Tongue

بِسْمِ اللهِ الرَّحْمنِ الرَّحِيم

Surgery of the TongueLECTURE (1)


The oral cavity Extent: from skin–vermilion border of lips ant. to junction of soft /hard palate superiorly to circumvallate papillae inferiorly and to ant. tonsillar pillars laterally Divisions: 7 sites: lips, alveolar ridges, oral tongue, floor of mouth, buccal mucosa, hard palate & retromolar trigoneDefence: The oral mucosa is resistant to injury ?1- Well keratinized2- Rapid turn over by desquamation3-Firm attachment to underlying structures4- Saliva & its continuous wash / antibacterial effect.


AGLOSSIA= absence ,associated with other congenital or developmental defects (limb / other cranio-facial defects). CLEFT or BIFID TONGUE failure of fusion of 2 lingual processes

DEVELOPMENTAL ANOMALIES OF TONGUE

TONGUE TIE(ANKYLOGLOSSIA): short thick lingual frenulum . Presentations 1. Impairment of tongue movements 2.Malocclusion, swallowing & speech defects. Treatment by division of frenum near floor of mouth (LA,GA) best at 3 years age


MACROGLOSSIA: Persistent painless enlargement of tongue; Congenital causes: cavernous hemangioma. Congenital AV fistula Lymphangioma. Neurofibromatosis. Acquired causes: Muscular hypertrophy in cretinism. Acromegaly. Amyloidosis. Diffuse carcinoma or sarcoma of tongue. Down syndrome Treatment Surgical correction is indicated in severe cases


.

GEOGRAPHIC TONGUE (benign migratory glossitis) : Benign condition in patients with cong. heart dis or acute GIT problems Alternating red & yellowish-white areas due to alternating hypertrophy / atrophy of filiform papillae BLACK HAIRY TONGUE (lingua villosa nigra) Benign painless temporary condition resulting from an overgrowth of bacteria or yeast on the papillae making Rbc pigments (porphyrins) giving the tongue a black appearance. The "hairy appearance " due to rapid growth of papillae or interruption of normal shedding of cells . Etiology 1-Changes in normal bacteria or yeast after antibiotic therapy or bismuth drugs .2-Poor oral hygiene3-Tobacco use4-Drinking excessive coffee or tea Treatment oral hygiene and controlling cause

Congenital syphilis

MEDIAN RHOMBOID GLOSSITIS Smooth, oval- or diamond-shaped nodule on the dorsum of tongue just ant.to circumvallate papillae. LINGUAL THYROID Red lobulated mass behind foramen cecum (failure of thyroid to descent) Treatment : excision after mTC99 scan to confirm presence of normal thyroid gland. CONGENITAL FISSURED TONGUE): The surface of the tongue furrowed with a deep median fissure Shorter fissures run transversely from a median groove unlike syphilis which run longitudinally. This sometimes get infected by yeast resulting in median rhomboid glossitis. 
.

TONGUE INJURIES

Mechanism: 1.Tongue biting (commonest) e.g. epileptics. 2. Associated with jaw # after road traffic accidents. 3- Blow to the jaw Why serious especially in unconscious? Tongue hematoma causes airway obstruction If laceration serious or delayed bleeding due to lingual vessels injury. Treatment: 1.Arrest bleeding by pressure = hooking tongue forwards by fingers & compress it against mandible. 2. Laceration is sutured under GA to estimate its depth 3. Big tongue hematoma if obstructs airways may require tracheotomy. .

INFLAMMATION OF TONGUE (GLOSSITIS)

1.ACUTE PYOGENIC GLOSSITIS Is extremely rare due to strept. infection e.g. scalding fluids or after wasp sting ,sepsis , diabetes , alcoholism & Plummer Vinson syndrome. Clinically superficial painful red shiny tongue (beefy) 2.CHRONIC SUPERFICIAL GLOSSITIS: It is pre cancerous condition Chronic irritation( Smoking, Sharp tooth, Sepsis, Syphilis, Spirits, &Spices ). It affects middle & old ages. Treatment: Elimination of irritating cause. Mouth washes & multivit. Excision of lesions in resistant cases Diathermy coagulation in superficial lesions

