Preface

Agam is a group of budding medicos, who are currently doing their under graduation in
various Medical Colleges across Tamil Nadu and Pondicherry. The group was initiated on 18th
November 2017, in the vision of uniting medicos for various social and professional causes.
We feel delighted to present you Agam ENT notes prepared by Agam Divide and Rule 2020
Team to guide our fellow medicos to prepare for university examinations.

This is a reference work of 2017 batch medical students from various colleges. The team
took effort to refer many books and make them into simple notes. We are not the authors of the
following work. The images used in the documents are not copyrighted by us and is obtained from
various sources.

Dear readers, we request you to use this material as a reference note, or revision note, or
recall notes. Please do not learn the topics for the 1st time from this material, as this contain just the
required points, for revision.
Acknowledgement

On behalf of the team, Agam would like to thank all the doctors who taught us ENT. Agam
would like to whole heartedly appreciate and thank everyone who contributed towards the making
of this material. A special thanks to Taher Hussain, who took the responsibility of leading the team.
The following are the name list of the team who worked together, to bring out the material in good
form.
 Jeyabharathi
 Manikandan
 Mohammed Salman
 Manisha
 Saranya
 Rajarajan
 Supriya
 Aarthi
 M Lavanya
 Kaviyathendral Agilan
 A Anusha Lakshmi
 Arivudainambi
 R M Ashwini
 Shree Lakkshmi K
 Mikun Manoj
 Catharine Maria J
 Aparna JM
 Dhikshitha P
 Ragha Dharshini K
 Sneha A
 Rajeshwar Venkatesan
 Satrajit Vijayaram V
 ANATOMY OF ORAL CAVITY

BOUNDARIES:

POSTERIOR: Oral cavity communicates with the oropharynx through oropharyngeal isthmus. This
oropharyngeal isthmus is bounded superiorly by the soft palate, Inferiorly by the tongue, on both
sides by palatoglossal arches.

FLOOR: it is small horse shoe shaped region.

Surface of the floor is formed by mucous membrane, connects the tongue to the mandible. Anterior
part of the floor is sublingual region. Lower part of the tongue is connected to the floor of the
mouth by frenulum linguae. On each side the frenulum there is elevation called as sublingual
papilla, on summit of it submandibular duct opens. On each side of frenulum the submandubular
gland projects into the membrane and produces an elevation called submandibular fold.
ROOF: Roof is formed by palate.

Anterior two third of the palate is made of bones called Hard palate. Posterior one third is made of
soft tissues called soft palate. From the posterior free margin there is a conical projection called
uvula hangs down in the median region.
 COMMON DISORDERS OF ORAL CAVITY

Ulcers are the most common disorders of oral cavity.

Most common causes of ulcer of oral cavity:

1. Infections

(a) Viral: Herpangina, herpes simplex (primary and secondary), hand, foot and mouth disease

(b) Bacterial: Vincent infection, TB, syphilis

(c) Fungal:Candidiasis

2. Immune disorders. Aphthous ulcer, Behçet syndrome

3. Trauma

(a) Physical: Cheek bite, jagged tooth, ill-fitting denture

(b) Chemical Silver nitrate, phenol, aspirin burns

(c) Thermal: Hot food or fluid, reverse smoking

4. Neoplasms

5. Skin disorders. Erythema multiforme, lichen planus, benign mucous membrane pemphigoid,
bullous pemphigoid, lupuserythematosus

6. Blood disorders. Leukaemia, agranulocytosis, pancytopenia, cyclic neutropenia, sickle cell

anaemia

7. Drug allergy. Mouth washes, toothpaste, etc. Reactions to systemic drugs

8. Vitamin deficiencies

9. Miscellaneous. Radiation mucositis, cancer chemotherapy, diabetes mellitus, uraemia

Infections:

Viral infections:

1.Herpangina: It is a coxsackie viral infection, mostly affect children.

Features: Multiple vesicles appear on faucial pillars, tonsil, soft palate & uvula. They rupture to form
ulcer with yellow base & red areola around them.

2.Herpetic gingivostomatitis:

Caused by Herpes simplex virus.

Primary infection: it mainly affects children. Features: clusters of vesicle, soon rupture to form
ulcer.

Additional symptoms: fever, malaise, headache with sore throat, lymphadenopathy.

Secondary or recurrent infection: It mainly affects adults & it is milder because of developed
immunity. most commonly it is seen in vermilion border of lip. Less is the chance of appearance
intraorally. In recurrent cases, virus present in dormant state in trigeminal ganglion. Once get
activated it affects peripheral sensory supply of that ganglion.

Treatment – acyclovir 200mg 5 times a day for 5 days.

3.Hand Foot Mouth Disease: It is also a viral infection affecting children. Oral lesions are seen on
the palate, tongue and buccal mucosa. Vesicles also develop on the skin of hands, feet buccal
mucosa buttocks.
Bacterial infections:

1.Vincent infection-also called as acute necrotizing gingivitis. The disease affects young adults and
middle-aged persons.

It starts at the intradental papillae & then spreads to free margins of the gingival, later it get covered
with necrotic slough. It also become red &edematous.

Similar infection if present in tonsil called as – Vincent angina.

Treatment : systemic antibiotics, frequent mouth wash and dental hygiene.

Fungal infections:

Moniliasis (candidiasis)- caused by candida albicans. It is seen in two forms

1.THRUSH-white grey patches on the oral mucosa and tongue, when it is whipped of it leaves a
erythematous mucosa. It is seen in infants and children, adults are also affected when they suffer
from malignancy, diabetes, taken broad spectrum antibiotics or cytotoxic drugs.

2.Chronic hypertrophic candidiasis: also called candidal leukoplakia. It appears as a white patch
and it cannot be whipped off. Mostly it affects anterior buccal mucosa just behind the angle of
mouth.

Immune disorders:

Aphthous ulcer: They are recurrent and superficial ulcers. Mainly involves inner surface of lips,
buccal mucosa, tongue, floor of mouth and soft palate, while sparing mucosa of the hard palate and
gingivae.
Minor form, is more common ulcers are 2–10 mm in size and multiple with a central necrotic area
and a red halo.

Major form, ulcer is very big, 2–4 cm in size and heals with a scar but is soon followed by another
ulcer.

CAUSES: unknown, it may be an autoimmune process, nutritional deficiency, viral or bacterial

infection, food allergy, stress.

These ulcers can be differentiated from the viral ulcers by their frequent recurrence, involvement of
movable mucosa in soft palate and cheek.

Treatment: topical application of steroids and cauterization with 10% silver nitrate. In severe cases
tetracycline 250 mg dissolved in 50 ml of water & it is given as mouth rinse and then it swallowed.

Behcet syndrome (oculo oro genital syndrome)

.TRIAD:

1. Aphthous like ulcer in oral cavity. 2. Genital ulceration 3. Uveitis.

Edge of the ulcers are punched out. Lesions are also seen in skin, joints and CNS.

TRAUMA:

Traumatic ulcer: it is mostly seen on the later border of the mouth, due to jagged tooth, ill-fitting
denture. Seen on the mucosa of cheek due bite and on the due to foreign object. Ulcers also result
from accidental ingestion of acids or alkali.
Aspirin burn when a tablet is kept against the painful tooth.

Neoplasm: Malignancies of the oral cavity or oropharynx may present as chronic ulcers. Though
most commonly it is squamous cell carcinoma, it could be carcinoma of minor salivary glands or
non-Hodgkin lymphoma.

Skin disorders:

Erythema multiforme: Disease of skin and mucous membrane. The cause is unknown but may be
associated with drug allergy (sulfonamides) or recent herpes simplex infection. Oral mucosal lesions
consist of vesicles or bullae which soon rupture to form ulcers covered with pseudo membrane.
Common sites are lips, buccal mucosa and tongue. The lesions bleed easily.

Distinctive feature: form haemorrhagic crusts on the lips.

Skin lesions consist of erythematous patches on the palms, soles and extensor surfaces of the
extremities.

2. Pemphigus vulgaris.

 It is an autoimmune disorder affecting older age group (50–70 years). Oral lesions are seen
in50% of the cases and may precede skin lesions.
 Oral ulcerations are superficial and involve palate, buccal mucosa and tongue. Treatment
consists of systemic steroids and cytotoxic drugs.
3. Benign mucous membrane pemphigoid (BMMP).

 It is a autoimmune disorder. Mucosal lesions mainly involve cheek, palate& gingivae.

Conjunctiva is also the important site where the infection occurs.
 Lesion starts as a bulla filled with clear or haemorrhagic fluid which ruptures to form
superficial ulceration covered with shaggy collapsed mucosa.
 Skin lesions may be absent.

4. Lichen planus. Both oral & skin lesions are seen. Skin lesions are pruritic, purple, polygonal
papules. Oral lesions occur in two forms:

(a) Reticular. White striae forming lace-like pattern are seen on the buccal mucosa on both sides.
They are asymptomatic and require no treatment.

(b) Erosive. It is characterized by painful ulceration on the buccal mucosa, gingiva or lateral tongue.
Each ulcer is surrounded by a keratotic periphery.

Treatment consists of topical steroids.

5.Chronic discoid lupus erythematosus. Oral lesions are almost always associated with skin lesions.
Oral lesions are similar to those of erosive form of lichen planus.
Blood disorders:

Blood dyscrasias cause ulcerations in the oral cavity and pharynx. Due to lack of defense
mechanism, e.g. granulocytes, infections quickly supervene causing ulcers.

Acuteleukaemia is mainly of two types types— acute lymphoblastic type, which occurs in young
children.

acute myeloid type, occurring in the middle aged or the elderly. Both cause hypertrophy of gums
with ulceration and bleeding

Agranulocytosis is characterized by ulcerations in throat with severe neutropenia.

Cyclical neutropenia: when gets infection& oral ulcerationthere will fall in neutrophil count.

Pancytopenia: there is a drop in RBC count, white cell count and platelets.

Drug allergy:

 Systemic administration of drugs like penicillin, tetracycline, sulfa drugs, barbiturates,

phenytoin, etc. may cause erosive, vesicular or bullous lesions in the oral cavity.
 Contact stomatitismay occur due to local reaction to mouth washes, lozenges, chewing gum,
toothpastes or to prosthetic dental materials
 Oral lesions may vary from erythema to vesicles and bullae formation.

Vitamin deficiencies:

Vitamin B12 and folic acid deficiency may cause ulcers.

MISCELLANEOUS:

1.Radiation mucositis: when radiation therapy for cancer in oral cavity or pharynx is given it also
affects the mucosa and forms ulcer. First the mucosa turns red and then they form spotty mucositis.
Later they coalesce to form large ulcerated lesion. Covered by slough.

2. Median rhomboid glossitis.

Red coloured rhomboid shaped lesion, seen on the dorsum of the tongue in front of the foramen
caecum. It is developmental anomaly occurs due to the presence persistence of tuberculum impar,
which fails to in vaginate. Lesions are devoid of papillae. The condition is
asymptomatic and no treatment is necessary.

3.Geographical tongue.:
 lesion is characterized by erythematous areas, surrounded by an irregular keratotic white
outline.
 The lesions keep changing their shape and hence the condition is also called “migratory
glossitis.”
 The condition is asymptomatic and may not require any treatment.
3. Hairy tongue.
 Due to excessive formation of keratin, the filiform papillae on the dorsum of the tongue
become elongated.
 They get colored, brown or black, due to chromogenic bacteria and look like hair.
 Smoking seems to be one of the factors.
 Treatment - scraping the lesions with a tongue cleaner, application of half-strength hydrogen
 peroxide and improving the nutritional status of the patient by vitamins.
 Causative factors, if known, should be removed

4. Fissured tongue. It may be congenital or seen in cases of syphilis, deficiency of vitamin B complex
or anaemia.
 Congenital fissuring associated facial palsy is seen in Melkersson–Rosenthal syndrome.
5. Ankyloglossia: also called as tongue tie.
 True tongue tie which produces symptoms is uncommon.
 If tongue can be protruded beyond the lower incisors, it is unlikely to cause speech defects.
 A mobile tongue is important to maintain
 orodental hygiene—to clean the debris and prevent formation of dental plaques.
 Treatment - significant tongue tie is transverse release and vertical closure.
 Thin mucosal folds can be simply incised.

6. Fordyce spots: There are aberrant sebaceous glands present under the buccal or labial mucosa.
They shine through it as yellowish or yellow-brown spots.
They are seen with equal frequency in both males and females and are considered normal.
7.Nicotine stomatitis:
 This lesion is seen in smokers particularly those in the habit of reverse smoking. Palatal
mucosa shows pin-point red spots in the center of umbilicated papular lesions.
 They are due to inflammation of the minor salivary glands and their duct openings as a
reaction
 to the heat of the smoke.
 The nicotine stomatitis is a misnomeras nicotine is not the cause.
 Treatment – elimination of smoking.

Submucosal fibrosis:

It is a chronic insidious process characterized by juxtaepithelial deposition of fibrous tissue in the

oral cavity and pharynx.
AETIOLOGY:
Socioeconomic status: poor socioeconomic status
has been associated with higher risk of precancerous
lesions like leukoplakia, erythroplakia and submucous fibrosis.
Tobacco chewing: It is a major risk factor in submucous fibrosis as it is in lesions of leukoplakia and
erythroplakia.
Areca nuts: Areca nuts are chewed alone, with tobacco or in the form of pan.
Betel quid without tobacco also increases the risk of oral precancerous lesions, but causes higher
risk for oral submucous fibrosis relative to leukoplakia, erythroplakia or multiple precancerous
lesions.

Alcohol: drinking increases the risk of

leukoplakia by 1.5-fold, OSF by 2-fold and that of erythroplakia by 3-fold.
Nutritional: Deficiency of vitamins and micronutrients has been suggested.
Therapy of OSF with vitamin A, zinc and antioxidants has shown some beneficial effect.
Immune process: OSF is considered a cell-mediated
immune reaction to arecoline in areca nuts
PATHOLOGY:
 The basic change is fibroelastotic transformation of connectivetissues in lamina propria
associated with epithelial atrophy, sometimes preceded by vesicle formation.
 In later stages, when fibrosis is marked, there is progressive trismus and difficulty to protrude
the tongue.
 Leukoplakia and squamous cell carcinoma may be associated with submucous fibrosis
possibly because of common aetiological factors involved.
 It is a premalignant condition and malignant transformation has been seen in 3–7.6% of
cases.
Pathogenesis:
Areca nut chewing

Collection of activated T-lymphocytes

and macrophages in subepithelial
layers of oral mucosa

Activated T-lymphocytes Macrophages

Reduced production of Increased production

antifibrotic cytokines of fibrinogenic cytokines

Less collagenase Mesenchymal cells

Proliferation of fibroblasts

Increased production of collagen

CLINICAL FEATURES:
1. Age and sex. No age or sex is immune but the disease mostly affects age group of 20–40 years.
2. Symptoms.
Patient often presents with:
(a) Intolerance to chilies and spicy food.
(b) Soreness of mouth with constant burning sensation; worsened during meals particularly of
pungent spicy type.
(c) Repeated vesicular eruption on the palate and pillars.
(d) Difficulty to open the mouth fully.
(e) Difficulty to protrude the tongue.
3. Findings.
Changes of submucous fibrosis are most
marked over
(i) soft palate
(ii) faucial pillars and
(iii) buccal mucosa
In initial stages, mucosa is red with vesicle formations, which rupture to form superficial ulcers.

 In later stages, when fibrosis develops in the submucosal layers, there is blanching of mucosa
with loss of suppleness.
 Fibrotic bands can be seen and felt in the affected areas.
 Fibrosis and scarring has also been seen in the underlying muscle leading to restrictive
mobility of soft palate, tongue and jaw.
 Trismus is progressive, so that patient may not be able to put his finger in the mouth or
brush his teeth.
 Orodental hygiene is affected badly and teeth become carious.
Examination of oral cavity is difficult particularly to
rule out other associated premalignant lesions or malignancy.

Treatment:
MEDICAL
1.Steroids. Topical injection of steroids into the affected area is more effective than their systemic
use.
It also has fewer side effects.
It may be combined hylase (hyaluronidase).
Dexamethasone 4 mg (1 mL) combined with
hylase, 1500 IU in 1 mL is injected into the affected area twice a week for 8–10 weeks.
This brings marked improvement in symptoms and relieves trismus.
2. Avoid irritant factors, e.g. areca nuts, pan, tobacco, pungent foods, etc.
3. Treat existent anemia or vitamin deficiencies.
4. Encourage jaw opening exercises.
Surgical:
It is indicated in advanced cases to relieve trismus. Various surgical techniques used are:

1.Simple release of fibrosis and skin grafting:

There is high recurrence rate due to graft contracture.

2. Bilateral tongue flaps:

Requires flap division at a second stage.

3. Nasolabial flaps. They are small to cover the defect completely,

cause facial scar and require division of flaps at second
stage.

4. Island palatal mucoperiosteal flap. It is based on greater palatine artery. Possible only in selected
cases. Requires extraction of second molar for the flap to sit without tension.
Not suitable for bilateral cases.

5. Bilateral radial forearm free flap. It is bulky and hair bearing. May require debulking procedure,
third molar may require extraction.

6. Surgical excision and buccal fat pad graft.

7. Superficial temporal fascia flap and split-skin graft.

8. Coronoidectomy and temporal muscle myotomy.

 TUMORS OF ORAL CAVITY

BENIGN TUMORS

a) Solid Tumors

1. Papilloma:
 Palate, uvula, tongue and lips.
 White, pedunculated and less than 1cm.
 Rx: Excisional biopsy.
2. Fibroma (Fibroepithelial Polyp):
 Anywhere in oral cavity.
 Mucosa-covered pedunculated, 1cm, soft to firm.
 Cause: Chronic irritation.
 Rx: Conservative surgical biopsy.
3. Haemangioma:
 m/c in children (spontaneous regression possible).
 3 types : (i)Capillary (ii)Cavernous (iii)Mixed
 Rx: Cryosurgery and laser.
Microembolization – Preoperative adjunct.
4. Lymphangioma:
 Ant.2/3rd tongue.
 Diffuse(Macroglossia) or localized (soft, compressible swelling).
 Rx: Small lesions  Surgical excision.
Large  Partial excision.
5. Torus:
 Submucosal bony outgrowth.

Palatine Torus Mandibular Torus

(common) midline of hard Bilateral; Lingual aspect
palate. of gingiva.
 Rx: Resection.
6. Pyogenic granuloma:
 Reactive granuloma; Ant. Gingivae
 Soft, reddish to purple, bleeds on touch.
 Cause: Trauma and chronic irritation.
 Rx: Surgical excision.
 7. Pregnancy granuloma:
 Similar to pyogenic granuloma(clinically and histology)
 Starts in 1st trimester; regresses once preg. ends.
 Rx: Excision (only if it persists after preg.)
8. Granular cell myoblastoma:
 Tongue; Schwann cell derived tumor.
 Firm submucosal nodule.
 Rx: Conservative surgical excision.
 Variant: Congenital epulis- Gums of future incisors in female
infants.
9. Minor salivary gland neoplasms:
 m/c Pleomorphic adenoma
 Soft or hard palate.
 Painless submucosal nodule
 Rx: Wide surgical excision (due to high recurrence).
10. Solitary fibrous tumor:
 Mean age: 49; Females (m/c).
 Haphazard arrangement of spindle cells, thick collagen bundles in between
(Mesenchymal tumor).
 Capillary proliferation and pericystic pattern (like Hemangiopericystoma).
 Immunohistochemistry : To differentiate from other spindle cell tumors(
neurofibroma, leiomyoma etc.)
 Rx: Complete surgical excision.
b) Cystic lesions

1. Mucocele:
 m/c – lower lip.
 Retention cyst of minor salivary glands.
 Soft, bluish cyst.
 Rx: Surgical excision.
2. Ranula:
 In floor of mouth on one side of frenulum, pushing tongue up.
 From sublingual salivary gland(due to duct obstruction).
 Variant- Plunging type: Extends into neck.
 Thin wall and ramification – complete excision not possible.
 Rx: Small Complete surgical excision.
 LargeMarsupialization.
3. Dermoid:
 Sublingual dermoid: Median or lateral; above mylohyoid.
 Submental dermoid: Below mylohyoid; submental swelling behind chin.

PREMALIGNANT LESIONS

1. Leukoplakia
 Clinical white patch that cannot be characterized clinically or pathologically as any
other disease.
 Etiological factors
i. Smoking
ii. Tobacco chewing
iii. Alcohol abuse
iv. Chronic trauma
v. Associated – Hyperplastic candidiasis, Plummer
Vinson syndrome, Submucous fibrosis.
 Sites – Buccal mucosa and oral commissures.
 Age and sex- Fourth decade; m/c in males.
 Clinical types (high chance of malignant transformation)
i. Homogenous – smooth or wrinkled white patch.
ii. Nodular (speckled) – white patches on erythematous base.
iii. Erosive (erythroleukoplakia) – interspersed with erythroplakia.
 Histology – Mild to severe epithelial dysplasia.
 Malignant potential – 5%
 Management
i. Causative agent removed: disappear spontaneously.
ii. Biopsy taken to rule out malignancy if high potential suspected.
iii. Small lesions: surgical excision or ablation with laser/cryotherapy.

2. Erythroplakia

 Red patch or plaque on mucosal surface.

 Dec. keratinization red vascular connective tissue of submucosa shines through
( Hence red).
  Sites – lower alveolar mucosa, gingivobuccal sulcus, floor of the mouth.
 Clinical types :
i. Homogenous
ii. Speckled / granular
iii. Erythroplakia interspersed with leukoplakia.
 Histology – severe dysplasia, carcinoma in situ or frank invasive carcinoma.
 Malignant potential – 17 times higher risk than leukoplakia.
 Rx: excision biopsy and follow-up.
3. Melanosis and hyper pigmentation

Benign pigmented oral May transform or Malignant

mucosal lesions sometimes resemble melanoma

Hence, Biopsy mandatory.

CARCINOMA ORAL CAVITY

Etiology:

1. Smoking
 Six times higher risk than in non-smokers.
 Reverse smoking- high incidence of carcinoma hard palate.
 2. Tobacco chewing
3. Alcohol
 Six times higher risk of cancer of upper aerodigestive tract.
4. Dietary deficiency
 Riboflavin def. in alcoholics.
 Iron def. anemia – Plummer-Vinson (Patterson-Brown-Kelly) syndrome
5. Dental sepsis, jagged sharp teeth and ill-fitting dentures.
Types:

1. Carcinoma lip
 m/c – lower lip.
 SCC; exophytic or ulcerative type.
 Site of predilection: between midline and commissure of lip.
 Lymph node metastases : Submental and submandibular
 Rx: Surgical excision and plastic repair of the defect.
Block dissection (Lymph node metastases).
Radiotherapy
2. Carcinoma buccal mucosa
 m/c site – angle of mouth,
line of occlusion of upper and lower teeth.
 Gross appearance:
a. Exophytic
b. Ulceroinfiltrative
c. Verrucous Ca – white papillary growth with keratinization.
 Histology: SCC - m/c type.
 Local spread:
Submucosa muscle subcutaneous fatskin.
 Lymphatic spread:
Submandibular and upper jugular nodes.
 Clinical features:
a. Pain and bleeding.
b. Buccinator, pterygoid and masseter muscles if involved  Trismus.
c. Fungating mass over cheek. Late
d. Foul smelling bleeding mass in oral cavity. Features
 Investigations:
a. Biopsy
 b. CT scan ( Mandible or maxilla involvement and extension into
infratemporal fossa )
 Rx :
a. Stage I (T1N0) – surgical excision
b. Stage II (T2N0)
i) Radiotherapy
ii) Surgery (excision of growth and marginal or segmental
mandibulectomy /maxillectomy) – if bone or muscle involved.
c. Stage III and IV
i) Surgical resection
ii) Reconstruction with skin or myocutaneous flap
iii) Post-op radiotherapy

3. Carcinoma oral tongue

 m/c site : middle of lateral border,

ventral aspect.
 Local spread :
a. Lingual musculature – ankyloglossia
b. Floor of mouth, alveolus, mandible.
 Lymphatic spread :
a. Submandibular and submental nodes
b. Upper jugular and jugulo-omohyoid nodes.
 Clinical types :
a. Exophytic – like papilloma
b. Nonhealing ulcer – grey white shaggy base
c. Submucous nodule.
 Symptoms:
a. Local pain
b. Pain in ipsilateral ear - Due to common N. supply of tongue (lingual
nerve) and ear (auriculotemporal) from mandibular division of trigeminal
N.
c. Lump in mouth
d. Enlarged lymph node mass in neck
e. Dysphagia, slurred speech.
f. Difficulty to protrude tongue.
 g. Bleeding from mouth.
 Rx :
a. Radiotherapy
b. Surgery
c. Commando operation – hemiglossectomy, segmental or
hemimandibulectomy and block dissection of neck nodes.

4. Carcinoma hard palate

 Glandular variety m/c than SCC.

 Lymphatic spread : submandibular and upper jugular nodes
 Rx:
a. Surgical excision with partial maxillectomy
b. Block dissection of nodes
c. Surgical defect in palate- closed by suitable prosthesis.
5. Carcinoma of alveolar ridges

 Gingival carcinoma
 m/c in men
 m/c site: lower jaw behind the first molar
 Rx :
a. Surgical excision
b. Block dissection
c. Partial maxillectomy or hemimandibulectomy
d. Radiotherapy avoided - risk of radio-osteonecrosis.
6. Cancer floor of mouth

 SCC ( ulcerative or infiltrative)

 m/c in males.
 Start near opening of submandibular ductobstructed submandibular gland
enlarges.
 Local and lymphatic spread.
 Rx: Surgery, radiotherapy and block dissection.
7. Carcinoma retromolar trigone
 Primary or secondary to growth extensions from gingiva, floor of mouth, buccal
mucosa and palatine arch.
 Rx: wide surgical excision, block dissection.
 NONSQUAMOUS MALIGNANT LESIONS

1. Minor salivary gland tumors

 m/c site: palate
 Types : a. Adenoid cystic variety ( m/c)
b. Adenocarcinoma
c. Mucoepidermoid carcinoma
 Rx: Wide surgical excision and block dissection.

