillary Antrum
Majority are squamous cell carcinoma
Most important method of spread is contiguous spread
Early presentation is rare because maxillary antrum
serves no important function
Tissue diagnosis is by biopsy of the mass protruding
through nasal cavity/oral cavity or transnasal needle
through medial wall of the maxilla
CT scan for bone involvement and MRI for soft tissue
involvement are investigations of choice
Clinical Presentation (Table 35.3)
1. Growth originating on the floor of antrum may
result in bulge of the hard palate. This results in pain
in the teeth and they may become loose.
2. When medial wall is involved, nasal obstruction and
epiphora occurs due to obstruction of the lacrimal
duct. Bleeding from the nose can also occur, if there
is ulceration.
. If anterolateral wall is involved (Fig. 35.42),
3
asymmetry of the face results in pain in the cheek.
Anaesthesia over the skin of the cheek including
upper lip occurs due to
involvement of infraorbital nerve, a branch
of maxillary division of
the trigeminal nerve.
4. If the roof is invaded,
proptosis and diplopia
occurs.
5. Posterior extension of
the growth is difficult to
Fig. 35.42: Maxillary antral
carcinoma
assess clinically. When it involves the pterygoid
muscles, it results in trismus. Paraesthesia over the
cheek, gums, lower lip, postnasal discharge are the
other features of these tumours. They carry poor
prognosis because of late presentation.
Lymphatic Spread
Nodal metastasis is uncommon in sinonasal malignancies.
Investigations
. Computed tomography (CT scan) can define a lesion,
1
its extent, bony destruction, posterior extension, etc.
Hence, it is the first investigation of choice.
2. Sinoscopy: Fenestration will provide tissue for
biopsy followed by curettage to reduce the tumour
bulk and to drain necrotic contents outside.
Treatment
• Radiotherapy is the main modality of treatment in
carcinoma maxillary antrum. Curative rate is around
70% in early cases. In advanced cases, radiotherapy
is given first. This reduces the tumour bulk so that
an unresectable lesion becomes resectable and
maxillectomy can be done.
• Surgery can be done in the form of total maxillectomy
when the growth involves entire maxilla or it is of
high grade followed by postoperative radio-therapy.
• Tumours of the lower half of the antrum are treated
by partial maxillectomy. It includes removal of the
entire hard palate, alveolus and medial wall of the
antrum up to and including middle turbinate.
Table 35.3 Clinical examination of a case of carcinoma maxillary antrum
• Palatine bulge Growth in the floor
• Unilateral nasal obstruction (he is asked to breathe, Growth in the medial wall
closing the nostrils one by one)
• Asymmetry of the face Growth exp
• Change in the level and sharpness of inferior orbital Growth on the roof (orbit
margin, proptosis
• Swelling (indurated) temporal region Posterior extension into infratemporal region and then into
temporal region
• Hard, fixed or mobile submandibular nodes Metastasis
anding anteriorly, superficial surface
al surface)
Section II • General Surgery
366
Manipal Manual of Surgery
• Indications and contraindications for surgery and
radiotherapy are in similar lines as discussed earlier
in this chapter.
NASOPHARYNX—CANCER
• Carcinoma arises in a small anatomic site bordered
by nasal fossae, posterior wall continuous with
posterior wall of oropharynx, body of the sphenoid
and basilar part of occipital bone and soft palate.
• >90% are squamous cell carcinoma out of which
40–50% are undifferentiated (lymphoepithelioma)
and 5% are lymphomas.
• Incidence is higher in Asia—Southern China,
Malaysia, etc.
• May be associated with Epstein-Barr virus (EBV)
• Present as high posterior cervical lymphadenopathy
• Cranial nerve syndromes are common due to tumour
invasion of base of skull.
. Retrosphenoidal syndrome from involvement of
1
cranial nerves II through VI manifests as unilateral
ophthalmoplegia, trigeminal neuralgia, ptosis, etc.
2. Retroparotid syndrome: Occurs due to com-
pression of cranial nerve IX through XII and causes
various symptoms depending on nerve involvement including Horner’s syndrome (refer Trotter’s
triad given in page 340).
• Diagnosis by endoscopy, biopsy, CT and MRI.
• Mainly managed by radiotherapy and chemotherapy.