Heals with scar Removal of cause biopsy if chronic precancerous

If 2ndary infection
Indurated
red
Hyperemic
Raised irregular
Painful
single
Irregular
tongue side
carious ,broken T or ill-fitted denture
Dental ( traumatic)
Open pulm. TB
Unknown occur about puberty
Cause
Tip
Tip & edge
site
Rounded
Round /oval<1 cm
shape
Heals with scar AntiTB
Heals in 7-10 days no scarring Hygien /triamcinalone in ora base
treatment
Enlarged
No LN
Cx LNs
indurated
sloughy
base
caseous
grey / yellow
floor
blue
Red hyperemic
margin
undermined
irregular
edge
multiple small shallow
single /multiple shallow clusters up to 5
no
Very painful
Very painful recurrent
symptom
TB
Aphthous (Dyspeptic)
TONGUE ULCERS: (commonest lesions )
Dental
aphthous
TB



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Enlarged elastic
Not indurated
Granulation tissue
congested
Sloping irregular
Recurrent painful
multiple
Small round shallow blisters that rupture
tip
H- simplex 1 in children
Herpetic
Leucoplakia, Chronic irritation
2ndary stage
cause
Lateral margin
Sides
site
irregular
Linear fissures or ulcers(snail track)
shape
Biopsy
penicillin
treatment
Enlarged hard
enlarged
Cx LNs
indurated
indurated
base
necrotic
yellow
floor
hard
hyperemic
margin
everted
sloping
edge
Usually single
Usually multiple
no
Ankyloglossia, fetor
painless
symptoms
Neoplastic malignant
Syphilitic= Gummatous
TONGUE ULCERS:
herpetic
syphilitic
malignant

Fungal infection of the tongue

1- Acute pseudomembrenous candidiasis:(thrush) occurs in infant or old aged or those using steroid for long time or cytotoxic as soft moist thin creamy white plaque 2- Acute hypertrophic candidiasis: as thick white mass usually in low immune person. 3- Acute atrophic candidiasis: as a complication of antibiotic causing burning sensation 4- Chronic atrophic candidiasis: in dentures with poor oral hygiene as painless red oedematous tongue. 5-Chronic hypertrophic candidiasis precancerous

The sixth most common ca in world. > 90% sq cell ca, Etiology• Age >60 years; & male > females (both smokers)• Geographical: India 40% (tobacco chewers /spicy food).• Predisposing factors Chronic irritation 6 S (Sharp broken tooth Smoking e.g. tobacco chewing or snuffing betel nut 4x, Sepsis, Syphilis (tertiary), Spirits 3x &Spices) . Premalignant lesionsHigh-risk lesions Leucoplakia, Erythroplakia &Chronic hyperplastic candidiasisMedium-risk lesions Oral submucous fibrosis,Syphilitic glossitis &Sideropenic dysphagia (Paterson–Kelly syndrome)3.lesion with doubtful risk: discoid lupus erythematosis,dyskeratosis congenita,& Lichen planus Oral cancer

Premalignant conditions

Leucoplakia White hyperkeratotic patch or plaque that cannot be characterized clinically or pathologically. Smooth or wrinkled, soft, nodular or indurated appearing as white paint coated tongue that can not be rubbed off Pathogenesis: irritation leads to atrophy / atypia of epith.cells The potential for malignant changes (5%) depends on Age, site of lesion (floor of mouth & ventral surface tongue) , induration & duration ( 2.4% for each 10 years) Management1- Adequate clinical examination of oral cavity2- Biopsy =incisional if small or excisional if big 3- CO2 LASER or surgery.4- Stop irritation. & regular follow up. Erythroplakia Bright red plaque cannot be characterized clinically or pathologically Asymptomatic red velvety or nodular lesion with irregular clearly demarcated margin, +/- leucoplakia (Speckled leucoplakia) Potential for malignant changes are17 X > white lesion, it should be totally excised by surgery or CO2 LASER


TONGUE CA PATHOLOGY :  Lateral margin of ant.2/3 & retromolar trigone (45-55%)  Posterior 1/3( 20%)  Less common sites :ventral, dorsal &tip(10% each)GROSS TYPES:1-Malignant ulcer:, deep, irregular margin with necrotic floor and everted edge2-Raised oval white plaque as cauliflower-like mass +central necrosis .(commonest) 3-Hard sub mucous nodule (less common) 4-Deep indurated chronic fissure that does not heal. 5-Diffuse infiltrative wooden base i.e frozen tongue (rare) MICROSCOPIC TYPES: Ant 2/3 well differentiated SCC >95%. Post 1/3 less differentiated BCC and adenoca of minor salivary gland (rare). (5%)