2. Melanoma
 Rare in oral cavity and oropharynx
 m/c sites : palate and gingiva
 Rx : Wide surgical excision
 Local recurrence and poor prognosis.

3. Lymphomas
 Palatine tonsils involved.
 Mostly non-Hodgkins
 Smooth, submucosal, ulcerated bulky mass
 Rx: radiation and chemotherapy

4. Kaposi sarcoma
 Multifocal vascular tumor
 High in AIDS pts.
 Reddish purple nodule or plaque on palate
 Spindle cells with haemorrhagic cleft-like spaces
 Rx in non-AIDS pts. : Chemotherapy
 NON NEOPLASTIC LESSON OF SALIVARY GLAND

1. MUMPS:
 CAUSE: Pararmyxo virus
 MOT:
 nasal , oral, and urinary secretions
 Fomites.
(most commonly occurs in children)
 INCUBATION PERIOD: 2-3 Weeks
 INFECTIVE PERIOD: Before appearance of clinical manifestations. Up to 7-10 days after
parotid swelling subsides
 CF:
 Fever (up to 103 degree), malaise , anorexia , muscle pain
 Parotid swelling 1st appears on one side followed by other
 Other glands may also be involved
 Swelling subsides after a week
 COMPLICATIONS:
 ORCHITIS: -Painful and tender testis on one side commonly
- Sterility is rare
 OPHRITIS: Causes lower abdominal pain. Female sterility never seen
 PANCREATITIS: Abdominal pain
 ASEPTIC MENINGITIS/ MENINGOENCEPHALITIS: Headache, neck stiffness, drowsiness
 UNILATERAL SENSORINEURAL HEARING LOSS: Sudden deafness
 OTHERS: Thyroiditis, myocarditis, nephritis, arthritis
 DIAGNOSIS:
 Usually clinical
 Serum ,urinary amylase,- 1st week of parotitis
 Serology:
 RECENT INFECTION: Serum IgM and 4 times serum IgG titre

 PAST INFECTION: Serum IgG : Past infection / immunization

 TREATMENT:
 Proper hydration, rest, analgesics
 PAROTITIS: Sold and hot compresses over parotid gland
 Avoid spicy food
 ORCHITIS: Cold compresses and support to scrotum analgesics
  PREVENTION: MMR vaccine -15 months

2. ACUTE SUPPORTATIVE PAROTITIS

 CAUSES: Staphylococcus aureus
 RISK FACTOR: Old age, dry mouth, dehydration
 ROUTE OF INFECTION: From mouth to stensens duct
 CF:
 Sudden onset, severe pain and enlargement of glands
 Jaw movements aggravate the pain
 Opening of stensens duct is swollen and red
 On gentle pressure over gland – pus discharges
 Patient is febrile and toxaemic
 INVESTIGATIONS:
 WBC count – Leukocytosis with increase polymorphs
 Culture of blood and pus
 TREATMENT:
 Antibiotics[ preferably through IV route]
 Adequate hydration –oral hygiene
 Promote salivary flow
 If doesn’t improve –SURGICAL DRAINAGE

3. CHRONIC RECURRENT SIALADENITIS:

 ACUTE EXACERBATION:
 Parotid gland – enlarge , tender with pus discharging
 Between acute episodes – gland firm
 CULTURE- Staphylococci/ streptococci
 TREATMENT :
 Antibiotics
 maintain good oral hygiene
 sialogogues [promote salivation]
 RISK FACTOR: OCPs, thiouracil, alcohol
 Involve parotid gland with recurrent bacterial infection
4. SIALECTASIS:
 Dialation of ductal system – stasis of secretion- infection
 CAUSES:
 Congenital

 Granulomatous disease

 SJogrens syndrome

 CF:
 Same as that of chronic recurrent sialadenitis
 Differentiate by sialography
 TYPES:
 Puncutate

 globular
 cavitatory

5. SIALOLITHIASIS: [salivary calculi]

 Calculi in duct of Submandibular [90 %] and parotid gland[10 %]
 Composition: calcium phosphate stones
 CF:
 Intermittent swelling – meal time
 Pain
 Subside in 1-2 hours
 80 percent – radio opaque
 INVESTIGATION:
 NCCT
 Sialography [translucent stones]
 Radiolucent stones- sialodoscopy [ diagnosis and treatment]

6. SJOGRENS SYNDROME: [SICCA SYNDROME]

 Also called lymphoepithelial sialadenitis, is an autoimmune disorder
 TYPES:

 PRIMARY SJOGREN SYNDROME

 Xerostomia- salivary glands involvement

 Xerophthalmia- Lacrimal gland involvement

 Mostly occurs in parotid gland , hence it is known as

 - benign cymphoepithelial cession of parotid
- Milkulicz s disease
 Both sexes are equally involved

 SECONDARY SJOGREN SYNDROME:

Three components-
1. Keratoconjunctivitis sicca- lacrimal gland
2. xerostomia
3. Rheumatoid arthritis/ SLE/ autoimmune connective tissue disorder
 HISTOPATHOLOGY: Destruction of acini and lymphocytic infilteration

 INVESTIGATION:

 Biopsy of lower lip [ minor salivary glands]

 SS -–A,AA-B, Antibody detection
 ESR increase, +RF,+ANA for associated Rheumatoid Arthritis/SLE

7. SIALOMETAPLASIA:
 Most commonly minor salivary glands in palate
 Male preponderance in their 40 s
 CF: Swelling / ulceration lesion
 HISTOLOGY: Pseudoepithelomatous hyperplasia [destruction of acini with squamous
metaplasia]
 INVESTIGATIONS: Biopsy
 TREATMENT: Spontaneous heating in 5-6 weeks

8.SIAILADENOSIS:

 Non inflammatory, non- neoplastic

 Bilateral or Unilateral parotid swelling
 RISK FACTOR: DM, alcoholism , malnutrition ,obesity and prolonged intake of
anticholinergic drugs
 HISTOLOGY:
 Acinar cells hypertrophy [2-3times normal;]

 Onlong standing , acini undergo degeneration and replacement with fatty tissues
  CF:
Bilateral parotid swelling


 Xerostomia [ long standing]

 INVESTIGATION:
- FNAC
- Gland biopsy
 TREATMENT:
- Treat the cause
- In later stage – artificial saliva, sialogogues

NEOPLASTIC LESION OF SALIVARY GLAND

Benign[percent] Malignant[percent]
PAROTID 80 20
SUBMANDIBULAR 50 50
SUBLINGUAL 25 75

FEATURES OF MALIGNANT SALIVARY TUMORS:

 Rapid growth
 Restricted mobility
 Fixity of overlying skin
 Pain
 Facial nerve involvement

BENIGN TUMOURS:

1. PLEOMORPHIC ADENOMA /MIXED TUMOURS

 Most common benign tumor –usually in females
 3rd/4th decade
 Slow growing –mostly arise in tail of parotid
  CF: Superficial lobe, painless, lifts earlobe upwards
 Histology: Has epithelial and mesenchymal elements. Stroma may be mucoid , fibroid,
vascular, chondroid/myxochondroid
 Diagnosis:
 FNAC
 Extent of swelling-MRI
 Management – surgical excision
In parotid [superficial parotidectomy]
 Recurrence rate is high
 Changes into mixed malignant tumor later.

2. WARTHIN TUMOUR/ADENOLYMPHOMA (PAPILLARY CYSTADENOMA LYMPHOMATOSUM):

 Common in males(5:1) usually in 5th and 7th decade
 Occurs bilaterally in 10% (most common B/L benign tumor)
 Gross: Rounded, encapsulated tumor, at times cystic with mucoid/brownish fluid
 Histology: Epithelial and lymphoid elements are seen.
 CF: Parotid swelling (tail of parotid gland)
 Diagnosis:
 FNAC
 Extent of swelling : MRI
 Treatment: Superficial parotidectomy (or) extracapsular dissection.

3. ONCOCYTOMA[oxyphil adenoma]
 Elderly
 Usually <5cm, involve superficial lobe of parotid
 Benign-cystic
 Arise from acidophilic cells [oncocytes]
 TREATMENT: Superficial parotidectoney

4. HEMANGIOMAS
 Most common in children mainly female
 CF: soft, painless mass, increased in size with crying/ straining
 TREATMENT:
  Tumour spontaneously regresses
 If not surgical excision

5. LYMPHANGIOMAS:
 Parotid and Submandibular glands
 PALPATION: Soft, cystic
 TREATMENT: Surgical exision
 Other tumor: LIPOMA, NEUROFIBROMA-Rare

MALIGNANT TUMOURS

1. MUCO EPIDERMOID CARCINOMA

 Most common malignant parotid tumor
 Seen in infancy
 Slow growing , invade facial nerve
 HISTOLOGY: Mucin producing cells and squamous cells present , hence the name
 TYPES:
 LOW GRADE – good prognosis, more common in children
 HIGH GRADE- Poor prognosis, aggressive
 TREATMENT:
 LOW GRADE- Superficial/total parotidectomy
 HIGH GRADE- Excision and post-operative radiotherapy
(Facial nerve preserved)

2. ADENOID CYSTIC CARCINOMA

 Slow growing- infiltrates into tissue planes and muscles
 Perineural invasion-
 Extremely painful
 7th nerve paralysis
 Metastasis – to lymph node
 distantly to lung, brain ,bone

 HISTOPATHOLOGY: SWISS- CHEESE APPEARANCE

  TREATMENT: Radical parotidectomy and post-operative radiotherapy

3. ACINIC CELL CA:

 Low grade benign mixed tumor
 GROSS- small, firm, movable, encapsulated tumor
 Metastasis- rare
 TREATMENT: Superficial/ total parotidectomy

4. MALIGNANT MIXED TUMOUR

 Malignant counterpart of pleiomorphic adenoma of salivary gland
 Rapid increase in size
 Facial nerve involvement
 Ulceration over swelling
 Hard swelling
 Painful
 TREATMENT:
 Radical parotidectomy
 Facial nerve sacrificed during operation is grafted immediately

5. SQUAMOUS CELL CARCENOMA

 Rapidly growing tumour that infilterates, causes pain and ulcerates through skin
 TREATMENT:
 Radical parotidectomy
 Radical neck combined if nodal metastasis are present
 Followed by post-operative radiotherapy

6. FREY’S SYNDROME [gustatory sweating]

 CAUSE: Complication of parotid surgery [several months later]
 SYMPTOMS: Sweating and flusting of preauricular skin
 PATHOLOGY: Aberrant innervation of sweat gland by parasympathetic(PS) secretomotor
fibers [destined for parotid gland]
 TREATMENT:
 Tympanic neurectomy [ intercept these PS fibers]
 Placing a sheet of fascia lata between skin and underlying fat
  subcutaneous infilteration of botulinium toxin

GRANULOMATOUS INFECTIONS OF SALIVARY GLAND

1. TB:TUBERCOLOSIS
 TYPICAL TUBERCULOSIS
 Involves parotid or Submandibular gland
 Parotid gland
1) Source of infection:
 Oral cavity to gland via parotid duct
 Hematogenous spread from lung
2) CF:
 Acute parotid sialadenitis (or)
 Long standing parotid mass-mimicking tumor
 Overlying skin changes or fistula seen
3) Investigation:
 PPD:-[Purified Protein Derivative] Skin test
 FNAC or biopsy:- Epithelioid granuloma or acid fast bacilli culture positively
 Chest x-ray maybe negative
4) Treatment :
 Antitubercular therapy
 Non responders – excisional biopsy
 ATIPICAL MYCOBACTERIAL
 Affect gland or lymph nodes
 Investigation:
 FNAC or biopsy- acid fast organisms culture and sensitivity established.

2. SARCOIDOSIS:
 Involves parotid gland
 CF: Uveoparotid fever
 Fever

 Enlargement of parotid and lacrimal gland

 Chorioretinitis

 Cranial nerve palsies

3. ACTINOMYCOSIS:
 Usually follows dental infection or manipulations
 Clinical Presentation: - Parotid swelling or fistula of skin that discharge sulfur granules.
 Investigation: Gram staining of pus: Nonacid gram + organisms
 Treatment: Penicillin, erythromycin, tetracycline- prolonged for months

4. TOXOPLASMOSIS:
 Causal organism: Toxoplasma gondil
 MOT:
 Eating undercooked meat of lamb, beef or chicken.

 Food contaminated by cats faces

 CF: Acute toxoplasmosis

 Cervical lymphadenothy with discrete , usually non-tender nods <3cm

 Fever malaise ,night sweats, myalgia, sore throat

 Retinochoroidits

 Investigation:
 Serological tests of acute convalescent sera

 Lymph node biopsy

 Treatment:
 Usually self-limiting

 Immunocompromised or pregnant women - PYRIMETHAMINE

 DEVELOPMENT OF TONGUE

Muscles of tongue formed by occipital myotomes,

Anterior 2/3rd of tongue (1st arch):

 Sensory: lingual branch of mandible,

 Taste: chorda tympani (PRETREMATIC NERVE),

Circumvallate papillae: It’s supplied by glossopharyngeal nerve,

Posterior 1/3rd of tongue (3rd arch): Sensory and taste both by glossopharyngeal nerve,

Posterior 1/3rd of tongue (4th arch): Sensory and taste both by superior laryngeal branch of vagus
 MANDIBULAR NERVE

It is a MIXED NERVE and branch of a TRIGEMINAL nerve

It’s a main nerve, supply oral cavity

Pass out through foramen ovale along with lesser petrosal nerve.

SENSORY SUPPLY OF MANDIBLE:

 Inferior alveolar nerve supplies lower part of the buccal cavity which pass
out through mental foramen form a MENTAL NERVE
 Lingual nerve supplies anterior 2/3rd of tongue
 Buccal nerve gives sensation of cheek
 Auriculo temporal nerve supplies lateral part of mandible

MOTOR SUPPLY OF MANDIBLE:

It supplies,

 Masticator muscle,
 Tensor tympani and Tensor palati,
 Mylohyoid and anterior belly of digastric (by Inf.alveolar nerve).

COVEYING PARA SYMPATHETIC SUPPLY:

To parotid gland,

 Carried by glossopharyngeal also through auriculo temporal nerve,

To submandibular and sublingual gland,

 Carried by chorda tympani also through lingual nerve.

 ANATOMY OF PHARYNX

THREE PARTS:

NASOPHARYNX:

 Also called Epi pharynx,

 Between base of skull and palate,
 Lies in front of C1 vertebra,
 Lined by ciliated columnar epithelium,

OROPHARYNX:

 Between palate and hyoid,

 Lies in front of C2,C3(upper part)
 Lined by stratified squamous epithelium

LARYNGOPHARYNX:

 Also called as HYPOPHARYNX,

 Between hyoid and cricoid,
 Lies in front of C3(upper part),C4,C5,C6,
 Lined by stratified squamous epithelium.
WALDEYERS RING:

 It is a group of lymphoid tissue,

 Present between nasopharynx and oropharynx,
 Provide immunity in children,
 Atrophied at latter age of life,

IT HAS FOUR TONSILS:

(LUSCHKA’S TONSIL) Adenoid tonsil both lined by

(GERLACH TONSIL) Tubal tonsil ciliated columnar epithelium

(FAUCIAL)Palatine tonsil both lined by

Lingual tonsil stratified squamous epithelium

POSTERIOR PHARYNGEAL WALL

 Anterior fascia,
 Between longitudinal and circular muscles of pharynx ,
 Posterior fascia,

Anterior fascia also known as PHARYNGOBASILAR FASCIA (it also forms a capsule of tonsils)

MUSCLES OF PHARYNX:

LONGITUDINAL MUSCLES:

It is also called as dilator muscles

 Stylopharyngeus(from styloid)
 Salpingopharyngeus(From ET) Connects to thyroid
 Palato pharyngeus(palate).

CIRCULAR MUSCLES:

It is also called as constrictor muscle

Three parts,

 Superior constrictor
 Middle constrictor
  Inferior constrictor

SUPERIOR CONSTRICTOR:

Superiorly it is not attached to base of skull

Above that FORAMEN OF MORGAGNI present

Contents of foramen of morgagni:

T TENSOR PALATI

A ASCENDING PALATINE ARTERY

A PALATINE BRANCH OF ASCENDING PHARYNGEAL

L LEVATOR PALATI

A AUDITORY TUBE (ET)

INFERIOR CONSTRICTOR:

It has two muscles,

 Thyropharyngeus
 Cricopharyngeus

Between that there is area of weakness called KILLIANS DEHISCENCE

Nerve supply,

 Glossopharyngeal,
 Vagus nerve,
Superior laryngeal which again leads to external and internal branches,
Recurrent laryngeal.

Glossopharyngeal nerve SUPERIOR and MIDDLE CONSTRICTOR

Superior laryngeal vagus of internal laryngeal nerve INFERIOR CONSTRICTOR

Recurrent laryngeal nerve OESOPHAGUS

ZENKERS DIVERTICULUM

 It is an out pouching of posterior pharyngeal wall,

 Site: killians dehiscence ,
 Seen common in elderly,
 It is an acquired condition of PULSION DIVERTICULUM,
 It is a FALSE DIVERTICULUM.

SYMPTOMS:

 Dysphagia,
 Hallitosis(foul smelling),
 Regurgitation of undigested food,
 Hoareness,recurrent cough.

ON EXAMINATION:

 Swelling in the neck goes anteriorly, due to posterior presence of vertebra(commonly seen
on left side),

ON PALPATION:

 Swelling gives a GURGLING SOUND,

 This condition called BOYCE SIGN,

INVESTIGATION:

 Endoscopy,
 Barium swallow(lateral view) is best,

MANAGEMENT: Cricopharyngeal myotomy,

  laser( for pouch less than 2 cm) called DOHLEMAN’S PROCEDURE
 endoscopic diverticulotomy (for pouch more than 2 cm)

CAVITY OF PHARYNX

NASOPHARYNX:

Inferior turbinate- 1 cm behind-Eustachian tube

Behind form a bulge called TORUS TUBARIS

And form a FOSSA OF ROSENMULLAR

(site of nasopharyngeal carcinoma)

It obstructs either one side of eustachian tube

(leads to unilateral serous otitis media)

Middle turbinate- 1 cm behind – sphenopalatine foramen (site of ANGIOFIBOMA)

OROPHARYNX:

Superior: soft palate

Antero inferior: base of tongue

Laterally: palatine tonsil ANTERIOR PILLAR

(palatoglossus)

POSTERIOR PILLAR

(palatopharyngeus) longitudinal muscles

It also gives some circular fibres

Fuses with superior constrictor

Form

PASSAVANTS RIDGE

 It moves anteriorly along with soft palate its move posteriorly to close
NASOPHARYNGEAL OPENING to prevent nasal regurgitation.

Defect in that passavant’s ridge and soft palate leads to,

VELO-PHARYNGEAL INSUFFICIENCY (regurgitate nasally)

HYPERNASAL VOICE (open) Caused by,

 Cleft palate
 Palate palsy
 Submucous cleft
It is known as RHINOLALIA APERTA.

HYPONASAL VOICE (close) Caused by,

 Nasopharyngeal carcinoma,
 Adenoid hypertrophy
 Polyp of nose.

It is known as RHINOLALIA CLAUSA

HYPOPHARYNX:

3 “P”s,

 Posterior cricoid,
 Pyriform fossa,
 Posterior pharyngeal wall.

NERVE SUPPLY OF PHARYNX

SENSORY:

Nasopharynx- Maxillary nerve

Oropharynx- Glossopharngeal nerve

(except base of tongue it is supplied by superior laryngeal nerve)

Hypopharynx- Vagus nerve

(upper part-superior laryngeal nerve

lower part-recurrent laryngeal nerve)

MOTOR NERVE:

 Pharyngeal plexus of vagus (with fibers of 11th cranial nerve) it supplies,

 Longitudinal muscles except STYLOPHARNYGEUS
 All constrictor muscles
 All palate muscles (except tensor palate supplied by mandibular nerve)
 SPACES OF PHARYNX

BEHIND MUSCLES OF PHARYNX (Three fascia [BAP])

 BUCCOPHARYNGEAL FASCIA
 ALAR FASCIA
 PREVERTEBRAL FASCIA

RETROPHARYNGEAL SPACE OF GILLET:

Upper limit: Base of skull

Lower limit: T4

Ant.Boundary: Buccopharyngeal fascia

Post.Boundary: Alar fascia

Content: lymph nodes of rouviere

Disease: retropharyngeal abscess is unilateral because it has midline

DANGER SPACE

Upper limit: base of skull

Lower limit: Diaphragm

Ant.Boundary: alar fascia

Post.boundary: pre vertebral fascia

PREVERTEBRAL SPACE

Upper limit:Base of skull

Lower limt: T4

Ant.boundary: prevertebral fascia

Post.boundary: vertebrae

Disease: prevertebral abscess is enlarged and diffuse bulge

PARAPHARYNGEAL SPACE

Smallest, most commonly infected

Also called as pharngo maxillary space

Divides into

 Anterior( pre styloid )

 Posterior ( post styloid)

Upper limit: base of skull

Lower limit: hyoid

Medial wall: buccopharyngeal fascia

Lateral wall: medial pterygoid, masseter, mandible, parotid

Contents:

Posterior (post styloid)

 Internal carotid artery,

 Internal jugular vein,
 9,10,11,12 cranial nerve,
 Cervical sympathetic chain.

Disease:

parapharngeal abscess push tonsils towards medially

lead to TRISMUS (lock jaw)

PERITONSILLAR SPACE

Medial wall: pharyngo basilar fascia

Lateral wall: superior constrictor muscle

Contents: Fat

Disease:

 Abscesss in that space called QUINSY

 Also leads to trismus
 It also pushes tonsils towards medial.
 ANATOMY OF PALATINE TONSILS

Two in number
Lymphoid tissue
Situated in Lateral wall of oropharynx between the anterior and posterior pillars
Extend upward into soft palate
Downward into base of tongue
Anteriorly into palatoglossal arch
TWO SURFACES: MEDIAL AND LATERAL
TWO POLES: UPPER AND LOWER.
Medial Surface:
 Covered by non-keratinizing stratified squamous epithelium.
 Dips into tonsil as crypts
 12 – 15 crypts seen on medial surface of tonsils.
 Crypt at Upper part of tonsil: very large and deep called Crypta magna or intratonsillar
cleft.
 Represent ventral part of second pharyngeal pouch.
 Crypts consists of epithelial cells, bacteria, food debris.
Lateral surface:

 Well defined fibrous capsule.

 Loose areolar tissue is present between capsule and bed of tonsil, helps in easy
dissection of tonsil during tonsillectomy.
 Site of collection of pus in peritonsillar abscess.
 Attachment of fibres of palatoglossal and palatopharyngeus muscles to capsule.

Upper Pole:

 Extend to soft palate.

 Medial surface covered by semilunar fold.
 Extend between anterior and posterior pillars, enclose SUPRATONSILLAR FOSSA.
Lower pole:

 Attached to tongue.
 Triangular fold of mucous membrane between anterior and anterior inferior part of
tonsil enclose ANTERIOR TONSILLAR SPACE.
  Tonsil separated from tongue by a sulcus: TONSILLO LINGUAL SULCUS (Seat of
carcinoma).

Bed of tonsil:

 Formed by superior constrictor and styloglossus muscles.

 Glossopharyngeal nerve and styloid process can be approached surgically through
tonsillar bed after tonsillectomy.
 Related to facial artery, submandibular salivary gland, posterior digastric muscles,
medial pterygoid muscles, angle of mandible.
BLOOD SUPPLY

 Tonsillar branch of facial artery.

 Ascending pharyngeal artery from external carotid.
  Ascending palatine artery from facial artery.
 Dorsal linguae branch of lingual artery.
 Descending palatine branch of maxillary artery.

VENOUS DRAINAGE

 Para tonsillar vein into common facial vein and pharyngeal venous plexus.
LYMPHATICS

 Deep cervical nodes: Jugulo digastric node. ( below angle of mandible )

NERVE SUPPLY

 Lesser palatine branch of sphenopalatine ganglion

 Glossopharyngeal nerve provides sensory nerve supply.
FUNCTION

 Act as sentinels
 Local immunity
 Surveillance mechanisms.
 Act through both humoral and cellular immunity
Local immunity:

 Tonsil and adenoid are lined by squamous epithelium.

 Increased surface area by crypt folds.
 They contain specialized epithelium: M Cells, Antigen processing cells, micropores.
 By this, antigenic material is brought in contact with lymphoid follicle.
 Follicles  germinal centre of B cells and a mantle zone in large lymphocytes.
 B cells transform into antibodies.
 Phagocytosis by macrophages.
 Utilised in Chronic infections.
Surveillance mechanisms:

 Identify antigen and alerts the body.

 Antigen load is high and B cells proliferate and enter blood stream.
 Antigen presenting cells, Memory cells, macrophages, T helper cells, T suppressor cells
are activated.
 Antibodies prepare antigens for phagocytosis.
 Tonsil is more active in
age: 4 to 10 years of age.
 Involution occurs after puberty
 Decrease in B cell production.
 Increased T:B cell ratio.
 Tonsillectomy do not affect general immuno surveillance function.
 ACUTE TONSILLITIS

Acute infection of tonsil involves these 3 components. Classified based on:

 Acute catarrhal or superficial tonsillitis: part of generalized pharyngitis; viral infection.

 Acute follicular tonsillitis: infection spread to crypts; has purulent discharge; present as
yellow spots.
 Acute parenchymatous tonsillitis: Tonsil uniformly enlarged; Red.
 Acute membranous tonsillitis: Stage next to acute follicular tonsillitis. Exudation from crypts

form a membrane on surface of tonsil.

AETIOLOGY:

 Haemolytic Streptococcus: Most common.