BENIGN LESIONS IN THE ORAL CAVITY
DIFFERENTIAL DIAGNOSIS OF ULCER IN THE TONGUE
(Fig. 35.43 and Key Boxes 35.17 and 35.18)
1. Aphthous ulcer
• Small, multiple, very painful ulcers, can occur at
any age group. More common in females at the
time of menstruation. These are called minor
aphthous ulcers.
Section II • General Surgery
Fig. 35.43: Ulcers of the tongue—see text for numbers
Key Box 35.17
Painful Ulcers in the Tongue
Aphthous ulcers
Dental ulcers
Tubercular ulcers
Key Box 35.18
Painless Ulcers in the Tongue
Carcinomatous ulcers
Gummatous ulcers
Systemic diseases
• When they are larger, deeper and painful, they are
called major aphthous ulcers.
• They are due to viral infection. These ulcers are
superficial ulcers with erythematous margin.
• They subside within a few days. Temporary relief
can be obtained by applying salicylate gel.
• Vitamin B complex is usually given for the satisfac-
tion of the patients.
2. Dental ulcer
• These ulcers occur due to broken tooth, sharp
tooth, ill-fitting dentures, prosthesis, etc. They are
very painful ulcers.
• Such ulcers are common on the lateral margin and
they heal when the tooth is removed. This is an
example for traumatic ulcer. It should not be confused with carcinomatous ulcer which commonly
occurs on the lateral margin.
3. Tubercular ulcer of tongue
• Tuberculosis affects tip of the tongue. These ulcers
are very painful with enlargement of regional nodes.
• It occurs in patients with fulminating pulmonary
tuberculosis.
• Ulcers have undermined edges. These ulcers are
sometimes multiple with serous discharge.
4. Gummatous ulcer
• Gumma is a complication of tertiary syphilis result-
ing in a firm swelling in the midline in the anterior
2/3 rds of the tongue. Induration is absent. Ulcer
is nontender. Severe endarteritis obliterans results
in the necrosis of gumma giving rise to gummatous
ulcer. It has punched out edges and wash leather
slough on the floor. Other sites of gumma include
testis, palate, clavicle and liver. These ulcers are
rare these days.
5. Systemic diseases
• Pemphigus
• Systemic lupus erythematosus (SLE)
• Lichen planus
Oral Cavity, Odontomes, Lip and Palate
367
6. Post-pertussis ulcer
• It occurs in children due to repeated coughing.
Typical location of the ulcer on the under surface
of the tongue and on the frenulum clinches the
diagnosis.
7. Carcinomatous ulcer
• Lateral margin
• Nonhealing ulcer
• Everted edge
• Edge and base are indurated
• Bleeds on touch
• Fixity
• Significant lymph nodes in the neck.
MACROGLOSSIA
Diffuse painless enlargement of the tongue is described
as macroglossia. It is a rare condition and can occur due
to various causes.
1. Lymphangioma: In this condition, the tongue
diffusely enlarges. Sometimes, it is a localised
swelling. It may be associated with lymphangiomas
elsewhere in the body such as cheek mucosa, lips,
etc. The tongue becomes larger, indurated and gives
rise to severe discomfort to the patients. Due to
repeated trauma, the surface becomes ulcerated. It is
treated by injecting sclerosants such as ethanolamine
oleate, hypertonic saline. Partial excision may be
necessary in cases of large lymphangioma.
2. Haemangioma: Cavernous haemangiomas occur in
the tongue, lips, etc. It is present since birth but
manifests during childhood. It presents with soft,
cystic, fluctuant swelling and at times, pulsatile.
Trauma due to teeth or food results in bleeding.
Haemangioma of the tongue is treated on the same
lines as lymphangioma. It is much more difficult to
excise it, especially a large haemangioma. Preoperative angiography and ligation of lingual artery on
both sides is necessary (Fig. 35.44).
3. Neurofibroma: It may be associated with von
Recklinghausen’s disease. It is treated by hemiglossectomy.
4. Muscular macroglossia: This condition, though rare,
is seen in cretins. The tongue is thickened and cannot
be held in place. Hence, it protrudes outside. It is
treated by partial excision.
SYPHILITIC LESIONS OF THE TONGUE
. Primary syphilis: Primary chancre that occurs in the
1
tongue is highly contagious. It affects the tip of the
tongue. It produces a painful ulcer with large significant enlargement of regional lymph nodes.