SPREAD: CA in situ=no invasion to BM + no spread. 1- Direct (local) spread :to nearby structure Ca of ant 2/3 invades lat. then to floor of mouth & to mandible. Post 1/3 ca invades tonsils, pharynx & larynx.. 2-Lymphatic spread: early to neck LNs ( 30% subclinical). Ca of ant. 2/3 to submandibular and then to deep cervical LN . Posterior 1/3 bilaterally upper deep cervical directly... Dorsum to bilateral submandibular LN Tip ca. drains bilaterally to submental then to jugul-omohyoid LN 3-Blood spread: very rare mainly in the post 1/3 4-Perineural invasion (bad prognosis)


Main clinical features■ Old, male +/- risk factors +general S/S of malignancy■ Asymptomatic painless unless deeply invasive. Or ■ Persistent oral swelling or ulcer >4weeks■ Deep indurated fissure Or ■ Oval raised papillated plaque and white keratin Or ■ Lobulated mass with overlying yellow patch of submucous necrosisLate stage■ Sore tongue the pain first due to infection then due to invasion of lingual n. it may refer to ear.■ Difficulty in swallowing with excess salivation (spitting) due to pain & decreased tongue movement (may be blood stained.)■ Foeter oris■ Jaw or facial swelling due to painless enlarged LNs ■ Trismus ■ Fixation of tongue (Ankyloglossia) or deviation of tongue to side of lesion when protrudes


Complications 1-Inhalation of necrotic tissue causes bronchopneumonia. 2-Cachexia & starvation due to pain & dysphagia. 3-Secondary bleeding due to erosion of lingual vessel or ICA in post 1/3 tumor 4-Asphyxia due to enlarged fixed LN or to glottic edema. Female show better prognosis with 50% 5 year survival in comparison with 25% in male

Investigations of ca tongue:

Biopsy Incisional = for any ulcer ,white or red patch or fissure >4 wks. FNAC for neck lump or enlarged cervical LNs.

-Plain XR of the jaw -A radioisotope bone scan of the facial skeleton shows high uptake in bone if mandible is involved
-MRI of head and neck for extent of intraoral tumor ,soft-tissue infiltration and LNs

Additional imaging studies

Ultrasound &CT for Cervical LN metastasis CT if bony invasion is suspected
T1 less than 2cm T2 2-4 cm T3 more than 4 cmT4 local invasion
N1- Single ipsilateral LN < 3cm N2a-single ipsilateral LN > 3cm N2b- multiple ipsilateral LN < 6 cm N2c-bilateral LN or controlateral LN < 6cm N3 any node > 6cm
TNM staging=
M1 no distal metastasis M2 positive distal metastasis

Definitive treatment of ca tongue Depends on

Site & age Biopsy,imaging &TNM stage Patient's nutritional status . Tumor <4 cm equally benefit from RT or surgery A- Surgery 1st choice CA in situ or small in tip or lateral margin = local excision +1 cm safety margin & 0.5 cm in depth & defect closed directly or flap from floor of mouth 2. Tumor > 2 cm= Partial or hemiglossectomy by diathermy or CO2 LASER. The defect closed by flap 3. CA post 1/3=either total glossectomy or ext. radiation 4. LN metastases = excision of tumor + neck dissection 5. Mandible invasion = hemiglossectomy +hemimandibulectomy +/- temporary tracheostomy +neck dissection to excise suspicious cervical LN + flap to close defect (commando operation. )


B- Radiotherapy usually alternative & indicated as palliative RT in Patient cannot tolerate surgery or Late stages of presentation or Post 1/3 ca or Post operative

Palliative treatment of ca tongue  Radiotherapy Palliative resection of primary to comfort patient Analgesia+NG feeding,??tracheostomy Chemotherapy Radiofrequency thermal ablation(minimal invasive therapy) Gene therapy (new treatment) gene manipulation to change genetic code in persons cells.