 Staphylococci , pneumococci , H.inflenzae
 Age: School going children.
 Rare in adults.
SYMPTOMS:

 Sore throat
 Difficulty in swallowing: Children refuse food due to pain.
 Fever : 38°C to 40°C
Associated chills and rigors
 Earache : Referred pain from tonsil or Acute otitis media
 Constitutional symptoms : Headache, General body aches , Malaise , Constipation ,
Abdominal pain ( enteric lymphadenitis )
SIGNS:

 Breath foetid
 Tongue coasted
 Tonsil: Red, swollen.
Acute follicular tonsillitis: yellow spots of purulent material presenting at opening of
crypts.
Acute membranous tonsillitis: Whitish membrane on medial surface of tonsil, wiped
away with swab.
Acute parenchymatous tonsillitis: Enlarged, congested, some oedema of uvula and
soft palate.
 Jugulo digastric node enlargement.
TREATMENT:

 Put to bed.
 Give plenty of fluids.
 Analgesics: According to age; to relieve local pain and fever.
 Antimicrobial drugs: Penicillin drug of choice. (Streptococcus)
Erythromycin is used in penicillin allergic patients.
For 7 -10 days.

COMPLICATIONS:

 Chronic tonsillitis, due to recurrent acute attacks.

 Peritonsillar abscess
 Parapharyngeal abscess
 Cervical abscess, suppuration of jugulo digastric node.
 Acute otitis media
 Rheumatic fever, Group A Streptococcal infection.
 Acute glomerular nephritis, rare.
 Sub-acute bacterial endocarditis, Streptococcus viridians infection.
 DIFFERENTIAL DIAGNOSIS OF MEMBRANE OVER TONSIL

Membranous tonsillitis:

Pyogenic infection.
Exudative membrane over medial surface of tonsil.

Diphtheria:

Slow in onset.
Less local discomfort.
Membrane extend beyond tonsil.
Color: Dirty grey.
Urine: Albumin ++
Smear and culture: Corynebacterium diptheriae.

Vincent angina:

Insidious in onset.
Less discomfort.
Formed over one tonsil.
Can be removed reveals an ulcer over tonsil.
Swab: Fusiform bacilli, Spirochetes.

Infectious mononucleosis:

Young adults
Tonsil enlarged, congested
Lymph node enlarged in posterior triangle of neck.
Splenomegaly
Due to failure of antibiotic therapy
Blood smear: 50% Lymphocytes, 10% atypical. WBC rises in second week

Agranulocytosis:

Ulcerative necrotic lesions all over tonsil and oropharynx.

Severely ill.
Acute fulminant form:
WBC < 2000/cu.mm. Polymorphs decreased by 5%.
Leukaemia:

Children: 75% ALL, 25% AML

Adults: 20% Lymphocytic, 80% Non-lymphocytic
Blood smear:
TLC >100,00/cu.mm
Anaemia present and progressive.

Aphthous ulcer:

Involve whole part of oral cavity.

Solitary

Malignant tonsil

Traumatic ulcer:

 Any injury to oropharynx heals by formation of membrane.

Candidal infections

DIAGNOSIS REQUIRES:

 History
 Physical examination.
 Total and differential count.
 Blood smear.
 Throat swab and culture.
 Bone marrow aspiration or needle biopsy.
 Paul bunnell or mono spot test
 Biopsy of lesion.
 CHRONIC TONSILLITIS

AETIOLOGY

 Complication of acute tonsillitis.

 Micro abscesses walled by fibrous tissue seen in lymphoid follicle of tonsils.
 Subclinical infections
 Children, young adults.

TYPES:

Chronic follicular tonsillitis:

Crypts are full of infected cheesy material – show yellow spots.

Chronic parenchymatous tonsillitis:

Hyperplasia
Enlarged, interfere with speech, deglutition, respiration
Sleep apnoea
Cor pulmonale: long standing cases.

Chronic fibroid tonsillitis:

Small but infected.

CLINICAL FEATURES

 Recurrent attacks of sore throat or acute tonsillitis.

 Chronic irritation in throat with cough.
 Bad taste in mouth and foul breath (halitosis) due to pus in crypts.
 Thick speech, difficulty in swallowing, choking spells at night.

EXAMINATION
  Tonsils: Varying degree of enlargement.
 Yellowish beads of pus on medial surface of tonsil.
 Tonsils are pus: Pressure on anterior pillar expresses frank pus or cheesy material.
 Flushing of anterior pillars of tonsil.
 Enlargement of Jugulo digastric lymph node.
 Acute attacks, nodes enlarge.

TREATMENT:

 General health
 Diet
 Treatment of co existential infection of teeth, nose, sinus.
 Tonsillectomy (on interference with speech, deglutition, respiration, recurrent attacks)

COMPLICATIONS:

 Peritonsillar abscess
 Parapharyngeal abscess
 Intratonsillar abscess
 Tonsilloliths
 Tonsillar cyst
 Rheumatic fever, acute glomerular nephritis, eye and skin disorders.
Tonsilloliths

Calculus of tonsil
Feature of chronic tonsillitis.
Crypt is blocked with retention of debris.
Calcium and magnesium deposits and lead to formation of stone.
Enlarge and ulcerate.
Local discomfort, foreign body sensation
Diagnosed by palpation or gritty feeling
TREATMENT: Removal of stone or tonsillectomy.

Intratonsillar abscess:

Accumulation of pus within tonsil

 Blocking of crypt opening in acute follicular tonsillitis
Tonsil: swollen, red
TREATMENT: Antibiotics, drain abscess,
Later tonsillectomy

Tonsillar cyst:

Blockage of tonsillar crypt

Yellow swelling over tonsil
Symptomless

DISEASES OF LINGUAL TONSILS

Acute lingual tonsillitis:

Unilateral dysphagia
Feeling of lump in throat
Enlarged, Congested
Cervical lymph nodes enlarged.
TREATMENT: ANTIBIOTICS

Hypertrophy of lingual tonsils:

It is a Compensatory hypertrophy of lymphoid tissue.

Due to recurrent infection of post tonsillectomy individuals
Discomfort in swallowing, feel of lump, dry cough, fever, thick voice.

Abscess of lingual tonsil:

Rare
After acute lingual tonsillitis
Severe unilateral dysphagia, Pain in tongue, Excess salivation Trismus
Jugulo digastric node enlarged.
Dangerous as it lead to laryngeal oedema.

ADENOID HYPERTROPHY

SYMPTOMS:
  Nasal obstruction (pinched up nose, naso labial crease absent, mouth
breathing, Palate become high arched, Crowding of teeth),
 Eustachian tube obstruction (serous otitis media (conductive hearing loss-dull
look) Recurrent acute otitis media),

Above conditions called ADENOID FACIES

 Rhinolalia clausa,
 Sleep apnea.

INVESTIGATIONS: X-RAY nasopharynx lateral view

ENDOSCOPY GRADING:

Grading one-1/3rd involved

Grading two-1/3rd to 2/3rd involved

Grading three-2/3rd to nearly complete

Grading four-Complete

MANAGEMENT:

Primary-Medical management (acute symptoms)

 Antiallergics
 Antibiotics(infection)
 Steroid nasal spray (decrease adenoid size)

Secondary-Adenoidectomy (chronic condition) Conditions like,

 Nasal obstruction-recurrent sinusitis (defect in hearing, learning, language

development),
 ET obstruction-(chronic serous otitis media Recurrent acute otitis media),
 Sleep apnea Greater than 5 apnea per hour OR Greater than 30 apnea per 7 hour

SURGICAL CORRECTION:

 Patient should lies on ROSES’S POSITION,

 Extension at atlanto-occipital joint,
  Extension at cervical joint also.

INSTRUMENTS:

 Tongue depressor-Boyle’s tongue blade, Davis mouth gag also used

 Connected by a device called DRAFFIN BIPOD STAND
 Curette used to remove adenoid- st clair Thomson adenoid curette
 Usage of micro debrider

ADVANCED TECHNIQUE:

COABLATION:

 Cutting and coagulating same time,

 It is depend on radio frequency.

CAUTERISATION: Diathermy

CONTRAINDICATIONS: Velo-pharyngeal insufficiency (cleft palate)

COMPLICATIONS:

 Heamorrhage,
 Injury to ET tube,
 Coroners clot,
 RARE: Grisel’s syndrome.
 THORNWALDT’S BURSITIS

 Remnant of communication

between primary pharynx and notochord normally disappear.

 If it is persist then it is called thornwaldt’s bursa

Site at roof of nasopharynx

Infection of thornwaldt’s bursa leads,

Recurrent post nasal drip,

Headache(occipital),

INVESTIGATIONS: CT/MRI scan

MANAGEMENT:

 Antibiotics,
 Excision,
 If cyst formed-MARSUPIALIZATION.
 ACUTE AND CHRONIC PHARYNGITIS

ACUTE PHARYNGITIS

Aetiology:

 Common
 Viral, bacterial, fungal
 Bacterial: Acute Streptococcal infection as aetiology to Rheumatic fever and post
streptococcal glomerulo nephritis.
Clinical features:

 Present as various grades.

 Milder: Discomfort in throat, malaise, low grade fever; Pharynx congested; No
lymphadenopathy.
 Moderate and severe: Pain in throat, Dysphagia, Headache, Malaise, High fever; Pharynx
show erythema; exudate and enlargement of tonsils and lymphoid.
 Very severe: Oedema of soft palate; Uvula of enlargement of cervical nodes.
 Viral infections are mild with rhinorrhoea and hoarseness of voice.
 Bacterial infections are severe.
 Gonococcal infection: Mild, asymptomatic.
Diagnosis:

 Throat swab: Bacterial pharyngitis

90% Group A Streptococcal infection.
Gonococcal pharyngitis
 Special media: Diptheriae
 Failure to obtain bacterial aetiology suggests viral aetiology
Treatment:

 General Measures
Bed rest, plenty of fluids, warm saline gargles or pharyngeal irrigations, Analgesics
Lignocaine viscous – Relieve Local discomfort
 Specific treatment
 Streptococcal pharyngitis – Penicillin G 2,00,000 to 2,50,000 units orally four times a day - 10
days.
Benzathine Penicillin G 6,00,000 units I.M, 60lb in weight , 1.2 million units once I.M for
patient > 60lb.
Penicillin sensitive: Erythromycin 20-40mg /kg Orally 10 days.
 Diptheriae: DPT antitoxin; Penicillin and erythromycin.
Viral infections causing pharyngitis:

 Herpangina :
Group A coxsackie virus.
Affect children
Feature: Fever, sore throat, Vesicular eruption- small, erythematous
 Infectious mononucleosis:
EB Virus.
Affect older children, young adults
Fever, sore throat, Exudative pharyngitis, lymphadenopathy, splenomegaly, Hepatitis
 Cytomegalovirus:
Affect Immunocompromised patients.
Mimics above condition; Heterophil antibody test -negative.
 Pharyngoconjuctival fever:
Adenovirus
Sore throat, fever, conjunctivitis;
Pain in abdomen; Mimicking appendicitis.
 Acute lymph nodular pharyngitis :
Coxsackie virus
Fever, Malaise, Sore throat
White yellow solid nodules – posterior pharyngeal wall
 Measles, Chicken pox :
Appearance of Koplik's spots (white spot around red areola) on buccal mucosa opposite to
molar teeth. Spots before 3-4 days of rash

Fungal pharyngitis:

Candida infections: Oral thrush.

In immunocompromised, taking high dose of antimicrobials

Pain in throat Dysphagia Drug of choice: Nystatin

Miscellaneous:

 Chlamydia trachomatosis :
Acute pharyngitis
Erythromycin or sulphonamides for treatment
 Toxoplasmosis:
Toxoplasma gondii - intra cellular parasite.

CHRONIC PHARYNGITIS:

 Chronic inflammatory condition of the pharynx.

 Hypertrophy of Mucosa, Seromucinous glands, Subepithelial lymphoid follicles and Muscular
coat of the pharynx
 Two types:
1. Chronic catarrhal pharyngitis.
2. Chronic hypertrophic (granular) pharyngitis.

AETIOLOGY

1. Persistent infection in locality.

 Chronic rhinitis and sinusitis - purulent discharge constantly trickles down the pharynx, act as
constant source of infection. Causes hypertrophy of the lateral pharyngeal bands.
 Chronic tonsillitis and dental sepsis cause chronic pharyngitis and recurrent sore throats.
2. Mouth breathing.

 Exposes the pharynx to air which is not filtered, humidified, adjusted to body temperature;
thus more susceptible to infections.
 Mouth breathing is due to:
Obstruction in the nose, e.g. nasal polyp, allergic or vasomotor rhinitis, turbinal hypertrophy,
deviated septum or tumours.
Obstruction in the nasopharynx e.g. adenoids and tumours
Protruding teeth which prevent apposition of lips
Habitual, No organic cause
3. Chronic irritants.

Excessive smoking
Chewing of tobacco
Pan; Heavy drinking
Highly spiced food lead to chronic pharyngitis

4. Environmental pollution.

Smoky or dusty environment

Irritant industrial fumes

5. Faulty voice production.

Excessive use of voice / Faulty voice production

Pharyngeal neurosis: Constant throat clearing, hawking or snorting, mainly hypertrophic variety.

SYMPTOMS

 Discomfort or pain in the throat, especially in the mornings.

 Foreign body sensation in throat. Constant desire to swallow / clear his throat.
 Tiredness of voice; make undue effort to speak as throat starts aching.
 Voice lose its quality; even crack.
 Cough. Irritable, Opening of the mouth may induce retching or gagging.
SIGNS

 Chronic catarrhal pharyngitis. congestion of posterior pharyngeal wall;

engorgement of vessels;
faucial pillars – thickened, increased mucus secretion
 Chronic hypertrophic (granular) pharyngitis
Pharyngeal wall - thick and oedematous; congested mucosa; dilated vessels
Posterior pharyngeal wall- reddish nodules (granular); Nodules are due to hypertrophy of
sub epithelial lymphoid follicles

Lateral pharyngeal bands - hypertrophied.

Uvula- elongated; oedematous.

TREATMENT

In Chronic pharyngitis, aetiological factor should be sought and eradicated.

 Voice rest
 Speech therapy - faulty voice production.
 Hawking, clearing the throat frequently or any such habit to be stopped.
 Warm saline gargles, especially in the morning for soothing and relieve discomfort.
 Mandl's paint - applied to pharyngeal mucosa.
 Cautery of lymphoid granules is suggested.
 Throat is sprayed with local anaesthetic and granules are touched with 10–25% silver
nitrate.
 Electro cautery or diathermy of nodules may require general anaesthesia.

ATROPHIC PHARYNGITIS

 Chronic pharyngitis - Patients of atrophic rhinitis.

 Pharyngeal mucosa along with mucous glands shows atrophy.
 Scanty mucus production leads to formation of crusts, get infected give rise to foul smell.
CLINICAL FEATURES

 Dryness ; discomfort in throat

 Hawking and dry cough may be present due to crust formation.
 Dry and glazed pharyngeal mucosa often covered with crusts.
TREATMENT

 Aim is to remove the crusts and promote secretion.

 Crusts can be removed by spraying the throat with alkaline solution, or pharyngeal
irrigation.
 Mandl’s paint applied locally has a soothing effect.
Potassium iodide, 325 mg, Orally Promote secretion and prevent crusting.
KERATOSIS PHARYNGITIS

 Benign condition
 Horny excrescences n the surface of tonsils; pharyngeal wall or lingual tonsils.
 Appear as white or yellowish dots.
 Excrescences result of hypertrophy and keratinization of epithelium.
 Firmly adherent.
 Cannot be wiped off.
 No accompanying inflammation nor constitutional symptoms
 Acute follicular tonsillitis - Show spontaneous regression; Do not require any specific
treatment except for reassurance to the patient.
 HEAD AND NECK SPACE INFECTIONS

1. PAROTID ABSCESS

Suppuration of the parotid space

Can burst through deep side of gland to form para-pharyngeal abscess

Etiology:

 Dehydration, stasis of salivary flow

 Bacteriology: Staphylococcus aureus, Streptococci, anaerobic organisms

Clinical features:

 Swelling, redness, induration, tenderness at angle of mandible.

 Fluctuation difficult to elicit; Stenson’s duct exude pus on pressure
 Toxic, running high fever

Diagnosis: By ultrasound or CT scan

Treatment: Correct dehydration, improve oral hygiene, promote salivary flow, intra venous
antibiotics given, surgical drainage under anesthesia.

2. LUDWIG’s ANGINA

Infection of submandibular space

Etiology: Dental infections: Submandibular sialadenitis, injuries of oral mucosa and fractures of
mandible

Bacteriology: Alpha hemolytic Streptococci, Staphylococci and bacteroides

Clinical features

 Difficulty in swallowing, tongue pushed up and back

 Sub mental and sub mandibular regions become swollen and impact wordy hard feel

Treatment: Antibiotics, drainage of abscess, tracheostomy (if airway endangered)

Complications: Spread of infection, airway obstruction, septicemia, aspiration pneumonia

3. PERITONSILLAR ABSCESS (QUINSY)

Collection of pus in peritonsillar space

Etiology: Usually arise following acute tonsillitis

Tonsillar crypt

Form

Intratonsillar abscess bursts

Form

Peritonsillitis

Abscess

Clinical features:

 Usually occur in adults and unilateral

 General – Fever, chills, rigor, malaise, body ache
 Local – odynophagia, ”hot potato voice”, foul breath, ear ache on same side

Examination: Congested tonsil, pillars, soft palate, uvula pushed, cervical lymphadenopathy.
Torticollis

Investigation: Contrast enhanced CT or MRI

Treatment:

 Antibiotic, analgesics, oral hygiene

 Incision and drainage of abscess
 Interval tonsillectomy
 Abscess or hot tonsillectomy

Complications: Parapharyngeal abscess, septicaemia, pneumonitis

4. RETROPHARYNGEAL ABSCESS
Infection of retropharyngeal space or prevertebral space

Etiology: Infection of adenoids, nasopharynx, posterior nasal sinuses, Penetrating injury of posterior
pharyngeal wall

Clinical features:

 Dysphagia, difficulty in breathing

 Stridor, croupy cough
 Torticollis
 Bulge in posterior pharyngeal wall

Investigation: Radiograph of soft tissue, lateral view shows widening of prevertebral shadow

Treatment: Incision and drainage of abscess and systemic antibiotics and Tracheostomy

5. CHRONIC RETROPHARYNGEAL ABSCESS OR PREVERTEBRAL ABSCESS

Etiology: Caries of cervical spine, Tuberculous infection of retropharyngeal lymph nodes

Clinical features:

 Dysphagia
 Tuberculous lymph nodes
 Posterior pharyngeal wall show fluctuant swelling

Treatment: Incision and drainage of abscess and Full course anti tubercular therapy

6. MASTICATOR SPACE

Lies between two layers of deep cervical fascia

Consists of three space: Masseteric space, Temporal space and Pterygomandibular space

It communicates with parotid and parapharyngeal space. Most common source of infection is dental
infections

Contents of this space include masseter muscle, maxillary artery, inferior alveolar nerve, ramus and
posterior part of mandible

7. PARAPHARYNGEAL ABSCESS
Also called pharyngomaxillary or lateral pharyngeal space

Infection of parapharyngeal space

Etiology: Infection can occur from

 Pharynx- acute/ chronic infection of tonsil and adenoid

 Teeth- Dental infection
 Bezold abscess and petrositis- ear
 External trauma

Clinical features:

Anterior compartment- prolapse of tonsil, trismus, swelling behind angle of jaw

Posterior compartment- bulge of pharynx. Paralysis of CN 9, 10, 11, 12.

Diagnosis: Contrast enhanced CT scan

Complication

 Acute edema of larynx

 Thrombophelibitis of jugular vein
 Spread of infection to other spaces

Treatment: Systemic antibiotics, drainage of abscess

 TUMOURS OF OROPHARYNX

Benign Malignant

Papilloma CA of post 1/3

tongue

Hemangioma Tonsillar fossa

Pleomorphic Faucial palatine

adenoma arch

Posterior and
Mucous cyst lateral
pharyngeal wall

Benign

1) Papilloma
a) Pedunculated, arise from tonsil soft palate faucial pillions
b) Treatment: Surgical excision
2) Hemangioma
a) Occur on tonsil, palate, posterior or lateral pharyngeal wall
b) Capillary or cavernous type
c) Treatment: diathermy, coagulation or injection of sclerosing agents
d) Cryotherapy, laser coagulation very effective
3) Pleomorphic adenoma
a) Seen submucosally on soft or hard palate. Potentially malignant and should be excised.
4) Mucous cyst
a) Seen in vallecula
b) Yellow in appearance, pedunculated or sessile
c) Treatment  Surgical excision if pedunculated or incision and drainage with removal of cyst
wall.
Malignant

Gross
1. Superficial spreading
2. Exophytic
3. Ulcerative
4. Infiltrative

Histologically
1. Squamous cell carcinoma
2. Lymphoepithelium
3. Adenocarcinoma
4. Lymphoma

TNM GRADING
Treatment
1. Surgery alone
2. Radiation alone
3. Combination of surgery and radiotherapy
4. Chemotherapy alone or adjuvant to surgery
5. Palliative therapy

CA posterior 1/3 of tongue

Patient presents with metastasis on cervical nodes their appearance

Early symptoms Late symptoms

Sore throat Referred pain in ear
Feeling of lump in throat Bleeding from mouth and change in quality
of speech
Discomfort in swallowing Dysphagia
1. Local: lesions are deeply infiltrative and spread to rest of tongue, epiglottis, pre epiglottic
space, tonsil, pillars.
2. Lymphatic: 70% of cases cervical metastasis(UL/BL) jugulodigastric is first to involve
3. Distant: Bone, lung, liver invovled

Diagnosis
1. Indirect laryngoscopy
2. Palpation under anesthesia  better idea of degree of infiltration of tissues
3. CT recommended tumour and nodal staging

Treatment
Tumour with radioactive such as anaplastic carcinoma, lymphoepithelioma or lymphoma are treated
by radiotherapy to primary and neck nodes.

1. T1T2 Squamous cell carcinoma with N0 and N1 neck, surgical excision with block dissection is
preferred
2. T3T4 require “surgical excision” with mandibular resection
3. T4 which also extend into anterior 2/3 of tongue and vallecula
CA tonsil and tonsilar fossa
 Squamous cell carcinoma most common presentation
 Presents as ulcerative lesion with necrotic base

Spread
1. Local: Soft palate, pillars, base of tongue, pharyngeal wall, hypopharynx, invade pterygoid
muscles and mandible
2. Lymphatics: 50% Initial cervical node involvement at time of presentation. Jugulo digastrics
are first to be involved

Diagnosis
1. Palpation of tumour is contraindicated
2. Biopsy is essential finding

Treatment
 Radiotherapy
Early and radio sensitive tumours
 Surgery
Excision of tonsil can be done for early superficial lesion
Large lesions and those invade bone wide surgical excision
 Combination therapy
Surgery + pre or post-operative radiation

CA of faucial (palatine) arch

 Soft palate, uvula, anterior tonsillar pillar compromise faucial arch
 CA of these sites are of squamous cell variety
 Lesion superficially spreading and undifferentiated with late tendency for nodal metastasis

Spread
Upper deep cervical and sub mandibular nodes

Patients with palatine arch cancer usually present with persistent sore throat, local pain, ear ache.
Growth may be noticed by patients.
Treatment
Surgical excision and irradiation

Carcinoma of posterior and lateral pharyngeal wall

Spread submucosally to adjoining areas such as ‘tonsil’, ‘soft palate’, ‘tongue’, ‘nasoharynx’, or
‘laryngopharynx’. They also invade parapharyngeal space.

60%  lymph node metastases

B/L node involvement

Treatment is irradiation or surgical excision of growth with skin grafting.

This is after combined with block dissection, when nodes are palpable

Access to post pharyngeal wall is through lateral pharyngotomy

 TUMOURS OF NASOPHARYNX

Benign Malignant

Carcinoma
Angiofibroma
nasopharynx

Chronal polyp Lymphoma

Squamous papilloma Rhabdomyosarcoma

Thornwaldt's cyst Chondroma

Hamartoma Plasma cytoma

Congenital tumour
• Hairy polyp
• Teratoma Melanoma
• Epignathism

Malignant salivary
gland tumour

JUVENILE NASOPHARYNGEAL ANGIOFIBROMA (JNA)

Most common tumour of nasopharynx

Etiology
 Most commonly seen in adult males
 Tumour is testosterone dependent
Site of origin
Posterior part of nasal cavity

1. Sphenopalantine foramen
2. Vidian canal
3. Basi sphenoid

Grows into
1. Nasal cavity
2. Nasopharynx
3. Pterygopalantine fossa

Pathology
Tumour made up of vascular and fibrous tissue with variable ratio

Most vessels endothelium lined spaces with no elastic or muscle lined coat

Extension

Cranial cavity anterior and middle cranial fossa

Orbit  proptosis and frog face deformity

Nose: Nasal obstruction, epistaxis

And nasal discharge

Paranasal sinus

Clinical features
1. Age: 10-20 (Most common in males)
2. Profuse recurrent and spontaneous epistaxis
3. Progressive nasal obstruction and denasal speech
4. Mass in the nasopharynx (Due to mass in the post nasal space)
5. Conductive hearing loss: Blockage of Eustachian tube
6. Broadening of nasal bridge
7. Proptosis
8. Swelling of cheeks
9. Involvement of CN 2,3,4,6
Diagnosis
Biopsy is contraindicated because of bleeding

Investigation
1. CT scan head with contrast  Investigation of choice
Shows
a. Extent of tumour
b. Bone destruction
c. Anterior bowing of posterior wall of maxilla  Holman Miller sign
2. MRI  Complementary investigation
Shows: soft tissue extension intracranially
3. Carotid angiography
Extension of tumour
a. External carotid artery  vascularity and feeding vessel
b. In large tumours  internal carotid artery
4. Arrangement for blood transfusion
2-3 units of blood

Treatment

Surgery
Surgical excision with radio and chemo therapy  treatment of choice

 Transpalatine
 Transpalatine and sublingual  Sardana’s approach
 Lateral rhinotomy + medial maxillectomy (Side effect : Scar)
o Facial incision
o Degloving approach
 Trans maxillary (le Fort’s)
 Infra temporal fossa approach
 Intracranial- extracranial approach
Transpalatal approach

1. Confined to nasopharynx
2. It can be extended into Sardana’s approach if tumour extends laterally
3. This avoids depression deformity on face

Trans maxillary le Fort’s approach

1. Wider access to remove the tumour which extends into maxillary and ethymoid sinuses and
pterygopalatine palatine fossa
2. For tumours of infra temporal fossa, maxillary swing approach, also called facial translocation
3. Pre-operative embolization lowers blood supply and cause less bleeding. Withdrawal of
tumour is performed within 24-48 hrs of embolization.
Management

1. Observation  tumour spontaneously regresses

2. Revision surgery and removal: if recur after revision surgery, Radiotherapy required
3. Radiation: reduces blood supply and tumour subsides

NASOPHARYNGEAL CARCINOMA
1. Multifactorial disease
2. Most common in china
3. Burning of incense or wood (polycyclic hydrocarbons), use of preserved salted fish and
vitamin C deficient diet are factors responsible in disease operation.