2. Secondary syphilis produces a white patch in the
tongue, lips and on the anterior pillars of fauces. In
the tongue, these are multiple which coalesce to form
snail track ulcers. The ulcers heal with fine tissue
paper scar. In some cases syphilitic organisms produce
a flat, hypertrophied epithelium which is described
as condyloma. This is called Hutchinson’s wart.
3. Tertiary syphilis: It produces gumma. Syphilis also
produces chronic superficial glossitis, which is
characterised by bald tongue with loss of papilla and
fissured tongue. It is a precancerous condition.
ODONTOMES
Definition: Odontomes are the cysts, malformations
arising from epithelial or mesothelial elements of tooth
resulting in swelling of
the jaw. As a developmental
anomaly, a few epithelial cells proliferate, persisting
as epithelial debris of Mallasez. Three important
odontomes have been given in Table 35.4.
DENTAL CYST: RADICULAR CYST/PERIAPICAL CYST
athogenesis
P
This arises from a normally erupted, chronically
infected, pulpless caries tooth. The caries tooth produces
a low grade, chronic inflammation which stimulates
epithelial debris to proliferate. Later this brings about
degeneration of epithelial and mesothelial cells resulting
in a cyst within the maxilla.
Clinical Features
• Common in women around 3rd–4th decades.
• Commonly affects the upper jaw (maxilla).
• It presents as a slow-growing swelling in the maxillary
region resulting in deformity of the face.
Fig. 35.44: Haemangioma. (Courtesy: Dr SV Mohan, Associate
Professor, Shivamoga Institute of Medical Sciecnes, Shivamoga)
Diagnosis
• Presence of caries tooth with expansion of maxilla.
• X-ray—large, unilocular cyst in maxilla or ortho-
pantomogram showing cyst in the mandible.
• Aspiration of the cyst demonstrates cholesterol
crystals.
Section II • General Surgery
368
Table 35.4 Comparison of three common odontomes
Dental cyst Dentigerous cyst Adamantinoma
1.Aetiology Caries tooth Unerupted tooth True neoplasm—ameloblasts
2.Site Maxilla Mandible Mandible
3.Age 30–50 years 20–30 years 40–50 years
4.Palpation Smooth, thin bone-eggshell Smooth, expansion of the Expansion of mandible in the 3rd
crackling outer table of mandible molar region, cystic areas
5.X-ray Radiolucent unilocular cyst Radiolucent unilocular cyst Large radiolucent area with fine
6.Treatment Subperiosteal excision Subperiosteal excision Wide excision even though benign
7.Spread Does not occur Does not occur Local spread, recurrence, late spread
Manipal Manual of Surgery
with unerupted teeth honeycombing
to the lung are the features
Treatment
Excision of cyst with its epithelial lining through intraoral approach. After excision of the epithelium, the cyst
wall should be curetted, followed by soft tissue ‘pushin’ to obliterate dead space.
DENTIGEROUS CYST: FOLLICULAR ODONTOME
• Common in lower jaw (mandible) in women
30–40 years (Fig. 35.45).
• It occurs in relation to unerupted, permanent, molar
tooth, most commonly the upper or lower third molar
tooth.
• This unerupted tooth constantly irritates the cells,
produces degeneration of the cells resulting in a dentigerous cyst. The cyst is lined by squamous epithelium
surrounded by connective tissue. Within the cyst, the
tooth lies obliquely or sometimes is embedded in the
wall of the cyst. As it grows further, the cyst displaces
the tooth to which it is attached. Thus, the tooth is
displaced deeper and deeper and prevented from
eruption.
Clinical Features
• Absence of molar tooth
• Expansion of mandible—since the inner table of the
mandible is strong, the expansion mainly occurs in
the outer aspect of mandible. The bone gets thinned
out resulting in egg-shell crackling.
Diagnosis
X-ray mandible orthopantomogram (OPG) (Figs 35.45
and 35.46)
. Tooth in the cyst
1
2. Soap-bubble appearance due to multiple trabeculations of the bone
Section II • General Surgery
3. Radiolucent well-defined swelling.
FIg. 35.45A: Dentigerous cyst
Fig. 35.46: Orthopantomogram showing unerupted tooth
Fig. 35.45B: X-ray of the
dentigerous cyst
Treatment
• Small cyst—excision of the cyst by intraoral approach.