Etiology
1. Genetic: Chinese have greater disease incidence
2. Viral: EBV is closely associated with nasopharyngeal carcinoma. Specific viral markers
developed to screen people.
EBV
a. Viral capsid antigen (IgA  97% specific & 95% sensitive)
b. Early antigen (IgA  sensitive)
Pathology

Histology types

I. Keratinizing
II. Non keratinizing differentiated carcinoma
III. Non keratinizing undifferentiated carcinoma

Gross

 Proliferative  when polyploid mass fills nasopharynx  obstructive nasal symptoms

 Ulcerative  epistaxis is common
 Infiltrative  growth infiltrates submucously
Spreads of nasopharyngeal carcinoma can be local, via Lymphatic or Distant
Clinical features
Age: 5th -7th decade. Also in younger age

Sex: Males are more prone to nasopharyngeal carcinoma

I. Blockage of Eustachian tube

a. Conductive hearing
b. Serous or suppurative otitis media
c. Tinnitus, dizziness
II. Nasal
a. Nasal obgstruction
b. Nasal discharge
c. Denasal speech
d. Epistaxis
III. Ophthalmoneurologic
a. Squint and diplopia (CN: 6)
b. Ophthalmoplegia (CN: 3, 4, 6)
c. Reduced corneal reflux(CN: 5, through foramen lacerum)
IV. Distant metastasis
a. Cervical lymphadenopathy
b. Hearing loss
c. Nasal obstruction
d. Epistaxis
e. Neckpain
V. Cervical node metastasis
a. Angle of jaw and mastoid

Diagnosis
1) Endoscopic evaluation: biopsy can be obtained
2) Imaging:
a) CT/MRI of nasopharynx, head with contrast
b) CT/X-ray: Secondaries of lung
c) CT abdomen: secondaries of liver
d) PET scan
3) Biopsy
4) Audiogram: Baseline audiogram is important not only to establish diagnosis of serous otitis
media but is also important for side effects and chemotherapy.

Treatment
1. Radiotherapy:
Treatment of choice for stage I and II of nasopharyngeal carcinoma
Stage III and IV – require concomitant radio and chemo
IMRT higher dose delivery with reduced damage
2. Chemotherapy
Some stage III and IV are cured by radiotherapy alone but cure rate is doubled when
chemotherapy is combined

Treatment of resistant and residual disease

1. Positive nodes in neck

Radical neck dissection with removal of sternocleidomastoid muscle, CNM, IJV
2. Recurrent or residual disease
First evaluated by CT and MRI
a) Second course external radiation (IMRT) used
b) Brachytherapy: (gold 198) is used
High dose to tumour less radiation surroundings
c) Nasopharyngectomy
i) Endoscopic approach
ii) Lateral rhinectomy, medial maxillectomy
iii) Maxillary swing
iv) leFort’s approach
 TUMOURS OF HYPOPHARYNX

Benign Malignant

CA Hypopharynx
Papilloma •Pyriform sinus
•Post Cricoid region
•Posterior pharyngeal wall

Adenoma

Lipoma

Fibroma

Leiomyoma

CARCINOMA OF PYRIFORM SINUS

 60% of all hypopharyngeal CA
 Mostly males above 40 years
 Growth of this region
o Exophytic or ulcerative
o Deeply infiltrative

Spread
 Locally
 Upwards  vallecula and base of tongue
 Downwards  post cricoid region
 Medially  Aryepiglottic fold
 Lymphatic
 75% patients; cervical lymph node metastases, bilateral
 Upper and middle groups of jugular cervical nodes
 Distant metastases
 Liver, lung and bones

Clinical features
Early symptoms  pricking sensation on swallowing, followed by

1. Referred otalgia, pain on swallowing, increased dysphagia

2. Hoarseness and laryngeal obstruction indicate laryngeal edema or spread of disease to larynx

Diagnosis
1. Barium swallow CT helpful to evaluate the extent of growth and status of lymphnode
2. Endoscopic biopsy is necessary for accurate assessment of extent of growth

Treatment
1. Growth without node involvement  radiotherapy
2. If growth limited to pyriform fossa; not extend to post cricoids  total laryngectomy, partial
pharyngectomy
3. Growth extended to post cricoid region  total laryngectomy, total pharyngectomy with block
dissection
4. Post-op radiotherapy is given routinely to all cases

CARCINOMA POST CRICOID REGION

Constitute 30% of laryngopharyngeal malignancy

Etiology
Plummer Vinson syndrome characterized by microcytic hypochromic anemia

Spread
1. Ulcerative type of lesion from post cricoid region
2. Local spread often occurs in annular fashion marked dsphagia
3. Growth often invades cervical oesophagus arytenoids or recurrent laryngeal nerve at
cricoarytenoid joint
4. Lymphoid spread  paratracheal lymph nodes

Clinical features
 Most common in female of young age group (20-30)
 Progressive dysphagia is predominant
  Sometimes voice change, aphonia due to infiltration of recurrent laryngeal nerve or posterior
cricoarytenoid muscle.

Diagnosis
1. Edema, erythema of post cricoid region and pooling of secretion in hypopharynx may not be
visible on indirect laryngoscopy
2. Lateral soft tissue radiograph
3. Barium swallow
4. Endoscopy to take biopsy

Treatment
1. Early case  radiotherapy; advantage of preserving of laryngeal function
2. If failed  laryngo pharyngo oesophagectomy with stomach pull up or colon transposition to
reconstruct pharyngo oesophageal segment

CARCINOMA OF POSTERIOR PHARYNGEAL WALL

Least common laryngopharyngeal malignancy; 10%

Spread
Growth is usually exophytic but may be ulcerative. It remains localized until late spreads to pre-
vertebral fascia, muscle, vertebra.

Lymphatic spread is bilateral due to midline nature of lesion. Retropharyngeal nodes not palpable
but involved.

Clinical features
1. Dysphagia, spitting of blood may be early symptoms
2. Palpable mass in nodes

Diagnosis
1. Indirect minor examination often reveals tumor
2. Lateral soft tissue radiography  vertical extent and the thickness of tumor
3. Endoscopy is essential for biopsy and accurate assessment of tumor

Treatment
1. Early lesion – radiotherapy
2. Early small lesion – excised surgically via lateral pharyngectomy
3. Advanced lesion – laryngopharyngectomy
PHARYNGEAL POUCH TUMOURS
Also called

1. Hypopharyngeal diverticulum
2. Zenker’s diverticulum

Etiology
Spasm of cricoid sphincter or in-coordinated contraction

Pathology
1. Herniation of pouch in the midline
2. It is first behind oesophagus and comes to lie on left
3. Mouth of sac is wider than oesophagus, this causes food accumulation

Clinical features
1. Dysphagia  appears after some food accumulates in the sac and presses the oesophagus
2. Ginging sound while swallowing
3. Regurgitation of food  cough, aspiration pneumonia
4. Patients have hiatus hernia

Diagnosis
Barium swallow shows sac and its size

Treatment
1. Excision of pouch and cricopharyngeal myotomy
2. Dohlman’s procedure  partition wall between oesophagus and pouch is divided by diathermy
through oesophagus
3. Endoscopic laser treatment  similar to Dohlman’s procedure; CO2 laser is used for partition
 SNORING

 Undesirable disturbing sound that occurs during sleep.

DEFINITION OF CERTAIN TERMS:

 Sleep apnea: Cessation of breathing for 10 sec or more during sleep.
Normal : < 5 episodes
 Apnoea index: No. of episodes of apnoea per hour
 Hypopnea: Reduction of airflow. i.e., drop of 50% of airflow from base line associated with
EEG defined arousal (or) 4% drop in O2 saturation.
 Respiratory disturbance index (RDI): Also called as apnoea-hypopnea index.
RDI = No. of apnoea and hypopnea events / hr
Normal : < 5
Classification:-
1. Mild = 5-14
2. Moderate = 15-29
3. Severe = >30
 Arousal: Transient awakening from sleep as a result of apnoea or respiratory efforts.
 Arousal index : No. of arousal events / hr
Normal : < 4
 Sleep efficiency : Minutes of sleep / Minutes in bed after lights are turned off
 Multiple latency test or nap study: Patient given 4-5 scheduled naps at day time.
Latent period: From wakefulness to onset of sleep and rolling eye movements are measured.
Performed when narcolepsy and daytime sleepiness is suspected.
MECHANISM OF SNORING :
Muscles of pharynx are relaxed during sleep

↓
Partial obstruction and breathing against obstruction

↓
Vibrations of soft palate, tonsillar pillars and the base of tongue

↓
SOUND

Maximum sound = 90 dB
It may be associated with or without Obstructive Sleep Apnoea (OSA).

ETIOLOGY:
Most common cause – Adenotonsillar hypertrophy
Can be due to lesions in
1. Nose/ Nasopharynx: Septal deviation, turbinate hypertrophy, nasal valve collapse, nasal
polyps, tumors.
2. Oral cavity/ Oropharynx: Elongated soft palate and uvula, tonsillar enlargement,
macroglossia, retrognathia, large base of tongue or its tumour.
3. Larynx/ Laryngopharynx: Laryngeal stenosis or omega shaped epiglottis.

SITES OF SNORING :
 Soft palate
 Tonsillar pillars
 Hypopharynx
SYMPTOMATOLOGY : Snorers with OSA
1. Excessive daytime sleepiness
2. Morning headaches
3. General fatigue
4. Memory loss
5. Irritability
6. Depression
7. Decreased libido
8. Risk of road accidents

TREATMENT:
 Avoidance of alcohol, sedatives and hypnotics
 Reduction of weight
 Sleeping on side rather than on back
 Removal of obstructing lesion with Radio-frequency
 Uvulopalatoplasty surgically with cold knife or assisted with radio-frequency or laser.
 SLEEP APNOEA

 No breathing at all. No movement of air at the level of nose and mouth.

TYPES:

1. Obstruction : Collapse of upper airway -> Cessation of airflow

2. Central: Patent airways; But brain fails to signal the muscles to breathe.
3. Mixed
PATHOPHYSIOLOGY OF OSA:

Apnoea

↓
Hypoxia and retention of CO2

↓
Pulmonary constriction

↓
Congestive heart failure, Bradycardia, Cardiac hypoxia, Cardiac arrhythmias, Sudden death

Frequent arousals causes sleep fragmentation and daytime sleepiness.

CONSEQUNENCES:

 Congestive heart failure

 Cor pulmonale
 Polycythemia
 Hypertension
 Atrial and ventricular arrhythmias
 Angina attacks
 Snoring spouse syndrome
 Loss of memory
 Decreased libido
PHYSIOLOGY OF SLEEP:

 Normal sleep : 7-8 hours

 Two phases : Non-REM sleep and REM sleep
 Occurs in semi-regular cycles – each 90-120 min
 3-4 cycles of sleep
NON-REM SLEEP:

 75-80% of sleep
 Occurs in 4 stages
Stage – 1: Transition from wakefulness to sleep.

2-5% of sleep

EEG – Alpha waves – Decrease

Theta waves – Rise

Muscle tone – Decreases

Easily aroused

Stage – 2: Sleep spindles

45-55% of sleep

Stage – 3: 3-8% of sleep

EEG – Delta waves

Deep sleep

Stage – 4: 10-15% sleep

EEG – Delta waves

REM SLEEP:

 20-25% of sleep
 Rapid eye movements
 Increased autonomic activity
 Erratic cardiac and respiratory movements
  Dreams – occur
 Muscular activity – Decreased

CLINICAL EVALUATION:

1. History to be elicited:
 Snoring during sleep
 Restless disturbed sleep
 Gasping
 Choking
 Sweating
 Symptoms similar to OSA
 Body position during sleep
 Use of alcohol, sedatives and hypnotics
 Mouth breathing
 H/O menopause and hormonal replacement therapy (HRT)
2. Physical examination:
Assess the risk factors – Male gender, obesity, age above 40 years.
 BMI : Body weight (in kg)
-------------------------
Height (in m²)
Normal BMI: 18.5 – 24.9
Overweight: 25 - 29
Obesity: 30- 34.9
 Collar size: Neck circumference at level of cricothyroid membrane.
Normal (in males): < 42 cms
(in females): < 37.5 cms
 Complete head and neck examination:
Look for any lesions in Nasopharynx, Oropharynx, Laryngopharynx.
 Muller’s manoeuvre: A flexible endoscope is passed through the nose and mouth
completely closed.
Look for collapse of soft tissues at the level of the base of tongue and just
above the soft palate.
 3. Systemic examination:
 Look for Hypertension, CHF, Pedal edema, truncal obesity and any sign of
hypothyroidism.
4. Cephalometric radiographs :
For craniofacial anomalies and tongue base obstruction
5. Polysomnography:
 Gold standard for diagnosis of sleep apnoea.
Includes various parameters:

 EEG: For non-REM or REM sleep and it’s stages.

 ECG: For heart rate and rhythm
 EOM: Electroculogram – For rolling eye movements
 EMG: Electromyography – Recorded from submental and tibialis anterior muscle
 Pulse oximetry: To assess O2 saturation of blood to know lowest SaO2 during
sleep.
 Nasal and oral airflow: For episodes of apnoea and hypopnea
 Sleep position: Helps to know whether apnoea and hypopnea episodes occur in
supine or lateral recumbent position.
 Blood pressure
 Esophageal pressure: Negative esophageal pressure helps to know degree of
breathing efforts by the patient.
Not done in all laboratories
 Split night polysomnography:
First part of night: Usual polysomnography
Second part of night: Filtration of pressure for continuous positive airway
pressure (CPAP)
Not recommended because episodes of sleep apnea occurs more in 2nd half of the
night and thus missed.

TREATMENT – NON SURGICAL:

 Change in lifestyle: Weight loss, dietary changes, quitting smoking and the use of alcohol,
sedatives and hypnotics.
 Positional therapy: Should sleep on side as supine position may cause obstruction apnoea. A
rubber ball is fixed to the back of shirt to prevent adopting supine position.
 Intraoral device: Alter position of mandible and tongue to open the retropalatal airway.
Relieves snoring and sleep apnea.
 1. Mandible advancement device(MRD): Keeps mandible forward. Mainly in retrognathia
2. Tongue retaining device(TRD): Keeps tongue in anterior position during sleep.
 Continuous positive airway pressure (CPAP): Provides pneumatic splint to airway and
increases its caliber.
Optimum airway pressure: 5-20 cm H2O

Disadvantage: Difficult to carry during travel

 Bilateral positive airway pressure: Delivers positive pressure at two fixed levels.
A higher inspiratory pressure and lower expiratory pressure.

TREATMENT – SURGICAL:

Failed and non-compliant medical therapy

 Permanent tracheostomy – GOLD STANDARD

 But has complications and not preferred by patients.
1. Nasal surgery:
Indications: Nasal obstruction
 Septoplasty – Correct deviated nasal septum
 Removal of nasal polyps
 Reduction of turbinate size
2.Oropharyngeal surgery:

 Uvulopalatoplasty(UPP) – Most common

 80% effective – Snoring
 50% effective – OSA (relapse because of another site becoming active)
 UPP with laser/ radio-frequency used

3. Tonsillectomy/adenoidectomy:
Tailored to the level of obstruction

 Nose and Nasopharynx (Level 1)

 Soft palate and tonsils (Level 2)
 Tongue base and pharynx (Level 3)
 4. Advancement genioplasty with hyoid suspension:
Indications:

 When base of tongue causes OSA

 Retrognathia
 Micrognathia
Procedure:

 Resection of rectangular portion of the mandible including genital tubercles

and genioglossal muscle.
 Rotate by 90° and fixation by plates.
 Hyoid bone is freed from its inferior musculature and suspended from the
lower border of mandible by wires.
 Helps to pull base of the tongue anteriorly.

5. Tongue base radio-frequency:

 Used in 5-6 sittings to reduce the size of tongue.
 Radio-frequency needle – inserted submucosally.
 Coagulates tissue and causes scarring – Reduction of the size of tissue.

6. Maxillomandibular advancement osteotomy:

 Performed on mandibular ramus and maxilla.
 Osteotomy of maxilla – Fixed in anterior position with plates and screws.
Disadvantage: Causes aesthetic facial changes
 ANATOMY OF LARYNX

Formed by three paired and three unpaired cartilages

Unpaired Paired
Epiglottis Arytenoid
Thyroid Corniculate
Cricoid Cuneiform

Laryngeal joints
 Cricoarytenoid joints- synovial joints
 Cricothryroid joints- synovial joints

Laryngeal membranes and ligaments

Extrinsic Intrinsic
Thyroid membrane Cricovocal membrane
cricotracheal membrane Quadrangular membrane
Hyoepiglottic membrane Cricothyroid membrane
Thyroepiglottic membrane

Muscles of larynx

Intrinsic
1. Acting on vocal cords
a. Abductors- posterior cricoarytenoid
b. Adductors- Lateral cricoarytenoid, transverse arytenoid, thyroarytenoid
c. Tensors- cricothyroid vocalis
2. Acting on laryngeal wall
a. Openers- thyroepiglottic of thyroarytenoid
b. Closers- intraarytenoid part of thyroarytenoid and aryepiglottic

Extrinsic
1. Elevators
a. Primary- stylopharyngeus, salpingopharyngeus, thyrohyoid, palatopharyngeus
b. Secondary- mylohyoid, digastric, stylohyoid, geniohyoid
2. Depressors- sternohyoid, sternothyroid, omohyoid
Cavity of larynx
 Inlet- bounded by anterior-free margins of epiglottis, on the sides by aryepglottic folds and
posteriorly by interarytenoid fold
 Vestibule- anterior wall-epiglottis, posterior wall- mucoid membrane over arytenoids
 Ventricle
 Vestibular folds- 2 in number, anterior extension across pharyngeal cavity
 Vocal folds- 2 in number, pearly white in appearance, extension from middle of thyroid to
vocal process of arytenoids
 Rima glottidis- elongated space between vocal cords

PHYSIOLOGY OF LARYNX

Important functions of larynx

1. Protection of lower airway
a. Cough reflexes
b. Cessation of respiration
c. Sphinteric closure of laryngeal opening
2. Phonation
a. Larynx is a wind instrument
b. Helps in producing sound  vocal cords are adducted  infraepiglottic pressure is
generated  air forces the vocal cords to open and vibrate and produce sound
3. Respiration
a. Larynx regulates flow of air into the lungs
4. Fixation of the chest
a. When larynx is closed, chest wall gets fixed. Helps in digging, pulling, climbing
coughing, vomiting etc.
 LARYNGOTRACEAL TRAUMA, CONGENITAL LESIONS OF LARYNX AND STRIDOR

LARYNGOTRACHEAL TRAUMA: Injury to the upper airway structures of larynx and trachea.
AETIOLOGY

 Automobile accidents(most common)

 Blow on neck
 Neck striking against stretched wire
 Strangulation
 Gunshot wounds
 Penetrating injuries

PATHOLOGICAL CHANGES

1. Hematoma and edema of supraglottic and subglottic region.

2. Tears in laryngeal and pharyngeal mucosa leading to subcutaneous emphysema.
3. DISLOCATIONS:
 CRICOARYTENOID JOINTS(arytenoid displaced anteriorly, dislocated or avulsed)
 CRICOTHYROID JOINT(recurrent laryngeal nerve paralysis occurs)
4. FRACTURES:
 HYOID BONE
 THYROID CARTILAGE (vertical or transverse, upper part fracture-avulsion of
epiglottis and one or both false vocal cords, lower part fracture-disrupt true vocal
cords)
 CRICOID CARTILAGE
 UPPER TRACHEAL RINGS
5. Trachea may separate from the cricoid cartilage
 Retract into upper mediastenum
 Injury to recurrent laryngeal nerve

CLINICAL FEATURES (vary depending on structures injured)

 Respiratory distress
 Hoarseness of voice or aphonia
 Dysphagia and odynophagia followed by aspiration of food.
 Local pain in the larynx marked on swallowing or speaking.
  Haemoptysis due to mucosal tears.
EXTERNAL SIGNS:
 Bruises or abrasions on skin.
 Tenderness
 Subcutaneous emphysema of mucosal tears.
 Flatulence of thyroid prominence and contour of anterior cervical region
 Thyroid notch may be palpable.
 Gap that can be felt which is formed by fractured fragments of thyroid and cricoid cartilage
 Bony crepitus between fragments of fractured bone.

Separation of cricoid cartilage between larynx and trachea

DIAGNOSTIC EVALUATION

METHOD USED FOR VISUALIZING

INDIRECT LARYNGOSCOPY Mucosal edema, haematoma, lacerations, exposed
(most valuable) fragments of cartilage, asymmetry of glottis, laryngeal
inlet
FLEXIBLE LARYNGOSCOPY VIA Mucosal edema, haematoma, lacerations, exposed
NOSE fragments of cartilage, arytenoid dislocation, vocal cord
palsy

CT OF LARYNX Mucosal edema, fractures of thyroid and cricoid

cartilages and dislocation of joints. To see about injuries
to cervical spine and vascular structures(3D CT used)

ADDITIONAL EXAMINATION OF  Injury to head, cervicalspine, chest, abdomen

and extremities.
 X-Ray chest for pneumothorax
 Gastrograffin swallow for oesophageal tears.

TREATMENT:

1. Hospitalized the patient and see for any respiratory distress

2. Voice rest is essential
3. Humidification of inspired air is essential
4. Steroid therapy to resolve oedema and hematoma, to prevent scarring and stenosis.
 5. Antibiotics to prevent perichondritis and cartilage necrosis.
6. If not resolved by this go for surgery

TRACHEOSTOMY: Tracheostomy enables breathing to be controlled by an intermittent positive

pressure respirator and bronchial secretions can be removed with suction. A prolonged obstruction
of the glottis may occur with juvenile papillomas, severe trauma to the larynx, or bilateral cord
palsies, making a permanent tracheostomy necessary. A tracheostomy tube with a speaking valve
allows air to enter during inspiration, but closes on expiration so that air passes through the larynx
for phonation. Patient with a speaking valve after tracheostomy

OPEN REDUCTION:done 3-5 days after injury within 10 days, in following cases:

 Fractures of hyoid bone,thyroid and cricoid cartilage can be wired and replaced in their
anatomic positions immobilised by titanium miniplates.
 Mucosal lacerations are repaired with catgut(tough cord used for suturing).
 Epiglottis is anchored in its normal position and if avulsed is excised.
 Arytenoid cartilage is repositioned in its normal position and if completely avulsed is
removed.
 End to end anastamosis- in laryngotracheal separation.
 Internal splintage of laryngeal structures using larygeal stent or silicone tube and removed
after 2-6 weeks.
 Webbing of anterior commissure prevented by silastic keel.
COMPLICATIONS
 Laryngeal stenosis: supraglottic,glottic or subglottic.
 Perichondritis and laryngeal abscess.
 Vocal cord palsy.
CLASSIFICATION OF LARYNGOTRACHEAL TRAUMA BASED ON THE DEGREE OF INJURY
 CONGENITAL LESIONS OF LARYNX

 Laryngomalacia (congenital laryngeal stridor- most common

 Congenital vocal cord palsy(2ndMC)
 Congenital subglottic stenosis(3rdMC)
 Laryngeal web
 Laryngeal-oesophageal cleft
 Laryngeal cyst
 Subglottic hemangioma

LARYNGOMALACIA:

 Most common congenital abnormality of the larynx.

 Child presents with inspiratory stridor, manifests at birth or soon after.
 There is excessive flaccidity of supraglottic larynx which is sucked in during
inspiration producing stridor and cyanosis( rare)
 It cannot be diagnosed in paralyzed patient.
 Cry of the child is normal.
 Stridor : inspiratory ( increases on crying and supine position ,decreases on prone
position)
DIAGNOSIS:
 Direct laryngoscopy(fibre optic):shows
1. Enlarged omega shaped epiglottis
2. Floppy aryepiglottic folds
3. Prominent arytenoid cartilage
 Flexible laryngoscope is best for diagnosis
TREATMENT
 Is CONSERVATIVE, REASSURE THE PARENTS, CONDITION USUALLY DISAPPEARS BY
TWO YEARS OF AGE
 If severe respiratory distress is present, tracheostomy is required.
 In severe cases, if supraglottic structures are damaged SUPRAGLOTTIC LASRY is
required.
CONGENITAL VOCAL CORD PALSY

 Second most common abnormality.

 Due to birth trauma to recurrent laryngeal nerve injury during breech or forceps
delivery.
 Also from anomalies of central nervous system.

CONGENITAL SUBGLOTTIC STENOSIS

 Third most common abnormality.

 Due to abnormal thickening of cricoid cartilage or fibrous tissue seen below vocal
cords.
 Asymptomatic till upper infection develops causing stridor and dyspnea.
 Cry is normal.
 Diagnosis made when subglottic diameter less than 4 mm in full term neonate
(normal4.5-5.5mm)or 3 mm in premature neonate .(normal 3.5 mm)
 Treatment: stenosis improves as the larynx grows.
 If not tracheostomy is required

LARYNGEAL WEB: due to incomplete recanalization of larynx.

  Seen between the vocal cords with concave posterior margin.
 Clinical features: airway obstruction, weak cry or aphonia from birth
 Treatment: depends on thickness of web
Thin web cut with knife or co2 laser
Thick web require excision via laryngo fissure and keeping silicon keel and balloon
dilatations.

SUBGLOTTIC HEMANGIOMA:

 Asymptomatic until hemangioma increases in size till 3- 6months of age.

 50% cases associated with cutaneous hemangiomas and some with mediastinal hemangioma.
 90%cases there is anterior web formation in glottic region.
 Present with inspiratory stridor and a normal cry.
 Stridor increases on crying and on agitation of patient due to venous filling
 Biopsy is sometimes associated with hemorrhage
 Diagnosis: Direct laryngoscopy shows reddish blue mass between vocal cords
 Treatment:
1.Tracheostomy as it may involute spontaneously
2.steroid: Tab DEXAMETHASONE 1 mg/kg/day *1 week followed by
Tab PREDNISOLONE 3 mg/kg in divided doses *1 year
3.Co2 laser excision, if lesion is small.

LARYNGO-OESOPHAGEAL CLEFT:

 Due to failure of fusion of posterior cricoid lamina, so there is cleft between oesophagus and
larynx through which food is aspirated.
 Clinical features: aspiration and pneumonitis,coughing,choking and cyanosis on feeding,
stridor and hoarse cry.
 Seen associated with laryngoscopy, laryngeal palsy
LARYNGOCELE:

 Is dilatation of laryngeal saccule which extends between thyroid cartilage and ventricle.
 Seen in glass blowers, trumpet players,carcinoma of ventricle
 May be external, internal or mixed.
 Diagnosis: On Valsalva maneuver, the swelling size increases
On compressing the swelling there is sudden rush of air into larynx and a hissing
sound produced- BRYCE SIGN.
 Treatment:Excision

LARYNGEAL CYST:

 bluish ,fluid filled smooth swelling in the aryepiglottic fold of supraglottic larynx.
 Tracheostomy done in respiratory obstruction.
 Emergency-needle aspiration/ incision/drainage of cyst done
 Treatment: reroofing the cyst or excison with Co2 laser.
 STRIDOR
Listen to the stridor sound https://youtu.be/JSdEK79J4dw

is the noisy respiration produced due to turbulent airflow via narrowed air passages.

AETIOLOGY:
 Other causes

 Nose: choanal atresia

 Tongue: Macroglossia, haemangioma, dermoid at base of tongue, lingual thyroid
 Mandible: Micrognathia, pierrerobin syndrome(due to falling back of tongue)
 Pharynx: congenital dermoid, adenotonsillar hypertrophy, retropharngeal abscess, tumors.

LARYNX TRACHEA &BRONCHI Lesions outside respiratory tract

Congenital Laryngeal web Atresia Vascular rings
Laryngomalacia Stenosis Oesophageal atresia
Vocal cord palsy Tracheomalacia Congenital goiter
Subglottic stenosis Cystic hygroma
Inflammatory Epiglottitis Tracheobronchial Retropharyngeal
Croup retrooesophageal abscess
Tuberculosis
Diphtheria
Neoplastic Hemangioma Tumors of trachea Masses in neck
Juvenile multiple papillomas
Traumatic Laryngeal injuries Foreign body FB Oesophagus
Foreign bodies Stenosis trachea
Oedema following endoscopy
Prolonged intubation

MANAGEMENT:

Stridor is a physical sign, not a disease., elicit the cause based on:
*Time of onset- congenital/ acquired
*Mode of onset-sudden (fb, oedema)/gradual&progressive (laryngomalacia, subglottic
stenosis, haemangioma)
*Duration-short (fb, oedema)/long (laryngomalacia, subglottic stenosis)
*Relation to feeding-aspiration in laryngeal cleft, vascular ring
*Cyanotic spells- need for airway maintenance
*Aspiration of any foreign body
*Laryngeal trauma blunt injuries to larynx, intubation, endoscopy

PHYSICAL EXAMINATION:
 1. It is always associated with respiratory distress.
2. There may be recession in suprasternal notch, sternum, intercostal spaces, epigastrium
during inspiration
3. Note stridor is inspiratory/expiratory/biphasic
4. See for associated features:
Snoring, or snorting or nasopharyngeal cause
Gurgling sound and muffles voice pharyngeal cause
Hoarse cry or voice laryngeal cause at vocal cords. Cry is normal in laryngomalacia and
subglottic stenosis
5. Associated fever shows infective condition eg: acute laryngitis, epiglottitis, croup,
diphtheria
6. Disappears in prone position: Laryngomalacia, Micrognathia, Macroglossia
7. Auscultation: with unaided ear and with stethoscope over nose, open mouth, neck and the
chest to localize the site of origin.
8. Examination of nose, tongue, jaw and pharynx to exclude local pathology

INVESTIGATION
 Soft tissue lateral and PA view and X ray chest in PA and lateral view to diagnose foreign body
 X ray chest in inspiratory and expiratory phases
 Contrast enhancement CT Scan
 Angiography for vascular anomalies
 Oesophagogram with contrast for tracheobronchial fistula or oesophageal atresia
 Direct laryngoscopy: microlaryngoscopy and bronchoscopy under general anaesthesia after
short direct laryngoscopy, bronchoscope is inserted to see for any obstruction from
subglottic to bronchi. Secretions can be also collected from this region after this the child is
intubated and examination of oesophagus and larynx is done. Can be done without
intubation also, oxygenation and gases being delivered via catheter or spontaneous
breathing
 ACUTE AND CHRONIC INFLAMMATIONS OF LARYNX

ACUTE LARYNGITIS (SIMPLE)

ETIOLOGY

 Secondary to inflammation of nose, throat, paranasal sinuses

 Air bond inflection by adenovirus, influenza- leads to secondary bracterial inflection by
damaging mucosa
 Most common oraganism are moraxella cartarrhalis, streptococcus pneumoniae,
haemophilus infunezae
 Unfavourable climate ,physical, psychological strain are predisposing factors

PATHOLOGY

 MUCOSAL INFLAMMATION – EXTRAVASTION OF FLUID

 Imfiltration of nutrophils/lymphocytes/plasma cells
 Muscles, joins, perichondrium affected
 Epithelial exfoliation, necrosis occurs
 In some instance fibrosis result with muscosal loss leading to chromic laryngitis

SYMPTOMS

 Hoarseness of voice
 Discomfort
 Pain
 Instant paroxysmal cough
 General cough
 Dryness of throat
 Malaise
 fever
SIGNS

 Erythema and edema of epiglottis, aryepiglottic folds, arytenoids and ventricular

bands
 Vocal cords appears normal in early stages
 In later stages congestion and swelling increases, vocal cords becomered and swollen
 Stricky secretion are seen between cords and intreraryteniod region
 Submucosal hemorrhages may be seen in the vocal cords

TREATMENT

 Vocal rest
 Avoid smoking and alcohol
 Steam inhalation with tincture benzoin
 Cough sedatives (codeine)
 Antibiotics (broads sprectrum penicillin)
 Analgesics
 Steroids

ACUTE FIBRINOUS LARYNGITIS

 Laryngotrachoebronchitis involving the entries respriation system

 Age:6 month – 7 yrs
 Super infections following influenza by hemolytic streptococcus

PATHOLOGY

 Affection entire respiratory tract

 The loose areolar tissue in the subglottic reagion swells up causes respiratory obstruction and
stridor
 This coupled with thick tenacious secretion and crusts may completely occlude the airways

SIGNS AND SYMPTOMS

 Hoarseness
 Croapy cough
 39=40 degree temprature
 Common cold
  Difficult to breath
 Inspiration stridor
 Increased muscular energy consumption
 Increased CO2 retention leads to metabolic respiratory acidosis , paralysis of respiratory
regulation centers
 CYNOSIS may be present

INVESTIGATIONS

 Blood gas analysis

 3mm flexible endoscopic examination
 Chest x-ray

TREATMENT

 Hospitilazion: isolated room

 Treatmet with moist air
 Antibiotics- broad spectrum penicillins – amoxicillin 50mg/kg
 Mucolytics: oral or aerosol
 Nasogastic feeding
 Hydration
 Steroids
 Intrubution / tracheostomy
 Ventilator support may be required

SUBGLOTTIC LARYGITIS (PSEUDOCROUP)

 Common in young children – 3years of age

 Caused by influenza virus
 Signs and symptoms: subglottic edema(+) croup, stridor, no fever
 Treatment: voice rest, stroid, tracheostomy may be needed
ACUTE EPIGLOTTITIS (SUPRAGLOTTITIS)

ETIOLOGY

1. Common in children between 2-7 yrs

2. Incidence 1:17000
3. In adult 1:100000
4. Caused by H.influenza type B

CLINICAL FEATURES

 Onset : abrupt/ rapid progressive

 Sore throat
 Dysphagia in adults
 Dyspnoea and stridor in children
 Tripod sign
 Drooling of saliva
 Fever 40 degree celsius

TREATMENT

 Hospitalization
 Antibiotics
 Fluids
 Steroids
 Humidification
 Intubation / tracheostomy
 Assisted respiration

OEDEMA OF THE LARYNX

 Oedema of mucosa can accompany any inflammatory reaction therefore not a specific
disease but rather a sign
 Solitary reaction to different type of stimuli like exogenous of stimuli like exgenous or known
/ trauma, infection , tabacco, radiation

ETIOLOGY

 Infection: acute epiglottities,croup,TB,syphilis

  From neighboaring strutures;quinsy, retro and parapharyngeal abscess, Ludwig’s angina
 Trauma;tongue ,larynx floor of mouth burns(physical,chemical),foreign bodies ,post
endoscopy
 Neoplasms :larynx, tongue ,pharynx
 Allergy
 Angioneurotic oedema
 Radiation
 Systemic diseases:nephritis,cardiac failure,myxedema

REINKE’S OEDEMA

 Named after German anatomist

 Reinke’s space bound between superior and inferior arcuate lines which is filled with loose
areolar tissue

ETIOLOGY

 Preciously not known

 Allergy ,infections local irritants like tobacco
 Common in men in 30 to 50 yrs

CLINICAL FEATURES

 On IDL examination vocal cord red swollen , slightly translucent,mucosa shows

polypoidal changes
 Hoarseness stridor cough present

TREATMENT

 Rehabilitation
 Microlaryngeal stripping:mucosa on both sides incides sagittally not up to anterior
commisure
 Voice rest and speech therapy

ANGIONEUROTIC OEDEMA

 May be allergic, non allergic OR herediatary and non hereditary

 Recurrent attacks of local swelling in various parts of the body:face,larynx,limbs,buttocks
 Death occurs because of the edema of the larynx
  Colic,nausea,vomiting

ETIOLOGY

Allergic: food, medicines, inhaled allergens (ACE inhibitors used in treatment of essential
hypertension)

 Heriditary angioneurotic edema :described by sir Williams osler (1888)

 Serum deficiency of C1esterase inhibitors protein thus inhibiting compliment activation of
kinin formation and fibrinolysis
 Traid of symptoms: abdominal pain, peripheral non pitting edema, laryngeal oedema

TREATMENT

 36000units of INH
 Recurrents attacs:use fibrinolytics inhibitors like epsilon amino caproic acid , tranexamic acid
or methyl testosterone derivative(danazol)these drugs stimulate C1 INH production

LARYNGEAL PERICHONDRITIS

 Inflammation of perichondrium covering laryngeal cartilages

 Etiology:Blood borne infection ,thypus ,typhoid and radiotherapy

RELAPSING POLYCHONDRITIS

 Autoimmune disease –collagen vasular disease

 Rheumatoid arthritis, SLE, ankylosing spondylitis
 Can effect recurrently pinna,nasal cartilages, larynx and trachea
 Treatment:corticosteroids

CHRONIC LARYNGITIS

 Diffuse inflammatory condition symmetrically involving whole larynx

ETIOLOGY

 Incomplete resolution of acute laryngitis and its recurrent attacks

 Chronic infection in paranasal sinuses, teeth ,tonsil and chest
 Occupational factor miners chemical industries
 Smoking, alcohol
  Chronic Lung disease
 Vocal abuse

CLINICAL FEATURES

 Hoarseness of voice easily tired becoming aphonic

 Constant hawking , dryness , compelled to clear throat
 Discomport in throat
 Dry irritating cough

SIGNS

 Hyperemia of vocal cords :dull , red , and round

 Viscid mucosa in vocal cord and interarytenoid region

TREATMENT

 Elimination of upper and lower respiratory infections

 Avoid irritating factors
 Voice rest
 Speech therapy
 Steam inhalation
 Supportive measures

CHRONIC HYPERTROPHIC ( HYPERPLASTIC) LARYNGITIS

 May be symmentric diffuse process or locallized

 Dysphonia plica ventricularis, vocal cord modules, vocal cord polyps , reinke’s oedema,
contact ulcers
 Starts in glottic region , later extends to super and subglottic region
 Muscosa, submucosa, mucosal glnds, intrinsic muscles and joints affected
 LARYNGEAL PARALYSIS

NERVE SUPPLY OF LARYNX

1. Recurrent laryngeal nerve (RLN)

a. Right RLN: Arises from right vagus nerve @ level of subclavian artery 
hooks and ascends between tracheo-oesophageal groove.
b. Left RLN: Arises from left vagus nerve @level of arch of aorta  Loops and
ascends in the tracheo-oesophageal groove.
2. Superior laryngeal nerve (SLN) – arises from inferior ganglion of vagus.
Branches of SLN
i. External branch of SLN.
ii. Internal branch of SLN.
I. MOTOR SUPPLY OF LARYNX

Cricothyroid muscle: external laryngeal (SLN)

All other muscles (Abductors, adductors or tensors) by recurrent laryngeal nerve
II. SENSORY SUPPLY OF LARYNX
Internal laryngeal nerve (SLN): Above vocal cords.
 Recurrent laryngeal nerve: Below vocal cords.

CAUSES OF LARYNGEAL PARALYSIS

 Supranuclear
 Nuclear
 High Vagal Lesion –
Intracranially / exit from the
jugular foramen /
parapharyngeal space
 Low Vagal Lesion Or RLN
 Systemic - Diabetes, syphilis,
diphtheria, typhoid, streptococcal or viral infections, lead poisoning.
 Idiopathic

RECURRENT LARYNGEAL NERVE PARALYSIS

A. UNILATERAL PARALYSIS
 Ipsilateral paralysis of all the intrinsic muscles except the cricothyroid.
 Vocal cord in median or paramedian position.

CLASSIFICATION OF LARYNGEAL
PARALYSIS

(may be unilateral
or bilateral)

Both recurrent and superior laryngeal

Recurrent laryngeal Superior laryngeal nerves (combined
nerve. nerve.
or complete paralysis).
 ETIOLOGY FOR RLN PARALYSIS

Clinical Features

 1/3rd patients are asymptomatic.

 Change in voice but no problems of aspiration or airway obstruction.

Treatment
1. Generally no treatment is required as compensation occurs due to opposite healthy
cord.
2. Laryngoplasty type I can be used if compensation does not take place.
3. Laryngoplasty type I with arytenoid adduction is done if posterior glottis is also
incompetent.
B. BILATERAL PARALYSIS

ETIOLOGY

 Onset : Acute
 Causes : Neuritis and surgical trauma (Thyroidectomy)

Clinical Features

Both the cords aligned in median or paramedian position  Inadequate pathway 

Dyspnoea and stridor.

Treatment
1. Tracheostomy - Emergency
2. Widening of respiratory tract without a permanent tracheostomy
i. Arytenoidectomy
 ii. Arytenoidopexy
iii. Lateralization of cords
iv. Laser cordectomy

Lesser invasive techniques

v. Transverse cordotomy
vi. Partial arytenoidectomy
vii. Reinnervation procedures
viii. Thyroplasty type II

SUPERIOR LARYNGEAL NERVE PARALYSIS

A. UNILATERAL PARALYSIS
 Rare
 Paralysis  Cricothyroid muscle.
 Anaesthesia  larynx above the vocal cord.

Clinical Features

Weak voice and inability to raise pitch

Paralyzed cord appears wavy due to loss tension  sags down during inspiration and
bulges up during expiration.

B. BILATERAL PARALYSIS
Etiology
 Uncommon condition;
 Surgical or accidental trauma, neuritis (mostly diphtheritic), pressure by cervical
nodes or involvement in a neoplastic process.
Clinical Features

Due to paralysis of Cricothyroid of both side and anaesthesia of upper larynx leads to
inhalation of food and pharyngeal secretions giving rise to cough and choking fits.
Treatment
 Neuritis  Recover spontaneously.
 Patients with repeated aspiration  Tracheostomy + esophageal feeding tube.
 Epiglottopexy (reversible procedure) protect the lungs from repeated
aspiration (Epiglottis folded backwards & fixed to arytenoids).

COMBINED (COMPLETE) PARALYSIS

A. UNILATERAL PARALYSIS
Paralysis of all the laryngeal muscles on one side except interarytenoid (receives
additional innervations from the opposite side).
Etiology
 Most common cause – Thyroid surgery.
 Lesion @ nucleus ambigius / lesion in the medulla / posterior cranial fossa /
jugular foramen / parapharyngeal space.
Clinical Features

 Paralysis of laryngeal muscles of one side  Cadaveric vocal cord position.

 Hoarseness of voice.
 Aspiration of liquid.

Treatment
 Speech therapy
 Procedures to medialize the cord towards the healthy cord.
 Injection of Teflon paste on lateral aspect of paralyzed cord.
 Thyroplasty type 1

B. BILATERAL PARALYSIS
 Rare condition.
  Paralysis of all laryngeal muscles on both side
 Cord position – Cadaveric (Both vocal cords)

Clinical Features

 Aphonia
 Aspiration
 Inability to cough
 Bronchopneumonia – Due to repeated aspiration and retention secretion.

Treatment
 Tracheostomy
 Gastrostomy – To prevent aspiration.
 Epiglottopexy
 Vocal cord placation – Surgical approximation of cords by suturing.
 Total laryngectomy
CONGENITAL VOCAL CORD PARALYSIS
i. Paralysis may be unilateral – more common
ii. Bilateral – Hydrocephalus/ Arnold-Chiari malformation, intracerebral hemorrhage
during birth, meningocele / Cerebral or nucleus ambiguus agenesis.

PHONOSURGERY
Surgical procedure to improve quality of voice.

1. By Laser / microlaryngeal surgery : Excision of benign/ malignant leison

2. Injection of teflon paste/ gelfoam to medialize the paralyzed cord
3. Thyroplasty
a. Type I: Medial displacement by inj of Teflon.
b. Type II: Lateral displacement – To improve airway.
c. Type III: Shorten / Relax vocal cords (Lowers pitch)
d. Type IV: Lengthen / Tighten vocal cord
4. Laryngeal Reinnervation
 BENIGN TUMOURS OF LARYNX

Benign tumors of larynx are not as common as malignant tumours.

Classified into i) Non- neoplastic & ii) Neoplastic

I. NON-NEOPLASTIC
These not true neoplasms but are tumour-like masses which form as a result
of infection, trauma or degeneration.

A. Solid Non-neoplastic

i. Vocal nodules (Singer’s or screamer’s nodules)

 Symmetrical on free edge at the junction of Ant 1/3rd to Post 2/3rd – area
of maximum trauma.
 Common among – Teachers, actors, vendors, singers etc.
 Clinical manifestation – Hoarseness of voice, pain in neck on prolonged
phonation.
 Rx- Early: Disappears in children; Large nodules: surgical resection.

ii. Vocal polyp

 Occurs as a result of vocal abuse; contributory factors – Allergy or
smoking.
 Affects Men of age grp 30-50yrs.
 Usually unilateral, arising same as vocal nodules.

iii. Reinke’s edema

 Collection of edema fluid in the sub epithelial space of Reinke  Bilateral
swelling
 Etiology – Vocal abuse & smoking.

iv. Contact ulcer/granuloma

 Ulceration or granuloma formation due to hammering of vocal processes
of arytenoids against each other’s.
 C/O Hoarseness of voice, pain throat, constant desire to clear throat.
 Unilateral or B/L ulcers.
 Management: Antireflus therapy; speech therapy; Inhaled or intralesion
steroids.

v. Intubation granuloma
 Trauma to vocal processes of arytenoid due to rough intubation.
  Mucosal ulceration Granuloma formation; bilateral involving posterior
third.
 C/O Hoarseness, if large causes dyspnoea.

vi. Leukoplakia
 Localized form of epithelial hyperplasia involving upper surface of
one or both vocal cords.
 White plaque or warty appearance  affects mobility.

vii. Amyloid tumours

 Amyloid deposits involving vocal cord, ventricular band, subglottic
area or trachea;
 Affect men in the age grp 50-70yrs.
 Presents as submucosal mass.
 Rx- surgical removal – good prognosis
B. Cystic

i. Ductal cysts
 Retention cysts due to blockage of seromucinous glands of
laryngeal mucosa.
ii. Saccular cysts
 Obstruction to orifice of saccule causes retention of secretion and
distension of saccule which presents as a cyst in laryngeal ventricle.
iii. Laryngocele
 Air filled swelling  dilation of saccule.
o Internal: confined to larynx and presents distension of false
cord and aryepiglottic fold.
o External: herniates through thyroid membrane.
o Combined: Both internal + external components seen.
II. NEOPLASTIC

A. Squamous papilloma
o Juvenile type :
 Most common in children
 HPV from infected birth canal.
 Diagnosed at age of 3-5yrs C/O hoarseness/ aphonia, respiratoy
difficulty.
 Pappiloma recuurent but rarely undergoes malignant changes.
o Adult-onset type :
 Single, smaller in size, common in males of age grp 30-50yrs
 Do not recur, less aggressive.
 Site: Anterior commissural.

B. Chondroma
 Most commonly arises from cricoid cartilage also occurs on thyroid
or arytenoid cartilages.
 Presents in subglottic area – Dyspnoea
 Male : Female (4:1)

C. Haemangioma

D. Granular cell tumours

E. Glandular tumours, e.g.

o Pleomorphic adenoma
o Oncocytoma

F. Other rare beningn laryngeal tumors

 Neurilemmoma
 Neurofibroma
 Rhabdomyoma
 Lipoma
 Fibroma
 CANCER LARYNX

Etiology

Risk factors

 Alcohol
 Tobacco
 Cigarette smoke[Benzopyrene and hydrocarbons]
 Previous radiation
 Occupational Exposure
 Asbestos
 Mustard gas
 Petroleum product

Histopathology
 m\c Squamous cell[90%]
 Other CA
 Verrucous CA
 Spindle cell
 Malignant salivary gland tumor
 Sarcomas
 Histopath –grading
Grade 1: Well differentiated
Grade 2: Moderately differentiated
Grade 3: Poorly differentiated

1. Supraglottic Cancer

 Less frequent
Areas of spread
Local spread
 Vallecula
 Base on tongue
 Pyriform fossa

Infrahyoid Epiglottis CA spread

 Pre-Epiglottis
 Thyroid cartilage
Nodal Spread
 Upper and middle jugular mode

Symptoms
 Silent
 Throat pain, Dysphagia and referred pain to ear
 Weight loss ,Respiratory obstruction, halitosis [late feature]
 Hoarseness-late feature
2. Glottic cancer

m\c site: Free edge, Upper edge of Vocal is its Anterior and middle third Spread
Ant: Anterior commissure
Post: Vocal process, arytenoid region
Up: Ventricle and false cord
Down: Subglottic region
 To thyroarytenoid muscle
 No nodal metastases Symptoms
 Hoarseness of voice-early sign
 So this CA-detected early
 In size => Oedema of larynx

3. Subglottic CA

Site: From glotti area to lower border of cricoid cartilage.