• Large cysts—managed by marsupialisation.
ADAMANTINOMA
• It is also called multilocular cystic disease, amelo-
blastoma, Eve’s disease (Fig. 35.47).
• This tumour arises from ameloblasts (enamel forming
cells).
• It is a benign tumour, very slow-growing and behaves
like a basal cell carcinoma. Inadequate treatment
results in local recurrence and later metastasis. Hence,
even though the tumour is benign, it has to be treated
like malignant tumour.
Oral Cavity, Odontomes, Lip and Palate
369
Images of Adamantinoma (Figs 35.47A to C)
A B
C
Figs 35.47A to C: Ameloblastoma. (A) Clinical presentation,
(B) CT scan image, (C) OPG. (Courtesy: Dr Abhay Kamath, Head,
Department of OFMS, College of Dental Sciences, Manipal)
Sites
• Mandible is the most common site.
• Tibia is the 2nd common site. It can be explained by
inclusion of abnormal embryonic epithelium.
• Pituitary is another common site where adaman-
tinoma can occur. Both pituitary stalk and enamel
arise from oral epithelium.
Clinical Features
• Patients in 4th or 5th decade are commonly affected.
• This is a slow-growing jaw tumour in the region of
angle of mandible and horizontal ramus of the
mandible.
• As the tumour grows, it undergoes cystic degenera-
tion resulting in multiple cystic spaces. Hence, it is
called multilocular cystic disease.
• As it grows it causes expansion of the outer table of
the mandible and causes fracture mandible.
• Patient may present with complaints of falling teeth.
Diagnosis
X-ray: A large cyst and small multiple cysts due to the
trabeculations giving it a ‘honeycomb’ appearance.
Key Box 35.19
Adamantinoma
Locally invasive solid tumour
Nonfunctional, intermittent in growth, unicentric,
multilocular
Spreads within the medullary bone
Invades soft tissues
Should not fragment the tumour cells
Subperiosteal excision should not be done as it may
result in recurrence
Incomplete excision results in recurrence and meta-
stasis to the lung
Hence, even though it is a benign tumour it is treated
by wide excision or hemimandibulectomy.
wide excision with 1 cm of healthy normal tissue should
be removed. It may amount to segmental excision of
the mandible or hemimandibulectomy (Key Box 35.19
and Table 35.4).
Differential Diagnosis
1. Giant Celled R
eparative Granuloma (Jaffe T
umour)
It is a benign tumour which occurs due to haemorrhage
within the bone marrow.
Pathology
• It affects antral part of maxilla or mandible causing
enlargement of the jaw.
• Stroma is vascular consisting of thin-walled blood
vessels, scanty collagen, connective tissue cells.
• Microscopic features mimic giant cell epulis or brown
tumour of hyperparathyroidism.
Clinical features
• Unlike an adamantinoma, this tumour affects females
in the age group of 10–25 years.
• Painless enlargement of the jaw is the presenting
feature. X-ray demonstrates radiolucent artery.
Treatment
• Calcitonin 0.5 mg (100 units) daily subcutaneous
injection over a period of one year has been
recommended as a first line of treatment. It has shown
resolution of the tumour.
• Curettage is the surgical line of treatment.
Treatment
Even though it is benign, simple curettage or enucleation may result in recurrence and chances of recurrent
adamantinoma turning into malignancy are high. Hence,
2. Osteoclastoma
• This is a rare tumour seen in the lower jaw.
• Males between the age of 25 and 40 years are
commonly affected.
Section II • General Surgery
370
Manipal Manual of Surgery
• Unlike adamantinoma, it is a rapidly growing
tumour.
• As the tumour enlarges, both tables of the lower jaw
are thinned out.
• X-ray may show a large, radiolucent cyst with pseudo-
trabeculation.
• Even though benign, it is radiosensitive.
• However, recurrence can occur and can turn into
malignancy like that of adamantinoma.
EPULIS
• Epulis means “upon the gum”. It refers to solid
swelling situated on the gum (Key Box 35.20).
• It arises from alveolar margin of the jaw.
• Very often patients present with swelling on the gum
which is painless.