Spread
 Anterior wall
 To trachea
 Cricothyroid muscle
 Thyroid gland
 Ribbon muscle
Nodal spread
 Pre\paratracheal node
 Lower jugular node
Symptoms
 Earliest sign: Stridor\larygial obstruction
 Hoarseness-spread to vocal cords
 Diagnosis of laryngeal cancer

Dictim-Having persistent\gradually increased hoarseness for Weeks must have laryngeal

examination

1. History given by patient

2. Indirect laryngoscopy
=>Apperance of lesion
 Suprahyoid epiglottis-Exophytic growth
 Infrahyoid epiglottis-ulcerative growth
 Vocal cord-Raised, nodular, ulcer or thickening
 Anterior commissure-granulation tissue like
 Subglottic area-Raised sub mucosal module
=>Vocal cord motility
 Impairment\fixation=infiltration to thyroarytenoid
muscle\invasion of recurrent laryngeal nerve
=>Other extend
 Vallecula
 Base of tongue
 Pyriform fossa
3. Flexible fiberoptic\rigid laryngoscopy\video laryngoscopy
4. Examination of neck.
 Perichondritis of thyroid palpation

Tender of palpation
 Check for nodal metastasis
5. Radiography
 X-ray chest 1)Check for coexist lung disease
2)pulmonary metastases
 Soft tissue lateral neck work
 Thyroid cartilage destruction
 CT and MRI
 CT scan
 Invasion of pre epiglottic or para epilgottic space, cervical
lymphnode involvement

6. Direct laryngoscopy
 To see the hidden area of larynx

 Infrahyoid epiglottis
 Subglottis
 Ventricles
7. Micro laryngoscopy
 Better to visualize and to take accurate biopsy
8. Supravital staining
 Biopsy site in leukoplakic lesion
 Toluidine blue-used
 Carcinoma in-situ: superficial CA
Take dyes
 Leukoplakia :Not takes

TREATMENT OF LARYNGEAL CANCER

1) Radiotherapy
2) Surgery
 Conservation laryngeal surgery
 Total laryngectomy

3)Combined therapy [surgery+radio]

4)Endoscopic resection with co2 laser

5)Organ preservation

1. Radiation

 Curative-early lesions
 Advantage-preservation of voice
2. Surgery
 Conservation laryngeal surgery
 To Preserve voice
  To avoid permanent tracheal opening
It includes
 Cordectomy via laryngofissure
 Partial frontolateral laryngectomy
 Excision of supraglottis and partial horizontal
laryngectomy
 Total laryngectomy
 The entire larynx (+) hyoid bone, pre-epiglottic space,
strap muscle,
 1\more tracheal rigs removed
 Lower tracheal stump sutured to skin for breathing

Indication

 T3 lesion (with coral fixed)

 All t4 lesion
 Invasion of thyroid\cricord, cartilage
 B\L arytenoid cartilage inv.
 Lesion of post commisure
 Failure of radio\conservational energy
 Transglottis cancers
C\I – pt.with distant mets
3. Combined therapy
=> Surgical ablation (+) pre\post op-radiation
4. Endoscopic resection with co2 laser

=> CA in mobile membranous vocal cord

Precisely excised with co2 laser

=>Low cost\duration\morbidity

=>Supra\ infrahyoid \ epiglosttis lesion(T1)

Can be resected
 5. Organ preservation

=>In T3 and T4 lesion

=>Induction chemotherapy followed by

Radiotherapy\con current

Better loco regional control

=>But chemo=more toxic

Glottics CA

Treatment: transroal endoscopic co2 laser

biopsy- CA-Radiotherapy and other management

CA Insitu-regular follow up

Invasive glottis CA Radiotherapy Conservative Complete Neck others

surgery laryngectomy dissection
T1-CA Best Endoscopic
co2
Excision
T1 Extend to anterior Best Fronto lateral Total excision
commisure partial
laryngectomy
{If failed}
T1- Ext to arytenoid Surgery Preferred
T2-No[K-LN][vocal cord If cord is mobile
+supraglottic/subglottic [1st] +\-Neck
extend] dissection
 Failure Performed
[if failed] Done
 Cord st
Performed[1 ]
immobile [if failed] Done
T3,T4 Done Done (if
palpable)
Advanced T4 Done (a)palliative
(+)postoperation treatment
radiation
Subglottic cancer

T1, T2 Radiotherapy

T3, T4 Total laryngectomy (+) post op-radiation

Supraglottic cancer

T1----Radiation

T2----Supraglottoic laryngectomy +/- Neck dissection

[if lung function good]

If poor lung function radiotherapy done

T3, T4----Total laryngectomy

(+)Neck dissection

(+)Postop radiation

Vocal rehabilitation after total laryngectomy

Speech lost completely

Methods of communication

 Written language (pen and paper)

 Aphonic lip speech(by trapping air in buccal cavity(+)sign language
 Oesophageal speech
 Electrolarynx
 Transoral pneumatic device
 Trans-oesophageal speech
 Blom-singer prosthesis
 Panje prosthesis
 VOICE AND SPEECH DISORDERS

1. HOARSENESS

 Roughness of voice
 Due to variation in periodicity, and/or intensity of consecutive sound
waves
 Symptom, not a disease

Normal vocal cord functions:

a. Ability to approximate with each other
b. Proper size and stiffness
c. Ability of regular vibration to air column

Any condition interfering with these functions Hoarseness

Examples of conditions:

a. Loss of approximation- vocal cord paralysis, tumour in vocal cord

b. Size of cords- increased in oedema; tumour. Decreased in partial excision;
fibrosis
c. Stiffness- reduced in paralysis; increased in spastic dysphonia, fibrosis
d. Inability to vibrate- congestion, submucosal haemorrhage, nodule, polyp
 EVALUATION OF HOARSENESS
 History
 >2 weeks- examination of larynx needed
 Age >40 yrs, exclude malignancy
 Indirect laryngoscopy for local laryngeal causes
 Examination of chest, neck, CVS, neurological system- to find cause of paralysis
 Lab investigations, radiological examinations based on clinical findings
 Direct laryngoscopy for detailed examination, biopsy and assessment of mobility
 Bronchoscopy, oesophagoscopy- paralytic lesions of cord, to exclude malignancy
2. DYSPHONIA PLICA VENTRICUARIS (VENTRICULAR DYSPHONIA)
 Voice produced by ventricular folds (false folds)
 Voice- rough, low pitched, unpleasant
 Maybe secondary to true cord impairment (paralysis, fixation, surgical
excision, tumours) as a compensatory function
 Difficult to treat
 Functional type-
 normal larynx; psychogenic
 voice starts normal, then becomes rough when false cords take over
true cord function
 Diagnosis- indirect laryngoscopy
- False cords obscure true cords on phonation
 Voice therapy, psych counselling
 3. FUNCTIONAL APHONIA (HYSTERICAL APHONIA)
 Emotionally labile women, 15-30 years
 Functional disorder
 Sudden onset, not associated with other laryngeal symptoms
 Patient whispers
 O/E vocal cords abducted, fail to adduct on phonation
 Normal adduction function (seen on coughing)
 Treatment- reassurance, psychotherapy

4. PUBERPHONIA (MUTATIONAL FALSETTO VOICE)

 Failure of vocal cord lengthening in puberty, persistence of childhood high pitched
voice
 Seen in boys who are emotionally immature, insecure, excessively fixated with
mothers
 Physical, sexual development normal
 Treatment- training body to lower voice pitch
 Gutzmann’s pressure test- Pressing thyroid prominence in backward and downward
direction
 Good prognosis

5. PHONASTHENIA
 Weakness of voice due to fatigue of phonatory muscles
 Due to abuse or misuse of voice; or following laryngitis
 Indirect laryngoscopy shows 3 characteristic findings :
 Elliptical space between cords- weakness of thyroarytenoid
 Triangular gap near posterior commissure- weakness of interarytenoid
 Keyhole appearance of glottis- both thyroarytenoid and interarytenoids
involved
 Treatment- voice rest, vocal hygiene, voice rest period after excessive use of
voice
 6. DYSPHONIA
 3 types
 Adductor
 Abductor
 Mixed

 ADDUCTOR DYSPHONIA
 Adductor muscles of larynx go into spasm, vocal cords adductor
 Voice strained, strangled, voice beaks
 Larynx is morphologically normal
 Severity variable
 Aetiology uncertain, however neurological conditions to be excluded. MRI and
CT useful for ruling out
 Treatment- botulinum toxin injections in thyroarytenoid muscle, dose
depends on severity
- Percutaneous EMG guided route through cricothyroid
space preferred
- Lasts up to 16 weeks
 Voice therapy
 Section of recurrent laryngeal to paralyse cord.
- Interferes with glottis closure
- Used if injections fail

 ABDUCTOR DYSPHONIA
 Spasms of posterior cricoarytenoid muscle (the only abductor). Hence glottis
open
 Breathy voice, breathy breaks
 Gradually progressive, symptoms aggravated on stress
 Unknown cause
 Treatment- Botulinum toxin injection in posterior cricoarytenoid muscle
- Either done by percutaneous EMG guided route or
endoscopy
- Results not as good as with adductor dysphonia
- Disadvantages: compromise vocal cord movement &
respiration => airway obstruction
  Not responding to toxin => thyroplasty type I or fat injection
 Speech therapy to be combined with injection therapy

 MIXED DYSPHONIA
 Both adductor and abductor functions affected

7. HYPONASALITY (RHINOLALIA CLAUSA)

 Lack of nasal resonance for words resonated in nasal cavity
 Due to blockage of nose or nasopharynx

8. HYPERNASALITY (RHINOLALIA APERTA)

 Words with little nasal resonance resonated through nose
 Defect- failure of nasopharynx to cut off from oropharynx; abnormal
communication between oral and nasal cavity

9.STUTTERING
 Disorder of fluency; consists of hesitancy, repetitions, prolongations, blocks
 Well established stutters give rise to secondary mannerisms
 Normal dysfluency of speech in children 2-4 years
 Too much attention and reprimanding by parents and peers give way to adult
stuttering
 Prevented by proper education by parents

Treatment- speech therapy, psychotherapy to improve self esteem

 RADIOTHERAPY IN HEAD AND NECK CANCERS

 Head and neck cancers is the eight most common malignancy worldwide, 3rd
most common in India.
 It’s common in males.
 Surgery is the most common treatment and effective in small to moderate sized
lesions.
 Radiation therapy is given for patients with
1. Early stage disease
2. Those who refuse surgery
3. Those who are not surgical patients
 For advanced lesions radiation and chemotherapy is given.
RADIOTHERAPY: is the medical use of ionizing radiations as part of cancer treatment to
control or kill malignant cells
 Propagation of energy from a radioactive source is called radiation.
 They belong to electromagnetic spectrum. (Visible light, X rays, gamma rays)
 SI unit of radiation is Gray(Gy). 1Gy=1J/kg
Types of radiation wave
1. Photon beams( X ray & gamma ray)
2. Electron beams
3. Particle radiation (neutron, proton)
 Energy of Photon beams (X rays and gamma rays) is expressed in kilovolts or
megavolts and electrons in mega electron volts
 Megavolts X ray energy: 1-25MV.
 Currently megavolts are used in radiotherapy.
MECHANISM OF ACTION: Radiation causes cellular death by break in DNA strands,
genetic mutation, and apoptosis.
RADIOSENSITISERS: substances which sensitize tumour cells to the effects of radiation
and increases cell killing.
  Use of hyperbaric oxygen which improves the function of white cells, and their
phagocytic activity.
 Inhalation of carbon (95%o2 +5%Co2)
 Use of nicotinamide improves oxygenation
 Patient prefers a good Hb level of 12 g before radiation
 Drugs like cisplatin, mitomycin c ,5 fluorouracil, paclitaxel, docetaxel and
hydroxyurea is used along with radiation to potentiate the effect.
 Cetuximab is used as a targeted chemotherapy along with radiation.
RADIOPROTECTORS
 Amifostine, antioxidants, lipoic acid and cysteine are used to scavenge normal
tissues from radiation effects.
FRACTIONAL RADIOTHERAPY:3 types
1. CONVENTIONAL: Most common type. Involves delivering 2Gy/ day for 5
days in a week.
2. HYPERFRACTIONATION: dose 1.1-1.2Gy/ fraction,2 fractions/ day are
given. It gives better loco regional control of disease used for aggressive
tumors, small cell lung cancer, head and neck cancers.
3. ACCELERATED FRACTIONATION: Multiple doses given and treatment time
is reduced but side effects are more.
 5 R's of RADIOTHERAPY
1. Inherent RADIOSENSITISERS
2. Tumour cell REPOPULATION
3. RECOVERY
4. REASSORTMENT
5. REOXYGENATION of tumour cells
 INDICATIONS OF RADIOGHERAPY IN HEAD AND NECK CANCERS
DEFINITIVE TYPE
 Recommended in early stage laryngeal cancer, nasopharyngeal tumour, and base
of tongue with radiation alone
PREOPERATIVE THERAPY
 Recommended in borderline operable lesions to improve resectability in cancer
of retromolar trigone and paranasal sinuses.
 Vascularity and oxygenation of tumours is not affected.
 Reduces the risk of tumour metastasis since lymphatics are blocked.
 Helps to eliminate microscopic disease beyond tumour mass and metastasis
 It reduces the vitality of tissues and favours chances of flap necrosis, fistula
formation, and carotid blow out.
 Preoperative dose is 4500 cGydelivered in 4-5 weeks to eradicate 90% of micro
metastases.
POSTOPERATIVE RADIOTHERAPY
 Recommended in following conditions
1. Positive resection margins
2. Extra capsular lymph node spread
3. Invasion of soft tissues
4. Involvement of 2or more lymph nodes
5. Vascular invasion
6. Poorly differentiated tumour
7. Stage3 or 4 disease
8. Multicentric primary
9. Insitu carcinoma at resection margins
 Surgical resection is easier and postoperative healing better
 A larger dose can be delivered to the target area and adjusted based on the
residual disease
 Blood supply to the tissues affected due to fibrosis after surgery
  If post-surgical complications occur, tumour cells regrow due to delay in
radiotherapy.
 During surgery there is increased chance of metastasis
 Complications: like flap necrosis, wound dehiscence, and infection, as surgery is
done on non-radiated tissues
PALLIATIVE RADIOTHERAPY: To control pressure symptoms on air and food passages
and on the nerves where control of the disease is not possible.

PLANNING
 Establishing an immobilisation cast so that the patient remains stable during
radiation
 Planning radiation treatment on CT Scan for contouring target volume and organs
at risk
 Planning radiation on a treatment planning system after specifying a prescription
dose for the tumour volume.

RADIOTHERAPY TECHNIQUES

CONVENTIONAL RADIOTHERAPY
 It comprises anatomically marking parallel opposed lateral fields or two
orthogonal fields depending upon the site including primary and nodal disease.
 Orthogonal films taken in the simulator with fields defined directly.
THREE DIMENSIONAL CONFORMAL RADIATION THERAPY
 In this the beams are shaped to confirm the dimensions of tumour mass, shield
the normal structures and thereby reduce toxicity
 A CT scan with patient positioned in the immobilisation device is a requisite
 This spares the normal tissues with 3 D radiation confirming with the dose to the
tumour using multiple fields
 Done by using computerized treatment planning system
INTENSITY MODULATED RADIATIONTHERAPY
 Highly precise and maximum dose delivery to the tumour
 Spares critical organs like spinal cord, parities, brainstorm
 Uses 3 D scans of the body to guide the beams of radiation to tumour from
different angles with varying intensity
 Shape of the beam changes according to shape of the tumour
IMAGE GUIDED RADIATIONTHERAPY(IMRT)
 More precise and accurate technique aimed for small tumors of eye, optic
nerves, spinal cord etc. during daily treatment delivery
 An IGRT image is obtained in the treatment room and positional information of
the target is also determined.
STEREOTACTIC BODY RADIATIONTHERAPY (SBRT)
 Specially designed stereotactic planning system for all body parts including head
and neck cancers & juvenile angiofibromas by 1 to 5 sessions
STEREOTACTIC RADIOSURGERY(SRS)
 Stereotactic radiation treatment for brain lesions done in 1 to 5 sessions
ADAPTIVE RADIOTHERAPY
Changing the treatment according to improvement in patient like tumour shrinkage,
weight loss, orinternal motion
TREATMENT MACHINE’S
1. COBALT 60(radioactive cobalt as source emit gamma rays)
2. LINAC( emit X-rays and electrons)
3. Gamma knife
4. Cyber knife
5. Tomotherapy
6. Proton therapy and heavy particle therapy( not used in India now)
Tomotherapy: radiation modality in which patient is scanned across a modulated strip
beam so that only one slice of the target is exposed at one time to the linear
accelerator.
DOSE AND FRACTIONATION
 Conventional dose:1.8-2 Gy/day for 5 days in a week.
 Definitive:66-74Gy/33-37 fractions /6-7 weeks
 Postoperative radiotherapy for negative margins:60Gy/30 fractions/ 6 weeks
 Postoperative radiotherapy for positive margins: 66 Gy/33fractions/6.3 weeks
BRACHITHERAPY

 Form of radiation therapy in which sealed radiation source is placed inside or

close to the tumour
 Used as a boost to extern beam therapy in early T1 to T2 tumors, cancers of
nasopharynx, lil and tongue
 It involves delivering radiation via thin tubes called catheter.
High dose is modality than giving low dose now. Gold (198, pallidum and radium,
caesium, tubes and needles and iridium wires and seeds are radioactive materials
being used.
SIDE EFFECTS: acute toxicity on rapidly dividing tissues such as skin, mucosa and bone
marrow
 Late toxicity is due to late responding tissues such as spinal cord, brain cells and
connective tissues
CARE OF PATIENT DURING THERAPY
 Side effects on skin : avoid exposure to sun, chemical irritants, and lotions ,don’t
rub the skin
 Care of oral cavity and dentition: Xerostomia and mucositis are main problems
oral hygiene maintained by gargling using nonalcoholic based salt and sodium
bicarbonate gargles. Mucositis by dietary modification. use fluoride dye
 Care of haemopoietic system: weekly hemograms to check the WBC, Hb, and
platelet count
 Care of infections: antibiotic, antifungal, and antiviral drugs as the patient is
immunosuppressed
 Care of nutrition: advised to take high protein diet with vitamins and minerals
and good hydration
 FOREIGN BODIES IN AIR PASSAGE

Etiology

 Children below 4 years while play or fight.

 Adults during coma, deep sleep, alcoholic intoxication
Common foreign bodies

Children:

 Peanut- most common

 Seeds, peas, beans, piece of carrot, etc.
 Plastics, safety pins, nails, wire, etc.
Adult: Loose teeth or denture may be aspirated during anaesthesia

Nature of foreign body

1. Non irritating type: plastic, glass, metals

2. Irritating type:
a. vegetable cause “vegetal bronchitis” – foreign body cause congestion
and oedema of tracheobronchial mucosa.
b. Areca nut – common in Rajasthan
c. Peanuts – USA
d. Watermelon seeds - Egypt
e. Pumpkin seeds – Greece
Clinical Features

Symptomology divided into 3 stages

1. Initial period of choking, gagging and wheezing.

a. Short time
b. Coughed out or lodge in air passage
2. Symptomless interval
a. Respiratory mucosa adapts to presence of foreign body
b. Initial symptoms disappear
c. Vary from few hours to few weeks depending on size and nature of
foreign body
 3. Later symptoms
Site of Symptoms and signs
foreign
bodies
Larynx ● Complete obstruction leading to death
● Partial obstruction: stridor, hoarseness, cough, respiratory
difficulty
Trachea
● Choking, stridor, wheeze, cough, palpatory thud, audible slap
Bronchi
(right
bronchus – ●Cough, wheeze and diminished air entry to lung forms a “triad”
common ) ● Respiratory distress with swelling of
foreign body
● Lung collapse, emphysema, pneumonitis, bronchiectasis or lung
abscess are late

Diagnosis

 History of foreign body ingestion

 History of sudden onset of coughing, wheezing and diminished entry of air
into lungs on auscultation forms a classical triad.
 Radiology is very useful.
1. Soft tissue posteroanterior and lateral view of the neck in its extended
position.
2. Plain X-ray chest in posteroanterior and lateral view. It shows
(a) radio-opaque foreign body—its size, shape and location,
(b) atelectasis (complete obstruction by foreign body),
(c) unilateral hyperinflation of lobe or segment or entire lung (if ball
valve obstruction),
(d) pneumomediastinum or pneumothorax,
(e) pneumonitis/bronchiectasis. - Prolonged stay of foreign body
3. X-ray chest at the end of inspiration and expiration. Atelectasis and
obstructive emphysema can be seen. They are indirect evidence of
radiolucent foreign bodies.
 4. Fluoroscopy/videofluoroscopy. Evaluation during inspiration and
expiration can be made.
5. CT chest.
MANAGEMENT

Laryngeal foreign body.

 For life threatening asphyxia, the measures include pounding on the back, turning
the patient upside down and following Heimlich manoeuvre.
 Heimlich manoeuvre. Stand behind the person and place your arms around his
lower chest and give four abdominal thrusts. The residual air in the lungs may
dislodge the foreign body providing some airway. Not be done in partial
obstruction.
 Cricothyrotomy or emergency tracheostomy - if Heimlich manoeuvre fails.
Tracheal and bronchial foreign body

 Removed by brochoscopy and done under general anaesthesia.

 Emergency removal of these foreign bodies is not indicated unless there is airway
obstruction or they are of the vegetable nature (e.g. seeds) and likely to swell up.
Methods to remove tracheobronchial foreign body:

1. Conventional rigid bronchoscopy.

2. Rigid bronchoscopy with telescopic aid.
3. Bronchoscopy with C-arm fluoroscopy.
4. Use of Dormia basket or Fogarty’s balloon for rounded objects.
5. Tracheostomy first and then bronchoscopy through the tracheostome.
6. Thoracotomy and bronchotomy for peripheral foreign bodies.
7. Flexible fibreoptic bronchoscopy in selected adult patients.
Equipment for foreign body removal include:

1. Bronchoscope, appropriate for the age of patient and a size smaller and
the other a size larger
2. Telescope or optical forceps.
3. Two laryngoscopes.
4. Foreign body forceps, Dormia basket, Fogarty’s catheter and a syringe to
inflate it.
 THYROID GLAND

Dimensions and weight

 Butterfly/H shaped
 Lobes 5*3*2cm
 Isthmus 1.2*1.2
 Weight 25g
 Larger in females
 Enlarges in pregnancy and menstruation

1. Pyramidal lobe
a. From isthmus
b. Close to left lobe
c. Towards hyoid bone
2. Capsules
a. True
i. Septa into thyroid tissue
ii. Surrounds thyroid
b. False
i. Loose alveolar tissue form middle cervical fascia
ii. Ensheaths larynx, trachea, and thyroid
3. Posterior sensory ligament/ Berry’s ligament
a. Connects thyroid lobes(posterior medial aspect) to cricoid and I and II
tracheal rings
b. Recurrent laryngeal nerve/its branches (if RLN divide extralaryngeally)
passes below it (or) through it.
c. Inferior thyroid artery passes close by  can cause bleeding
d. May connect thyroid tissue – small amount
i. Causes radionuclide uptake of thyroid bed
ii. Causes increase in thyroglobulin levels after thyroidectomy
4. Anterior suspensory ligament
a. Pre tracheal fascia
 b. Connects ant-sup-medial position of thyroid and isthmus to laryngeal
complex
c. Moderate sized vessels present
5. Superior laryngeal nerve
a. Ext branch supply cricothyroid muscle (injury bowing and Tnf placement
of vocal cord; loss of pitch)
b. Sup thyroid artery and vein close; during ligation- be close to upper
thyroid lobe, also downward traction of gland helps prevent injury to
nerve.
6. Recurrent laryngeal nerve
a. Branch of vagus
b. Right side hooks around subclavian
c. Left side hooks around aortic arch, lateral to ligament of ductus arteriosus
d. Relation to inferior thyroid nerve runs superficial, through branchespr
deep to artery to reach post suspensory ligament
7. Non recurrent laryngeal nerve
a. Anomalous RLN – no recurrent course
b. Origin from vagus – direct supply to larynx through inferior thyroid artery
c. More common in right (associated with anomalous right subclavian
artery left to descending aorta behind esophagus)
8. Arteries
a. Inferior thyroid
i. Branch of thyrocervical trunk
ii. Supplies thyroid and parathyroid
b. Superior thyroid
i. Branch from external carotid
ii. Runs close to sup laryngeal nerve
c. Sometimes thyroid ima
9. Veins
a. Superior thyroid- upper pole to int. jugular vein
b. Middle thyroid vein- lateral surf to internal jugular vein
c. Inferior thyroid vein- multiple- form plexus, drain into right and left
brachiocephalic trunk
10. Lymphatic drainage

a.
b. Pre laryngeal, para and pre tracheal – level VI
Sup mediastinal nodes – level VII
And also level II, III, IV
c. Nodes are of significance when treating thyroid malignancies
11. Parathyroid gland (PTG)
a. Should be preserved in case of benign thyroid disease
b. Superior PTG (more consistent location than inf. PTG)
i. Above inferior thyroid artery
ii. Posterior of RLN
iii. Close to cricoid cartilage
c. Inferior PTG
i. Below inferior thyroid artery
ii. Ant to RLN
iii. Can lie anywhere b/w hyoid bone above to sup. Mediastinum below
iv. Descends along thymus
12. Strap muscles N supply
a. Sternothyroid, sternohyoid, omohyoid  motor supply- Ansa hypoglossi in
the lower half of muscles
b. Significance- div. during goiter exposure  transect at upper part preserve
nerve
13. RLN triangle(of Lose)
a. Lower lobe of thyroid

Retracted strap muscles trachea and oesophagus

RLN
Inferiorly- thoracic inlet
b. Borders
i. Medial – trachea and oesophagus
ii. Lateral – retracted strap muscles
iii. Sup – lower lobe of thyroid gland
c. Apex – thoracic inlet
d. Content – RLN (lateral to medial in right side); Left – straight along
trachea-oesophageal groove
14. Lingual thyroid
a. 1 in 3000/4000 pts with thyroid disease
b. Only thyroid tissue or in addition to nerve or ectopic thyroid
c. Large- airway obstruction/difficulty in swallowing
d. Indirect laryngoscopy- mass at base of tongue
e. Diff diagnosis-lymphoma, sq. cell carcinoma, minor salivary gland tumour,
lingual tonsil, rarely thyroglossal cyst
f. Treatment
i. If symptoms - surgical removal by suprahyoid trans pharyngeal
approach
ii. Lifelong thyroid hormone replacement – if only tissue
Physiology of thyroid gland
1. Two types of cells

a. Follicular cells lining acinus synthesize and liberate T3 and T4

b. Parafollicular cels liberate calcitonin Ca2+ lowering effect
2. Synthesize and release of thyroid hormone
a. Uptake of iodine
b. Iodine to iodide(oxidation by peroxidase) + binding to tyrosine (diiodo
tyrosine and monoiodo tyrosine)
c. Coupling  T3 (1MIT and 1DIT) and T4 (2 DIT) by peroxidase
DIT, MIT, T3, T4, thyroglobulin bound together – colloid stored in follicles
d. Colloid taken by thyroid cells peptide bond between thyroglobulin and
others broken by peptidase release T4, T3, DIT,MIT
e. MIT and DIT (uncoupled iodinate tyrosine) deiodinated by iodotyrosine
deiodinase iodine
3. Congenital absence of iodotyrosine deiodinase  MIT and DIT appear in urine
loss in urine  iodine deficiency
4. T3 – active hormone – only 20% by thyroid gland
5. 80% by peripheral deiodination of T4
6. Hypothalamo pituitary thyroid axis
Important term for thyroid diseases
1. TRH
a. by hypothalamus
b. acts on pituitary
2. Thyrotropin
a. TSH
b. By ant pituitary
c. Acts on TSH receptors of follicular cells
3. Thyroglobulin (Tg)
a. Glycoprotein
b. By follicular cells of thyroid
c. After total thyroidectomy/ radioactive I ablation; Tg level 0; otherwise
disease recurrence
4. TSH receptor Ab
a. In Graves’ disease
 b. Lead to increased T4 and T3 hormones
c. Symptoms of hyperthyroidism
5. Tg Ab
a. In Hashimoto thyroiditis
b. Associated with thyroid peroxidase Ab
c. Symptoms of hypothyroidism
6. Calcitonin
a. By parafollicular C cells
b. Decreased no. of activity – osteoclast- bone resorption
c. Increased in medullary Ca
7. Peroxidase
a. Iodide iodine
b. Tyrosine MIT
c. Coupling of DIT T4
8. Anti-microsomal AB/ Anti peroxidase Ab
a. Seen in auto immune disease
b. Nearly 100% in Hashimoto’s
c. 80% in Graves
9. Propylthiouracil and methimazole
a. Impair organification of Iodine

Decrease T3 and T4

Used in hyperthyroidism
b. Propylthiouracil preferred in pregnancy- does not cross placental barrier
10. Increased iodine inhibit thyroid hormones decreased T3 and T4 in blood(Wolff-
Chaikoff effect)
Lugol iodine/KI – treatment for hyperthyroid patients before surgery
 Benign disorders of thyroid

Hashimoto thyroiditis
1. Also called chronic lymphocytic thyroiditis
2. Auto immune disorder
3. Anti Tg Ab and anti TPO Ab
4. Thyroid parenchyma infiltrated with lymphocytes
5. Fibrous septa extends into parenchyma
6. Thyroid size- normal, enlarged or small
7. Nodules(1/many) may progress to lymphoma papillary CA
8. More common in females
9. Diagnosis levels of Ab
10. Treatment thyroxine therapy- combat hypothyroiditis
Auto Ab

Thyroid inflammation with destruction of thyroid tissues and fibrosis

Increase TSH

Multiple micronodules/ solitary large nodule lymphoma/ papillary CA

Responds to exogenous thyroid

Hypothyroidism
1. Decreased thyroid hormones
2. Causes
a. Iodine deficiency(most common)
b. Hashimoto disease
c. Total / partial thyroidectomy
d. Radiation for lymphoma/ H&N CA
e. Radioactive iodine for Graves
f. Drugs: Amiodarone, lithium, para amino salicylic acid, antithyroid drugs,
goiterogenic drugs
3. Symptoms
 a. General: fatigue and weakness; intolerance to cold; coarse and sparse hair
b. CNS: poor memory and lack of concentration
c. GI: weight gain; constipation
d. Special senses: dry skin; hearing loss; hoarseness of voice
e. FGT: increased menstrual bleed, followed by
oligomenorrhoea/amenorrhoea
4. Signs
a. Dry coarse skin
b. Loss of hair
c. Puffy face
d. Bradycardia
e. Puffy feet and hands
5. Treatment: exogenous thyroid hormone
6. Neonates
a. 1 in 5000
b. Cretinism: lethargy, stunted growth, mental retardation and hearing los
c. Causes: inadequate iodine in mother’s diet, anti-thyroid drugs, radioactive
iodine, agenesis of thyroid in infant
d. Important to maintain euthyroid in pregnancy

Graves’ disease
1. Autoimmune disorder
2. Hyperthyroidism, goiter, ophthalmopathy and dermopathy
3. Common in females than males
4. Genetic and environmental causation
5. Anti TSH Ab increased T3 and T4
6. Diagnosis- clinical features of hyperthyroidism and lab tests(TSH decrease and T 4
increase)

Hyperthyroidism
1. Increased thyroid hormones
2. Causes
a. Graves
b. Toxic multinodular goiter
 c. Autonomous nodule
d. TSH secretory pituitary tumour
e. Functioning thyroid CA/metastasis
f. Thyrotoxicosis factitia(exogenous intake of thyroid hormone)
g. Thyroiditis
3. Symptoms
a. General: fatigue, weakness(myopathy)
b. CNS: nervousness, irritability, hyperactivity
c. GI: weight loss despite increased apetite, diarrhea
d. CVS: palpitations
e. FGT: oligomenorrhoea
4. Signs
a. Myopathy proximal
b. Tremors
c. Tachycardia, AF, increased PP
d. Diffuse alopecia
e. Goiter(difuse/nodular)
5. Signs of hyperthyroidism due to goiter
a. Lid retraction
b. Periorbital oedema
c. Exophthalmos
d. Myxoedema

Malignant disorders of thyroid

1. Types
a. Well differentiated
i. Papillary CA
ii. Follicular CA
iii. Hurthle cell CA
b. Undifferentiated : anaplastic CA
c. Medullary
i. Sporadic
ii. Familial
1. MEN type IIa
2. MEN type IIb
 d. Lymphoma
e. Metastases to thyroid
2. Papillary thyroid CA
a. Most common type
b. Females> males
c. Arises from follicular cells of thyroid
d. Cancerous fibrovascular stalk forming papilla
e. Risk factors
i. Ionizing radiation: several years ago, especially Chernobyl,
Hiroshima, Nagasaki
ii. Familial
1. Cowden syndrome: hamartomas+ breast tumour+ skin tags+ papillary or follicular
cancer
2. Gardener’s syndrome: colonic polyposis+ thyroid CA
f. Clinical presentation
i. Asymptomatic mass
ii. Metastatic nodes in the neck
iii. Local invasion
iv. Pulmonary (or) bone metastases (or) occult- 10 of thyroid
g. Diagnosis
i. History, clinical examination, FNAC- important
ii. FNAC
1. Annie eye nucleus- dull cytoplasm prominent nucleoli
2. Psammoma bodies- laminated Ca2+ bodies
iii. Thyroid function test- may be hyperthyroidism though most
patients – euthyroid
iv. CT-MRI- for retrosternal invasion
h. Treatment
i. Microcarcinoma
1. <1.5 cm, hardly palpable
2. No capsular invasion/ cervical nodes
3. Lobectomy with isthmusectomy
ii. Intrathyroidal tumour
1. >1.5 cm
2. No nodes/nodules contralaterally
3. Lobectomy with isthmusectomy
iii. Gross involvement of both lobes without nodes  total/ near total
thyroidectomy
iv. High risk- total thyroidectomy
v. Tracheal invasion- tracheal segmental excision and repair in
addition to excision of growth
vi. Cervical LN dissection in case of palpable nodes
i. Follow up
i. After total thyroidectomy disease may remain berry
ligament/sup poles/pyramidal lobe of thyroid gland requires
post-operative radioiodine ablation
3. Follicular CA
a. Arises from follicular cells
b. 10-15%
c. Females more than males
d. Solitary nodule/ increase in preexistent nodule
e. Metastasis- blood. LN involvement less common
f. Diagnosis
i. FNAC- follicular neoplasm to be reported
ii. CA diagnosed only after removal of specimen as it requires capsular
or vascular invasion
g. Treatment
i. FNAC- follicular neoplasm(NOT cancer) – lobectomy with
isthmusectomy include pyramidal lobe
ii. Lobectomy specimen- CA- completion of thyroidectomy by
removing other lobe followed by radioiodine ablation
iii. FNAC- follicular CA- total thyroidectomy
iv. Nodule size > 4cm, elderly follicular neoplasm perform total
thyroidectomy risk of CA
v. Nodes palpable- neck dissection
h. Prognosis- poor if age> 50, size of tumour> 4cm, distant metastases
present
4. Hurtle cell CA
a. Oncocytic CA
b. Oncocytes- large cells rich in mitochondria; stain pink
 c. Multifocal, bilateral, LN involvement, distant metastasis
d. Aggressiveness: hurtle cell CA> follicular CA> papillary CA
e. Clinical presentation: thyroid nodule
f. Diagnosis:
i. FNAC- Hurtle cells.
ii. Cannot differentiate Hurtle cell adenoma form CA
iii. Histology finding of capsular/vascular invasion
g. Treatment
i. Adenoma – benign – lobectomy with isthmusectomy
ii. Capsular/ vascular invasion +  total thyroidectomy
iii. CA on FNAC  total thyroidectomy with clearance and paratracheal
LN
h. Follow up
i. Technetium scan – Hurtle cell do not take up radio iodine
i. Prognosis- worse than follicular and papillary CA
5. Anaplastic CA
a. 5%
b. Females> males
c. Aggressive
d. Clinical symptoms: Hoarseness. Stridor, dyspnoea, dysphagia, thoracic
inlet obstruction
e. Cervical LN- 80%
f. Thyroid and cervical lymph node fuse together; difficult to distinguish
g. Difficult from lymphoma- it is painless unlike thyroid lymphoma
h. Distant metastases- long bone and brain
i. Treatment:
i. Unsatisfactory
ii. Palliation by tracheostomy and nutritional support- only treatment
6. Medullary CA
a. Sporadic (80%)
i. Unifocal
ii. No endocrinopathy
b. Familial
i. Multifocal
ii. Bilateral
 iii. Common in Young age
iv. MEN II A
1. Pheochromocytoma
2. Hyperparathyroidism
v. MEN II B
1. Pheochromocytoma
2. Mucosal and intestinal neuroma
vi. Non MEN
1. No endocrinopathy
2. Rare
c. Cell of Origin – Parafollicular C cells
d. Equal occurrence in male and female
e. Clinical Features:
i. Neck mass
ii. Cervical nodes
iii. Hoarseness,
iv. Pain
v. Dyspnoea
vi. Dysphagia
f. Diagnosis
i. Increased calcitonin
ii. RET proto onco gene mutation
iii. Serum calcium for parathyroid
iv. 24 hrs urine for catecholamine / metanephrine
g. Treatment
i. Total thyroidectomy
ii. Level VI node removal
h. Follow up – calcitonin levels
7. Lymphoma
a. B-call; Non – Hodgkin type
b. Risk factor – Hashonotos thyroiditis
c. Clinical Features:
i. Painless mass
ii. Hoarsness
iii. Stridor
 iv. Dyspnea
v. Dysphagia
vi. Inlet obstruction
vii. Lymph node enlargement
d. Differential diagnosis
i. Hashimoto thyroiditis
ii. Anaplastic CA
e. Treatment
i. Stage 1 – surgery
ii. Stage 2 – surgery
iii. Stage 3 – both side of diaphragm - Radio and chemo continued
iv. Stage 4 – disseminated; Radio and chemo continued

Thyroid Nodules and Management

1. Solitary nodule
a. Colloid nodule
b. Ademona
i. Follicular
ii. Hurtle cell
c. Thyroid cyst
d. Regenerative nodule
e. Dominant nodule – multinodular goiter
f. Autonomous / toxic nodule
g. CA
h. Metastatic deposit
2. Colloid nodule
a. Adenomatous nodule
b. Benign condition
c. Follicular cell hyperplasia
d. Treatment – exogenous thyroid hormone
3. Follicular adenoma
a. Well demarcated capsulated benign
b. Cystic degeneration, hemorrhage, calcification, fibrosis
 c. Differential diagnosis; follicular CA – cannot differentiate by FNA.
4. Hurtle cell adenoma
a. Hurtle cell – oncocyte rich in mitochondria
b. Well demarcated, capsulated
c. Cannot be deferentiated from CA by FNAC
5. Thyroid cyst
a. It may be:
i. Simple thyroid cyst
ii. Papillary cyst and cystic change
iii. Parathyroid cyst
iv. Hemorrhage in colloid nodule
v. Thyroglossal duct cyst
b. Diagnosis: (from aspirate
i. Brown fluid
1. Simple thyroid cyst
2. Cystic compound in colloid nodule
ii. Blood – papillary Ca
iii. Clear and colourless – parathyroid cyst
iv. Columnar cell – thyroglossal cyst
c. Treatment –
i. >4cm – excision
ii. >4cm - suppression therapy
6. Dominant nodule
a. Clinically 1 of many nodules palpable
b. Multinodular goiter
c. Dominant nodule maybe malignant
7. Regenerative nodule
a. Hashimitos thyroiditis
b. TSH is high
8. Autonomous / toxic nodule
a. 1 nodule
b. Independent of TSH
c. Diagnosis – Thyroid scan, mild thyrotoxicosis, low TSH
d. Treatment – Surgery preferred, radioactive iodine.
9. Carcinoma
 a. High risk – Male
b. Age - <20 and >45
c. History of radiation to neck
d. Family history
e. Rapid growth
f. Fixed hard painful lesion
g. Stridor, dyspnea, dysphagia
h. Size - >4cm
i. Recurrent / rapid filling cyst after aspiration

Evaluation of thyroid nodule

1. Physical examination
a. Size >4cm
b. Fixed to underlying structure
c. Firm
d. Laryngoscope – fixed vocal cords
2. Thyroid function
a. TSH, T3, T4 – Normal – colloid nodule
b. Low TSH / high T3 and T4 – hyperfunctioning nodule
c. Calcitonin levels – for family history of medullary CA
3. Ultrasound
i. Small nodule
ii. Multiple nodules
iii. Accurate size
iv. Custic / solid
v. Associated cervical LN
vi. Vascularity of gland / nodule
4. Thyroid Scan:
a. Differentiate cold and hot nodules
b. Chances of malignance in cold > hot nodules
5. FNAC
a. Benign / malignant / intermediate
b. Follicular & hurtle cell – reported as neoplasm
6. CT / MRI
a. Size and extent of retrosternal goiter
 b. Extent of tracheal compression

THYROID SURGERY

TYPES

1. Hemithyroidectomy

 Complete removal of one lobe of isthmus

 Indication: benign nodule
Intra thyroidal cancer

2. Subtotal thyroidectomy

 Removal of both lobes and isthmus leaving 3g on each side

 Indication : Thyrotoxicosis

Mulitinodular goiter

3. Near total thyroidectomy

 Removal of gland and isthmus leaving 1g on each side to protect RIN and PTG
 Indication : some malignancies

4. Isthmusectomy

 Complete removal of isthmus

 Indication :nodule of isthmus
 Diagnostic biopsy

5. Completion thyroidectomy

 Removal of remaining to convert it to total/subtotal thyroidectomy due to

histological findings
 If total thyroidectomy proves capsular and vascular invasion – other lobe is
excised

INDICATIONS- 4c’s

1. Cancer thyroid
2. Cancer suspicion

3. Compression symptoms of trachea, oesophagus, veins, etc,.

-substernal extension causing thoracic inlet syndrome

-And +ve PEMBERTON’S sign –raising arms above neck causes respiratory
distress, suffusion of face,neck vein engorgement

4. Cosmetic

PRE-OP WORKUP

1. Histological

2. Physical examination

3. ThyroId profile

4. Indirect laryngoscopy-FNAC

5. FNAC

6. TPO-Graves’ disease

7. Calcitonin-medullary

8. Serum Ca 2+

9. USG NECK- size and number of nodes

-Lymphnode status

10. Thyroid scan-autonomous nodule

11. CT-rectosternal goiter

12. Iinvestigation for surgical fitness

4. ANAESTHESIA –endotracheal intubation –general

5. POSITION-supine –extended neck

STEPS OF OPERATION
1. Incision

 Horizontal-sternocleidomastoid to other –cutting skin and subcutaneous tissue

 Women-heavy breast-higher-prevent hypertrophic scar due to drag to
manubrium

2. Elevation of flap

 Platysma –diathermy
 Upper flap-thyroid notch
 Lower flap-clavicle

3. Strap

 Mid line vertical incision-separates sternohyoids

 Separate sternothyroid from gland

4. Palpate thyroid for undetected nodularity

5. Ligate

 Mid thyroid vein- drain into IJV

 Inferior thyroid vein-venous plexus anterior to trachea
 Thyroidoma-infront of trachea
 Branches of inferior thyroid-ligate medially
 Preserve B.S to parathyroid
 RLN-anterior/posterior/thyroid branches-preserve carefully
 May be injured near berry ligament- if cut indiscriminately

6. Superior thyroid pedicle and upper pole

 Divide sternothyroid in upper parts

 Ligate superioir thyroid artery and vein individually
 Preserve exterior branch if SLN(Posterior medial to vessel
 Traction of thyroid inferior helps save nerve

7. Parathyroid

 Preserve B.S
  If removed – implant on sternocleidomastoid after histological confirmation by
frozen section

8.Division of isthmus and separation of thyroid lobe

9.Irrigation of wond by saline /Betadine

Surgical drainage to avoid hematomas

10.closure of wound

 Vasalva monoeuvre - +ve pressure on venous ooze

 Strap muscle and platysma approximated
 Subcutaneous tissue subcuticular suture(cosmetic purpose)
 Steristrips to strengthen incision lines

COMPLICATIONS

1. Haematoma

2. Airway obstruction

3. Injury to RLN

4. Injury to SLN

5. Wound infection

6. Hypocalcaemia- Removal/devascularisation of PTG

7. Pneumothorax –injury to pleura /lower neck

8. Hypothyroidism
 DISEASES AND DISORDERS OF OESPHAGUS

1. Acute oesophagitis
a. Acute inflammation of oesophagus
b. Causes:
i. Ingestion of corrosives
ii. Ingestion of hot liquids
iii. Infections
iv. Laceration due to foreign body
v. Systemic disorders (pemphigus)
c. Complains:
i. Dysphagia
ii. Retrosternal burning
iii. Haematemesis
d. Diagnosis:
i. X-ray
ii. Oesophagoscopy
iii. History
2. Corrosive burns of oesophagus
a. Etiology:
i. Acid or alkali, accidentally or suicide purpose
b. Factors deciding severity:
i. Nature of substance
ii. Quantity
iii. Quality (concenteration)
iv. Duration of contact.
v. Alkalis are more corrosive
c. Pathogenesis: (3 stages)
i. Stage 1: Acute necrosis
ii. Stage 2: Granulation
iii. Stage 3: Stricture
d. History:
 i. Type of substance ingested,
ii. peritonitis,
iii. mediastinitis,
iv. upper airway obstruction,
e. Investigation:
i. Acid-base imbalance
ii. Chest X-ray
iii. Associated burns of face, lip and buccal cavity.
f. Management:
i. Hospitalization
ii. Tracheostomy – air way obstruction
iii. IV Fluids – Shock
iv. Electrolytes – Acid-base imbalance
v. Relieve pain
vi. Neutralization – oral route, within 6 hours.
vii. Parenteral antibiotics for 3 to 6 weeks
viii. Steroids for 4 to 6 weeks, to prevent stricture.
ix. Nasogastric tube
1. To feed the patient
2. To maintain lumen
x. Oesophagoscopy – assess severity (every 2 weeks)
xi. Oesophagogram every 2 weeks to check prognosis
xii. Management of stricture
1. Prograde dilatation
2. Retrograde dilatation
3. Oesophageal reconstruction

3. Benign strictures of oesophagus

a. Etiology
i. Ulcers
ii. Burns
iii. Foreign body trauma
iv. Surgical sites
v. Congenital
b. Clinical Features
i. Dysphagia
ii. Regurgitation and cough (complete obstruction)
 c. Diagnosis
i. Barium swallow
ii. Oesophagoscopy (to exclude malignance)
d. Treatment
i. Prograde dilatation.
ii. Gastrostomy
iii. Excision and reconstruction surgery

4. Perforation of oesophagus
a. Etiology
i. Spontaneous rupture
1. Boerhaave syndrome – postemetic rupture
ii. Instrumental
b. Clinical feature
Cervical oesophagial rupture Thoracic oesophagial rupture
Pain Interscapular pain
Fever Fever
Dysphagia Signs of shock
Local tenderness
c. Diagnosis
i. Chest and neck X-ray
5. Hiatus hernia
a. Displacement of stomach into chest.
b. Types
i. Sliding hernia
ii. Rolling hernia

6. Plummer-Vinson (Patterson-Brown-Kelly) Syndrome

a. Clinical Features
i. Dysphagia
ii. Iron deficiency anemia
iii. Glossitis
iv. Angular stomatitis
v. Koilonychia
vi. Achlorhydria
vii. Atrophy of luminal mucus membrane
b. Investigations:
 i. Barium swallow
ii. Oesophagoscopy
c. Treatment:
i. Iron – oral/parenteral
ii. Dilatation of webbed area

7. Globus Pharyngeus
a. Functional disorder,
b. Patients complain of lump in throat, but examination reveals none.

8. Motility disorders:
Hypomotility Hypermotility
Cardiac achalasia Cricopharyngeal spasm
GERD Diffuse spasm
Scleroderma Nut cracker oesophagus
Amyotrophic lateral sclerosis

9. Neoplasm:
a. Benign
i. Leiomyoma
ii. Mucosal polyps
iii. Lipomas
iv. Fibromas
v. Hemangioma
b. CA Oesophagus
i. Risk factors
1. Smoking
2. Alcohol
3. Pre-existing lesions
ii. Type :
1. Squamous cell carcinoma
2. Adenoarcenoma
iii. Metastasis:
1. Direct / local spread
2. Lymphatic
 3. Hematogenous
iv. Clinical Features:
1. Substernal discomfort
2. Progressive Dysphagia
3. Pain – referred to the back
4. Mediastinitis
5. Aspiration
v. Diagnosis
1. Barium swallow
2. Oesophagoscopy
3. Bronchoscopy
4. CT scan
5. Chest X-ray
vi. Treatment:
1. Radiotherapy is the treatment of choice
2. Surgery
a. Bypass operation
b. Permanent gastrostomy
c. Feeding jejunostomy
d. Laser surgery
vii. Prognosis – Bad
 DYSPHAGIA

Difficulty in swallowing

1. Etiology
a. Preoesophagial causes
i. Oral phase
1. Disturbance in mastication
2. Disturbance in lubrication
3. Disturbance in motility of tongue
4. Defects of palate
5. Lesions of buccal cavity and floor of mouth
ii. Pharyngeal phase
1. Obstructive lesions
2. Inflammatory conditions
3. Spasmodic conditions
4. Paralytic conditions
b. Oesophagial causes
i. Luminal – obstruction
ii. Wall – Oesophagitis and motility disorders.
c. Outside the wall – causes obstruction
2. History
a. Sudden onset – foreign body obstruction
b. Progressive - malignance
c. Intermittent - spasm
d. Intolerance to acid - ulcer
3. Investigation
a. Chest and neck X-ray
b. Barium swallow
c. Manometric and pH studies
d. Oesophagoscopy
e. Bronchoscopy
4. Examination
a. Examination of buccal cavity for preoesophagial lesions
b. Haemogram (Plummer-Vinson syndrome)
 FOREIGN BODIES OF FOOD PASSAGE

Location of lodging

1. Tonsil
2. Base of tongue / Vallecula
3. Posterior pharyngeal wall
4. Pyriform fossa
5. Oesophagus
Etiology

1. Age
a. Children below 5 years
2. Loss of protective mechanism
a. Loss of consciousness
b. Epileptic seizures
c. Deep sleep
d. Alcoholic intoxication
3. Carelessness
a. Improper mastication
b. Hasty eating
4. Narrowed oesophagus lumen
5. Psychosis
Symptoms

1. Discomfort of pain
2. Dysphagia
3. Drooling of saliva
4. Respiratory distress
5. Substernal or epigastric pain
6. In partial obstruction.
Management

1. Endoscopic removal
 a. Oesophagoscopy under general anesthesia
2. Cervical oesophagotomy
a. Removal through incision
b. For bodies lodged in cervical oesophagus
3. Transthoracic oesophagotomy
a. Incision in chest
b. For bodies lodged in thoracic oseophagus
Complications:

1. Respiratory obstruction
2. Abscess
3. Perforation
4. Tracheo-oesohagial fistla
5. Ulceration and stricture
 RECENT ADVANCES

LASER SURGERY

LASER is an acronym for Light Amplification by Stimulated Emission of Radiation.

Depending upon the lasing medium, various types of lasers with differing wavelength
can be created. Lasing medium can be solid (ruby, Nd: YAG or potassium titanyl
phosphate); gas (CO2 or Helium–Neon) or liquid (pumped inorganic dye in a glass tube).

Various types of lasers are

• Argon

• KTP (Potassium titanyl phosphate)

• Nd: YAG (Neodymium: yttrium aluminium garnet)

• CO2 (Carbon dioxide)

• Ho: YAG (Holmium: YAG)

• Er: YAG (Erbium: YAG)

• Diode laser

• Tunable dye lasers

When the LASER hits the tissue it can

1. Reflect

2. Absorbed

3. Scattered

4. Transmission
Lasers which are reflected or transmitted through the tissue do not cause any effect on
tissues.

Effect of laser on the tissues depends on the absorbed energy.

Lasers can be used to cut (make incision), coagulate blood vessels or vaporize the tissue.
When a burn is created by laser beam, it always causes some degree of collateral
damage. Zones of tissue damage can be divided into:

1. Zone of vaporization. A crater is created due to tissue ablation and vaporization

leaving behind only a few flakes of carbon.

2. Zone of thermal necrosis. This is just adjacent to the above zone. There is tissue
necrosis. Small blood vessels, nerves and lymphatics are sealed.

3. Zone of thermal conductivity and repair. This zone recovers with time.

Lasers approved by FDA for otological work include:

• Argon – 514 nm

• KTP – 532 nm

• CO2 – 10,600

• Er: YAG – 2960

Otologic lasers have been used to vaporize small glomus tumours, acoustic neuromas,
small A-V malformation, granulation tissue or adhesions in the middle ear. Lasers have
also been used to do a myringotomy, drilling a hole in incus or malleus for ossicular
reconstruction, welding of grafts in tympanoplasty or coagulating membranous
posterior semicircular canal in benign paroxysmal positional vertigo and in stapes
surgery to make a hole in stapes footplate.

Advantages include precise incision, easy and rapid ablation of tissues, excellent
haemostasis, and minimal postoperative pain and oedema of tissues. Some lasers can
be passed through optical fibres and can thus be used through flexible endoscopes,
straight or curved tubes to ablate tumours situated in difficult locations in the
tracheobronchial tube or nasal crevices or clefts. Disadvantages include high cost in the
purchase of equipment and its maintenance, special training in operating with lasers,
hazards in the use of laser requiring special precautions, and safety measures and
special anaesthesia requirements to avoid fires.