Key Box 35.20
Epulis
Soft epulis – Granulomatous
Firm epulis – Fibrous
– Giant cell
Hard epulis – Carcinomatous
Malignant epulis – Carcinomatous
Dangerous epulis – Fibrosarcomatous
Fibrous Epulis (Fig. 35.49)
It is the commonest form. A simple fibroma arising from
periodontal membrane, presents on the gum. It may
undergo sarcomatous change. It is a firm polypoidal
mass, slowly growing and nontender.
Giant Cell Epulis
• It is also called myeloid epulis.
• It is an osteoclastoma arising in the jaw. It presents
as hyperaemic vascular, oedematous, soft to firm
gums with indurated underlying mass due to
expansion of the bone. It may ulcerate and result in
haemorrhage. X-ray shows bone destruction with
ridging of walls (pseudo-trabeculation).
• Small tumours are treated by curettage.
• Large tumours are treated by radical excision.
Carcinomatous Epulis
• This is an epithelioma arising from mucous mem-
brane of the alveolar margin.
• Typically, it presents as a nonhealing, painless ulcer.
It slowly infiltrates the bone.
• Hard regional lymph nodes are due to metastasis.
• Treated by wide excision which includes removal of
segment of the bone.
Types
Granulomatous Epulis (Fig. 35.48)
• Precipitating factors are
caries tooth, dentures,
poor oral hygiene.
• It manifests as a mass of
granulation tissue around
the teeth on the gums. It
is a soft to firm, fleshy
mass and bleeds on touch.
• Pregnancy epulis refers to
this variety (gingivitis
gravidarum).
65-year-old man was (Fig. 35.50) getting recurrent attacks
of pain and swelling beneath the chin. Sometimes there
was purulent discharge. He was treated with antibiotics
and incision drainage had been done twice. Sinus
persisted. Chief cause of his problems was his incisor
teeth. Nobody had examined the oral cavity. He had caries
teeth. Once these were removed, sinus healed. This case
highlights the importance of clinical examination.
Section II • General Surgery
Fig. 35.48: Granulomatous
epulis
Fig. 35.49: Fibrous epulis Fig. 35.50: Median mental sinus
MEDIAN MENTAL SINUS
This is a sinus in the midline just beneath the mentum.
Aetiopathogenesis
It is produced by an apical abscess of lower incisors which
penetrate buccal cortical plate below the origin of mentalis
muscle. This muscle takes origin from labial surface of
alveolar process just above the labial sulcus.
Hence, pus
discharges through a sinus in the centre of chin.
Clinical Presentation (Fig. 35.50)
• Patients present with recurrent swelling in the sub-
mental region which bursts open spontaneously
discharging at times mucus and seropurulent fluid.
Oral Cavity, Odontomes, Lip and Palate
371
• Repeated history of swelling, discharge and healing
are common presentations.
• Diagnosis is established by examination of the oral
cavity, which reveals evidence of caries tooth.
Treatment
Once the caries tooth is extracted, sinus will heal
spontaneously.
VINCENT’S ANGINA
It is an acute ulceromembranous stomatitis or acute ulcerative gingivitis and stomatitis. The disease is caused by
Vincent’s organisms—Borrelia vincentii, an anaerobic
spirochaete and fusiformis. These are gram-negative rods
which are the normal pathogens of oral cavity. However,
streptococci and staphylococci are the common organisms
involved here resulting in severe symptoms and toxicity.
PRECIPITATING FACTORS
• Malnutrition, diabetes mellitus, caries tooth, warm
seasons, winter, etc.
• The disease starts in the intergingival defects as a deep
penetrating ulcer which results in a spontaneous
gingival haemorrhage. There is a thick membrane
covering the ulcer.
• Once infection spreads to tonsillar region, it is called
Vincent’s angina—very severe painful condition.
Clinical Features
• Common in children and young adults between
20 and 40 years of age.
• It presents with very painful gums with fever, malaise
and toxaemia.
• Gums are swollen, red, inflamed with or without
slough.
• Difficulty in swallowing, painful swallowing
(odynophagia), foetor oris, features of toxaemia and
high grade fever are characteristic of this condition.
Treatment
• Improve nutrition. Mouthwashes with hydrogen
peroxide help in washing away the membrane. Broad
spectrum antibiotics such as Piperacillin-tazobactum
combination are given, metronidazole 400 mg thrice/
day for 7–10 days should be given.
CLEFT LIP
• Cleft lip results from abnormal development of the
median nasal and maxillary process.
• Cleft palate results from a failure of fusion of the two
palatine processes.
Epidemiology and Etiology
Cleft lip-palate has a varied incidence of 1 in 500–2,500
live births depending on geographic location, maternal
risk factors, prenatal exposure, ancestry, and socioeconomic status. The latest CDC reported incidence is
1 in 940 live births, with the highest rates in Asians and
Native Americans (1 in 500 births) and the lowest rate
in Africans (1 in 2,500 births)
Cleft lip is seen in a Male:Female ratio of 2:1 and in
contrast to cleft palate has a 1:2 ratio. It is postulated
that maternal hormones may be involved in both sex
determination and orofacial clefts.
The sporadic causes are multifactorial and involve
genetics, environmental factors, and teratogens
Syndromes: Most commonly van der Woude
•
syndrome, Stickler syndrome, Hardikar syndrome,
Treacher-Collins syndrome.
• Genetics-IRF 6 which is commonly implicated in the
syndromic forms, ch8q24, VAX1, FGFR2, BMP.
• Maternal risk factors: Smoking, alcohol consumption,
pre-gestational and gestational diabetes, advanced
maternal age, folate deficiency, zinc deficiency.
• Teratogens: Medications like anti-epileptics
(valproate/phenytoin), retinoic acid, occupational
exposure to pesticides/solvents etc.
Types of Cleft Lip (Figs 35.51 and 35.52)
I. Central: It is very rare and occurs due to failure of
fusion of two median nasal processes.
II. Lateral: It is the commonest variety wherein there
is a cleft between the frenulum and the lateral
part of the upper lip. This is due to imperfect
fusion of maxillary process with median nasal
process. The lateral variety can be unilateral or
bilateral.
CLEFT LIP AND CLEFT PALATE
SU19.1: Describe the etiology and classification of cleft lip
and palate.
Figs 35.51 and 35.52: Types of cleft lip (I and II)
Section II • General Surgery
372
Manipal Manual of Surgery
III. Complete or incomplete: In cases of complete
variety, cleft lip extends to the floor of the nose. In
cases of incomplete variety, the cleft does not
extend
up to the nostril.
IV. Simple or compound: Compound refers to cleft lip
associated with a cleft in the alveolus.
Clinical Features (Figs 35.53 and 35.54)
. In 80% of the cases, cleft lip is unilateral and in about
1
60% of the cases, it is associated with cleft palate.
2. In many cases, nostril is widened.
3. Maldevelopment or malalignment of the teeth in
relation to the cleft is common.
Functional Effect
1. Presence of cleft lip does not interfere much with
sucking. However, there may be some difficulty in
bottle feeding.
. Some degree of difficulty in speech (dysarticulation)
2
is present.
Figs 35.53 and 35.54: Cleft lip (Courtesy: Dr CG Narasimhan,
Senior Consultant Surgeon, Mysore)
CLEFT PALATE
Development of Palate
• Palate is developed around 6–8 weeks of intrauterine
life from 3 components. The premaxilla is developed
from the median nasal process and maxillary process
contributes one palatine process on each side.
• The line of fusion of these processes is in the form of
a letter Y.
• Imperfect fusion or developmental anomalies results
in cleft palate.
Types (Fig. 35.55)
I. Complete: Failure of fusion of palatine processes and
premaxilla results in complete cleft palate. In such
situations, the nasal cavity and mouth are interconnected. When premaxilla is not fused with both
palatine processes, it hangs down from the septum
of nose. Thus, complete cleft can be of two types as
Section II • General Surgery
shown below in the diagram.
Fig. 35.55: Types of cleft palate (I, IIa and IIb)
II. Incomplete: When the fusion of three components
of palate takes place, it starts from uvula and then
backwards. Thus, various types of incomplete fusion
result.
• Bifid uvula.
• The whole length of soft palate is bifid.
• The whole length of soft palate and the posterior
part of hard palate are involved. On the other hand,
anterior part of palate is normally developed. In
about 25% of cases, cleft palate alone and in 50%
of cases, both cleft palate and cleft lip are encountered.
Effects of Cleft Palate
1. Presence of cleft palate interferes with swallowing
to some extent.
. They are unable to pronounce the consonant sounds
2
such as B, D, K, P, T.
3. Teeth: Upper lateral incisors may be small or even
absent. The maxilla tends to be smaller. Teeth are
crowded.
4. Nose: Oral organisms contaminate the upper respiratory mucous membrane through cleft palate.
5. Hearing: Even with repair, acute and chronic otitis
media and hearing problems can occur.
SU19.2: Describe the principles of reconstruction of cleft
lip and palate.
Management of Cleft Lip and Palate
• A multidisciplinary approach involving plastic
surgery, orthodontics, speech pathology, ENT
department, prosthodontics and paediatrics department is needed to rehabilitate the cleft palate cases.
This approach to the problem results in aesthetically
acceptable end result without much functional
deficiencies.
• Feeding advice:
Cleft palate babies are unable to suck
mothers’ milk because intraoral negative pressure
cannot be created due to communication between oral
and nasal cavity. Thus, expressed mother’s milk is
given by spoon with head end of baby elevated by
Oral Cavity, Odontomes, Lip and Palate
373
45 degrees. Swallowed air during feeding is released
frequently by burping.
Cleft Lip Repair (Key Box 35.21)
Timing: Majority of surgeons follow “RULE OF 10” as
a guide for timing of lip and anterior palate repair. At
the time of repair, haemoglobin should be more than
10 g%, age approximately 10 weeks, weight more than
10 lb (4.54 kg) and total leucocyte count less than 10,000/
cu mm (i.e. no infection).
Key Box 35.21
Rule of 10
Hb >10 g%
Age approx : 10 weeks
Weight >10 lb (4.54 kg)
TC <10,000/mm
3
Types of Cleft Lip Repair
• For unilateral cleft lip repair most commonly used
methods are Millard rotation advancement flap and
Tennison-Randall triangular flap method.
• Bilateral cleft lip can be repaired in single stage
or in two stages at the interval of 3–6 months. For
two-stage repair, any one of the methods described
for unilateral cleft lip can be used. For bilateral repair
in one stage, Veau III method is simple and gives
satisfactory results. Other single stage methods which
give good results are Millard’s single stage procedure and Black procedure.
Basic Steps of Lip Repair
• Markings are made according to the method selected
(e.g. Millard’s repair, Fig. 35.56A and TennisonRandall repair, Fig. 35.56B).
• Adrenaline-saline solution (1:200,000) is injected in
the lip and labial sulcus for haemostasis.
• Full thickness of lip is incised along the marking.
• Lip repair is done in three layers—mucosa, muscle
and skin. For better aesthetic result, Cupid’s bow
A B
Figs 35.56A and B: Basic steps of lip repair
should become horizontal, white line continuity
should be repaired and there should be no vermilion
notching.
Cleft Palate Repair
Timing: Early repair results in retarded maxillary
growth due to surgical trauma to growth centre and
periosteum. Delay in repair results in speech defect. Best
balanced result is achieved by repairing between one
and a half years.
Types
• Palate repair: Palate is repaired by palatal shelves.
Mucoperiosteal flaps raised from various methods
are available for palate repair.
• Most commonly used method is V-Y, pushback
palatoplasty.
Steps of ‘V-Y’ pushback palatoplasty
(Fig. 35.57)
• Palate is infiltrated with 1:2 lakh
adrenaline-saline solution.
• Two mucoperiosteal flaps are
elevated, one from either side of
palatal shelves. Then, nasal layers
are mobilised.
• Palate is closed in three layers—
nasal layer, muscle layer, oral layer.
• In V-Y pushback palatoplasty,
palatal lengthening is achieved by
V-Y plasty. Hook of hamulus can
be fractured to relieve tension on
Fig. 35.57: V-Y
palatoplasty
suture line by relaxing the tensor palati muscle.
MISCELLANEOUS
ECTOPIC SALIVARY GLAND TUMOUR
• Palate is the most frequent site.
• These tumours can also occur anywhere in the mouth
or pharynx.
• It is a slow-growing and painless tumour. At this
stage, it may feel firm or hard without ulceration of
mucous membrane.
• Slowly it ulcerates. Thus, it can have the shape of a
‘verrucous’ carcinoma. Such lesions are ulcerated,
hard, and painful with irregular margins.
• They are of low-grade malignancy.
• Neglected cases can invade base of skull and spread
to lymph nodes.
• Wide excision with or without reconstruction is the
treatment of choice.
Section II • General Surgery