Clinical use of lasers is determined by:

1. Wavelength of laser

2. Selective absorptive property of tissues

3. Ability of laser to pass through flexible optical fibre

4. Mode of delivery (continuous wave mode or pulsed mode)

RADIOFREQUENCY SURGERY IN ENT

Radiowaves have been used surgically to reduce the volume of tissues. It has been used
on inferior turbinates to relieve nasal obstruction; on soft palate to relieve primary
snoring, upper airway resistance and sleep apnoea; and on the base of tongue to relieve
sleep apnoea. It has also been used for the treatment of lingual thyroid.

The radiofrequency (RF) device generates electromagnetic waves of very high frequency
between 350 kHz and 4 MHz. Usually 460 kHz is used. RF is delivered through various
probes according to the site of ablation. The probe, inserted into the tissues, causes
ionic agitation, heats up the tissues which result in protein coagulation and tissue
necrosis but no charring. Later scar formation occurs in 3 weeks with reduction in size of
tissue.

Using different types of electrodes, radiofrequency has also been used to perform
tonsillotomy, microlaryngeal surgery (to remove granulomas, papillomas, cysts),
myringotomy, uvulopalatoplasty, correction of rhinophyma and cosmetic removal of
skin lesions.

HYPERBARIC OXYGEN THERAPY IN ENT

Hyperbaric oxygen therapy (HBOT) is a treatment modality involving the intermittent

inhalation of 100% oxygen in chambers pressurized above 1 atmosphere absolute (ATA).
HBOT has been used as an adjunctive therapy for sudden sensorineural hearing loss
(SSNHL) as it raises the amount of oxygen in the inner ear by diffusion, which activates
cell metabolism leading to restoration of ionic balance and electrophysiological
functions of cochlea

INDICATIONS Approved by UHMS

1. Healing in problem wounds, diabetic or venous

2. Necrotizing soft tissue damage including malignant otitis externa

3. Radiation tissue damage

4. Carbon monoxide poisoning

5. Crush injury and other acute traumatic ischaemia

6. Decompression sickness

7. Air/gas embolism

8. Compromised skin grafts and flaps

9. Osteomyelitis

10. Thermal burns

11. Clostridial myonecrosis

12. Intracranial abscess

13. Exceptional blood loss (anaemia)

14. Sensorineural hearing loss

COBLATION

The term coblation was derived from controlled ablation or cold ablation, as the
temperature used in ablation of tissues is much lower than that used in electrosurgical
ablation or even coagulation. Coblation uses a radiofrequency above 200 kHZ to break
tissue bonds. It is a chemical process whereby highly energized ions are created in a
saline medium. A plasma field causes dissolution of tissue, unlike that in electrosurgical
dissection which works on thermal reaction causing tissue burning or coagulation with
collateral damage.

It has been used to perform:

• adenotonsillectomy,

• a reduction of tongue base,

• uvulopalatoplasty for sleep disordered breathing,

• turbinate reduction in nose,

• nasal polypectomy,

• cordectomy,

• laryngeal papillomas and other benign lesions of larynx and

• transverse cordectomy (Kashima operation) for bilateral abductor paralysis.

CRYOSURGERY

Rapid freezing of tissues to temperatures of −30 °C and below and their slow thawing
causes destruction. This fact has been used to treat various lesions of the head and neck
including benign, premalignant and malignant neoplasms. Agents used in freezing the
tissue are used either by an open method (liquid nitrogen spray or carbon dioxide snow)
or through a closed system such as a cryoprobe.

Freezing causes cell death through several mechanisms:

 Dehydration
 Denaturation
 Thermal Shock
 Vascular Stasis
 Cryoimmunisation
Cryotherapy can be applied under local or light general anaesthesia. Sometimes, no
anaesthesia is used as freezing itself causes numbness. The area to be frozen should be
insulated. A suitable cryoprobe is applied into or upon the tissues and the latter frozen
quickly for 3–8 min and then allowed to thaw slowly. The procedure is repeated once or
twice. Area frozen should include a margin of normal tissue. A thermocouple can be
implanted to ensure freezing at an adequate depth. After cryotherapy, the area is
allowed to heal by secondary intention. The necrotic slough falls off in 3–6 weeks.
Repeat cycles of cryotherapy may be required to achieve the desired result.

It is used in the treatment of Benign Vascular Tumours, Pre Malignant lesion, Malignant
lesion.
 BRONCHOSCOPY

Bronchoscopy is an endoscopic technique of visualizing the inside of the airways for

diagnostic and therapeutic purposes. An instrument (bronchoscope) is inserted into the
airways, usually through the nose or mouth, or occasionally through a tracheostomy.

Types- a. Rigid

b. Flexible fibreoptic

RIGID BRONCHOSCOPY - INDICATIONS

1Diagnostic
1. To find out the cause for wheezing, haemoptysis or unexplained cough
persisting for more than 4 weeks.

2. When X-ray chest shows:

 Atelectasis of a segment, lobe or entire lung

 Opacity localized to a segment or lobe of lung.

 Obstructive emphysema—to exclude foreign body.

 Hilar or mediastinal shadows.

3. Vocal cord palsy.
4. Collection of bronchial secretions for culture and sensitivity tests, acid
fast bacilli, fungus and malignant cells.
Therapeutic

1. Removal of foreign bodies.

2. Removal of retained secretions or mucus plug in cases of head injuries,
chest trauma, thoracic or abdominal surgery, or comatosed patients.
Anaesthesia: General anaesthesia

Position: sniffing postion.

Technique: There are two methods to introduce bronchoscope:

1. Direct method. Here bronchoscope is introduced directly through the

glottis.
2. Through laryngoscope. Here glottis is first exposed with the help of a
spatular type laryngoscope and then the bronchoscope is introduced through the
laryngoscope into the trachea. Laryngoscope is then withdrawn.

This method is useful in infants and young children, and in adults who
have short neck and thick tongue.
Postoperative care
1. Keep the patient in humid atmosphere.
2. Watch for respiratory distress. This could be due to laryngeal
spasm or subglottic oedema if the procedure had been unduly prolonged or the
bronchoscope introduced repeatedly. Inspiratory stridor and suprasternal retraction will
indicate need for tracheostomy.
Complications
1. Injury to teeth and lips.
2. Haemorrhage from the biopsy site.
 3. Hypoxia and cardiac arrest.
4. Laryngeal oedema.
Precautions during bronchoscopy
1. Select proper size of bronchoscope according to patient’s age.
2. Do not force bronchoscope through closed glottis.
 OESOPHAGOSCOPY

Oesophagoscopy is the examination of your gullet (swallowing tube) while you are
under a general anaesthetic. It is done to help problems of the gullet, such as difficult or
painful swallowing

Oesophagoscopy is of three types:1. Rigid oesophagoscopy.

2. Flexible fibreoptic oesophagoscopy.
3. Transnasal oesophagoscopy.
RIGID OESOPHAGOSCOPY- INDICATIONS

Diagnostic
1. To investigate cause for dysphagia, e.g. cancer oesophagus, cardiac
achalasia, strictures, oesophagitis, diverticulae, etc.
2. To find cause for retrosternal burning, e.g. reflux oesophagitis or hiatus
hernia.

3. To find cause for haematemesis, e.g. oesophageal varices.

4. Secondaries neck with unknown primary (as a part of panendoscopy).
Therapeutic
1. Removal of a foreign body.
2. Dilatation in case of oesophageal strictures or cardiac achalasia.
3. Endoscopic removal of benign lesions, e.g. fibroma, papilloma, cysts, etc.
 4. Insertion of Souttar’s or Mousseau-Barbin tube in palliative treatment of
oesophageal carcinoma.
5. Injection of oesophageal varices.

Contraindications
1. Trismus-makes the procedure technically difficult.
2. Disease of cervical spine, e.g. cervical trauma, spondylosis,
tuberculous spine, osteophytes and kyphosis.
3. Receding mandible.
4. Aneurysm of aorta for fear of rupture and fatal haemorrhage.

5. Advanced heart, liver or kidney disease may be a relative

contraindication.
Anaesthesia
General anaesthesia .
Position

Same as for direct laryngoscopy. Patient lies supine, head is elevated by 10-15
cm, neck flexed on chest and head extended at atlanto-occipital joint. The purpose of
this position is to attain the axes of mouth, pharynx and oesophagus in a straight line to
pass the rigid tube easily. This position can be achieved with the help of an assistant or a
special head rest.
Postoperative care
1. Sips of plain water followed by usual diet may be given in an uneventful
oesophagoscopy.
2. Patient is watched for pain in the interscapular region, surgical emphysema of neck
and abrupt rise of temperature. They indicate oesophageal perforation.
Complications
1. Injury to lips and teeth.

2. Injury to arytenoids.

3. Injury to pharyngeal mucosa. They are all the result of careless technique and can be
avoided.
4. Perforation of oesophagus. Most often it occurs at the site of Killian’s dehiscence
(near cricopharyngeal sphincter) when undue force has been used to pass the
oesophagoscope. Surgical emphysema develops within an hour or so and the patient
complains of pain in the interscapular region. This may be complicated by abscess in
retropharyngeal space or mediastinum.
5. Compression of trachea. Oesophagoscope may press on posterior tracheal wall,
especially in children, causing obstruction to respiration and cyanosis. Treatment is
immediate withdrawal of oesophagoscope.

FLEXIBLE FIBREOPTIC OESOPHAGOSCOPY

Its main advantage over the rigid oesophagoscopy is that it is an outdoor procedure,
does not require general anaesthesia and can be used in patients with abnormalities of
spine or jaw where rigid endoscopy is technically difficult. The oesophagus, stomach and
duodenum can all be examined in one sitting. Good illumination and magnification
provided by the fibrescope helps in the accurate diagnosis of the mucosal disease
affecting these sites and permits taking of precision biopsies, removal of small foreign
bodies or benign tumours, dilatation of webs or strictures and even injection of bleeding
varices with sclerosing agents. In cases of malignant disease, oesophageal stent can be
placed as a palliative measure.The procedure is performed under local anaesthesia with
or without intravenous sedation. The patient lies in left lateral position and fibrescope is
passed through a plastic mouth prop into the pharynx, postcricoid area and oesophagus,
insufflating air as the endoscope is advanced, to open the lumen of oesophagus. These
days flexible fibreoptic oesophagoscopy has practically replaced rigid oesophagoscopy
except in some cases of foreign bodies.

TRANSNASAL OESOPHAGOSCOPY

In contrast to flexible fibreoptic oesophagoscopy, which is performed through the oral

route by gastroenterologists, transnasal oesophagoscopy is performed through nose.
This flexible fibrescope has a working of 2 mm and the air can also be inflated through it
to distend the walls of oesophagus to look for any lesion in its mucosal folds.
Oesophagus can be examined up to gastric fundus. It is being used:
1. to look for pathology in oesophagus in cases of dysphagia.
2. as a part of panendoscopy in the work-up of a cancer patient to look for a second
primary and take a biopsy.
3. to remove foreign bodies from the oesophagus.
4. to perform tracheoesophageal puncture for oesophageal speech in laryngectomized
patient.
5. to take a laryngeal biopsy.
 TONSILLECTOMY

Indications
They are divided into:

A. ABSOLUTE
1. Recurrent infections of throat. This is the most common indication. Recurrent
infections are further defined as:
(a) Seven or more episodes in 1 year, or
(b) Five episodes per year for 2 years, or

(c) Three episodes per year for 3 years, or

(d) Two weeks or more of lost school or work in 1 year.

2. Peritonsillar abscess. In children, tonsillectomy is done 4–6 weeks after abscess has
been treated. In
adults, second attack of peritonsillar abscess forms the absolute indication.

3. Tonsillitis which causes febrile seizures.

4. Hypertrophy of tonsils causing
(a) airway obstruction (sleep apnoea),
(b) difficulty in deglutition and
(c) interference with speech.
5. Suspicion of malignancy. A unilaterally enlarged tonsil may be a lymphoma in children
and an epidermoid carcinoma in adults. An excisional biopsy is done.
B. RELATIVE
1. Diphtheria carriers, who do not respond to antibiotics.
2. Streptococcal carriers, who may be the source of infection to others.
3. Chronic tonsillitis with bad taste or halitosis which is unresponsive to medical
treatment.

4. Recurrent streptococcal tonsillitis in a patient with valvular heart disease.

C. AS A PART OF ANOTHER OPERATION
1. Palatopharyngoplasty which is done for sleep apnoea
syndrome.
2. Glossopharyngeal neurectomy. Tonsil is removed first and then IX nerve is severed in
the bed of tonsil.
3. Removal of styloid process.
Contraindications

1. Haemoglobin level less than 10 g%.

2. Presence of acute infection in upper respiratory tract, even acute tonsillitis. Bleeding
is more in the presence of acute infection.

3. Children under 3 years of age

4. Overt or submucous cleft palate.

5. von Willebrand disease. Bleeding disorders, e.g. leukaemia, purpura, aplastic

anaemia, haemophilia or sickle cell disease.
6. At the time of epidemic of polio.
7. Uncontrolled systemic disease, e.g. diabetes, cardiac disease, hypertension or
asthma.
8. Tonsillectomy is avoided during the period of menses.
Anaesthesia
General anaesthesia with endotracheal intubation. In adults, it may be done under local
anaesthesia.
Position
Rose’s position, i.e. patient lies supine with head extended by placing a pillow under the
shoulders. A rubber ring is placed under the head to stabilize it . Hyperextension should
always be avoided.

STEPS OF OPERATION (DISSECTION AND SNARE METHOD)

1. Boyle–Davis mouth gag is introduced and opened. It is held in place by Draffin’s
bipods or a string over a pulley.
2. Tonsil is grasped with tonsil-holding forceps and pulled medially.

3. Incision is made in the mucous membrane where it reflects from the tonsil to anterior
pillar. It may be extended along the upper pole to mucous membrane between the
tonsil and posterior pillar.
4. A blunt curved scissor may be used to dissect the tonsil from the peritonsillar tissue
and separate its upper pole.
5. Now the tonsil is held at its upper pole and traction applied downwards and medially.
Dissection is continued with tonsillar dissector or scissors until lower pole is reached

6. Now wire loop of tonsillar snare is threaded over the tonsil on to its pedicle,
tightened, and the pedicle cut and the tonsil removed.
7. A gauze sponge is placed in the fossa and pressure applied for a few minutes.
8. Bleeding points are tied with silk. Procedure is repeated on the other side.

Postoperative care
1. Immediate General Care
(a) Keep the patient in coma position until fully recovered from anaesthesia.
(b) Keep a watch on bleeding from the nose and mouth.
(c) Keep check on vital signs, e.g. pulse, respiration and blood pressure.
2. Diet. When patient is fully recovered he is permitted to take liquids, e.g. cold milk or
ice cream. Plenty of fluids should be encouraged.

3. Oral Hygiene. Patient is given Condy’s or salt water gargles three to four times a day.
A mouth wash with plain water after every feed helps to keep the mouth clean.

4. Analgesics.
5. Antibiotics. Patient is usually sent home 24 h after operation unless there is some
complication. Patient can resume his normal duties within 2 weeks.
Other methods for tonsillectomy.
1. Guillotine method.
2. Electrocautery.
3. Laser tonsillectomy.

4. Laser tonsillotomy.
5. Intracapsular tonsillectomy.
6. Harmonic scalpel.
7. Plasma-mediated ablation technique.
8. Coblation tonsillectomy.

9. Cryosurgical technique.

Complications
A. IMMEDIATE
1. Primary haemorrhage.

2. Reactionary haemorrhage.
3. Injury to tonsillar pillars, uvula, soft palate, tongue or superior constrictor muscle due
to bad surgical technique.
4. Injury to teeth.
5. Aspiration of blood.
6. Facial oedema.

7. Surgical emphysema.
ADENOIDECTOMY
Adenoidectomy may be indicated alone or in combination with tonsillectomy. In the
latter event, adenoids are removed first and the nasopharynx packed before starting
tonsillectomy.

Indications
1. Adenoid hypertrophy causing snoring, mouth breathing, sleep apnoea syndrome or
speech abnormalities, i.e. (rhinolalia clausa).
2. Recurrent rhinosinusitis.
3. Chronic otitis media with effusion associated with adenoid hyperplasia.
4. Recurrent ear discharge in benign CSOM associated with adenoiditis/adenoid
hyperplasia.

5. Dental malocclusion. Adenoidectomy does not correct dental abnormalities but will
prevent its recurrence after orthodontic treatment.
Contraindications
1. Cleft palate or submucous palate. Removal of adenoids causes velopharyngeal
insufficiency in such cases.
2. Haemorrhagic diathesis.
3. Acute infection of upper respiratory tract.

Anaesthesia
Always general, with oral endotracheal intubation.
Position
Same as for tonsillectomy. Hyperextension of neck should always be avoided.
Postoperative care
Same as in tonsillectomy. There is no dysphagia and patient is up and about early.
Complications
1. Haemorrhage.
2. Injury to eustachian tube opening.
3. Injury to pharyngeal musculature and vertebrae.
4. Grisel syndrome. .
5. Velopharyngeal insufficiency.
6. Nasopharyngeal stenosis.
7. Recurrence.
 SUBMUCOUS RESECTION OF NASAL SEPTUM

INDICATION:

Deviated nasal septum causing nasal obstruction and recurrent headaches.

Deviated nasal septum causing obstruction to ventilation of paranasal sinuses
and middle ear resulting in recurrent infections.
Recurrent epistasis from septal spur.
As a part of septorhinoplasty
Harvesting cartilage graft for tympanoplastyand rhinoplasty.
As an approach to surgeries of sphenoidal sinus, vidian nerve and pituitary gland.

TREATMENT - SURGERY:

It is generally done in adults.

It consists of elevating mucoperichondrial and mucoperiosteal flap on either side
of septum,removing the deflected parts of bony and cartilagenous septum and
then repositioning the flaps.

STEPS:

Infiltration: subpericondrial infiltration with 2% xylocaine with adrenaline.

Incision: killian's incision- curvilinear incision 2-3mm behind the anterior end of
septal cartilage.

Elevation of flaps: the mucoperichondrial and mucoperiosteal flap is elevated.

Incision of the cartilage- cartilage is incised just posterior to the first incision.

Elevation of opposite mucoperichondrial and mucoperiosteal flap.

Removal of cartilage and bone- cartilage can be removed with Ballinger swivel
knife or luc's forceps. Bony spur is removed using gouge and hammer.
Preserve a strip of 1cm wide cartilage along the dorsal and caudal borders (L-
struts).
Nasal packing.
CONTRAINDICATIONS:

Acute URTI.
Patient below 17 years of age.
Bleeding disorders.
Uncontrolled hypertension and diabetes mellitus.

LIMITATIONS AND COMPLICATION:

Caudal end deformities.

Poor access to nasal spine.
Dorsal deformities.
Saddle back deformity.
Septal hematoma.
Collapse of nasal tip and columella.
Nasal obstruction.
Mucosal tear.
TSS.
Septal perforation.
Cartilage and bone may return to original deformed position.
 DIRECT LARYNGOSCOPY

Indications

1. Diagnostic

 Indirect Laryngoscopy not possible as in infants and when symptoms points

to larynx

 Indirect Laryngoscopy not successful as in gag reflax and over hanging

epiglottis

 To find extent of growth and take biopsy

 To examine hidden areas of larynx and hypopharynx

2. Theraputic

 Removal of foreign body and benign lesions

 Dilate the strictures

Contraindications

 Injured cervical spine

 Difficult respiration

 Coronary occlusion and cardiac decompensation

Anesthesia

 General anesthesia

 Infants and children not needed in case of diagnostic purpose

Position

Supine neck with elevated 10 to 15 cm. Barking dog position

Procedure

1. Gauze in upper throat to prevent them from trauma

2. Laryngoscope lubricated with parrafin or jelly

3. Left hand to handle Laryngoscope

Right hand to manage other instruments and guide the Laryngoscope

4. Laryngoscope is pushed by one side of tongue till posterior part is reached then it is
pushed to anterior part go bring epiglottis in view.

5. Laryngoscope behind epiglottis for view of interior of larynx.

6. Ant commissure Laryngoscope it is sent past ventricular band and ant commissure
and between vocal folds for view of subglotic region.

7. Base of tongue , right and left valecule , epiglottis, both pyroform sinuses,
Ariepiglottic folds, artenyoid , post cricoid region, both false cords , ant post commissure
, right and left ventricles and right and left vocal cords then subglottic are are serially
checked.

Post-operative care

 Patients kept in coma position to prevent aspiration

 Patients respiration should be watched for cyanosis and laryngeal spasm

 Repeated Laryngoscopy leads to laryngeal edema and respiratory distress

Complications

 Injury to teeth mag fall into pharynx

 Laryngeal edema

 Aspiration
 NECK MASSES

Name Location and Features Treatment

dimension

Thyroglossal duct Cystic midline Increase in size with Sistrunks operation

cyst swelling 2to4 cm in upper respiratory
Recurrence if the
diameter (anywhere infections. Moves
whole tract ia not
between foramen with protrusion of
removed.
caecum to thyroid tongue.
gland)

Sublingual dermoid From floor of the Doesn't move with Surgical excision
cyst mouth , above
Protrusion of tongue
Suprastrnal notch

Submental nodes In submental triangle 2 to 8 Draining areas should

between platysma be looked for
and mylohyoid infection or
malignancy when
nodes get enlarged.

Pre laryngeal and pre Front of larynx and Juxtavisceral chain of Examine draining
tracheal nodes trachea nodes areas when enlarged.

Thymic cyst 3rd pharyngeal pouch Unilocular cyst (solid Sternotomy if extends
to neck , to or cystic) into mediatinum
mediastinum

Branchial cyst Anterior to SCM has Ext opening-Mucoid Surgical excision

an ext opening discharge from sinus
or fistula

Int opening in
tonsillar fossa. Both
are present, called as
branchial fistula.

Plunging ranula Transilluminant Extravasation of Total excision and

submandibular mucus from removal of sublingual
 swelling obstruction to salaivary gland
sublingual salivary
gland.

Carotid body tumor From chemedectoma Pulsatile , bruit heard CT and MRI are
diagnostic. FNAC
Extend to
shouldn't be done.
Parapheryngeal sapce
and present in Surgical and
Oropharnyx. radiotherapy can be
done.

Para pharyngeal Retromandibular area Majority are salaivary Diagnostic imaging

tumour gland tumor. and fnac

Cystic hygroma or Posterior triangle Obstruction of jugylar Surgical excision and

lymph sac bipolar diathermy.
Lymphangioma or Supraclavicular region
Solid cystic
Cavernous Other sites
multilocular
lymphangioma
Tongue and mouth
Transiluminant
Axilla and groin
Painful and increas in
size on infections

Tubercular lymph Any lymph node. Adherent to skin or Drugs Rntcp regimen
node draining sinus may
Matted due to peri If fails surgical
develop
adenitis excision.

Metastatic lymph Most common: Secondaries from

nodes pyriform sinus tonsil lung breast colon
base of tongue and stomach kidney ovary
nasopharynx and testis

SCM Tumor Fibrosis and Torticollis face facing Excersice in early

shortening of the opposite sude and stages and surgery in
muscle head tilted on case of this leading to
shoulder facial hemihypoplasia
 CHEMOTHERAPY OF HEAD AND NECK

 Drugs used alone or in combination with other forms of treatment.

 Squamous cell cancers-methotrexate, cisplasitin,bleomycin,5-flurouracil.
 Adriamycin- nonsqumous carcinomas
 Dacarbasin-melenomas

Types of chemotherapy:

Palliative chemotherapy: Cytotoxic drugs used to treat advanced ,recurrent /metastatic

drug to treat symptoms and prolong life.

 Used before surgery/radiation-induction or anterior chemotherapy.

 Used simultaneously with radiotherapy (acts as radiosensitizer )
 Used after surgery-posterior chemotherapy.

Single agent Vs multiple drug combination therapy:

Methotrexate, cisplastin, bleomycin, 5-fluorouracil – used as single agents

Can also be used in combination with other drugs to improve response and duration of
response.

Drugs used in cancer therapy:

1. Methotrexate :
Sq.cell cancer, (ALL)Acute leukaemic lymphoma.
S/E: Bone marrow suppression, mucositis of oral and GI cancer.
Maculopapular rash
Renal and hepatic toxicity.
2. 5-fluorouracil: Squamous and non-squamous cell cancer of breast and GI tract
S/E: Myelosuppression(neutropenia, thrombocytopenia)
Mucositis(nausea, vomiting, stomatitis, diarrhoea)
Skin (alopecia,hyperpigmentation, maculopapular rash, hand-foot syndrome)
3. Cyclophosphamide: Sq.cell cancer, lymphoma. Leukaemia, neuroblastoma,
multiple myeloma.
S/E: Haemorrhagic cystitis
Nausea, vomiting ,Alopecia
Cessation of menses
 Neutropenia
Permanent infertility
4. Dacarbasin: Melanoma, sarcoma
S/E: Nausea, vomiting
Myelosuppression
Flu-like symptoms
Alopecia
5. Adriamycin: Lymphoma, sarcoma, Esthesioneuroblastomas, salivary gland
cancer.
S/E – cardiotoxic
Alopecia
Stomatitis, nausea, vomiting, diarrhoea
Neutropenia

Pretreatement work-out of patients:

 History of clinical examination

 Haematological tests
 Urine tests
 Biochemistry
 Radiology
 Pulmonary function test
 ECG
 Audiogram
 Nutritional status
ENT MANIFESTATIONS OF HIV INFECTIONS:

Three types of lesions are seen:

 Opportunistic infections: All types of infection
 Unusual malignancies :Kaposi sarcoma, Hodgkin and non-hodgkin
lymphoma
 Neurological disorder

1. Ear:
 Kaposi sarcoma
 Seborrhoeic dermatitis of external canal
 Malignant otitis externa
 Serous otitis media
 Acute otitis media
 Pseudomonas and candida infections
 Mycobacterial infections
 Sensorineural hearing loss
 Herpes zoster (Ramsay–Hunt syndrome)
 Facial paralysis
2. Nose and paranasal sinuses
 Herpetic lesions of nose
 Recurrent sinusitis
 Chronic sinus infection
 Fungal sinusitis
 Kaposi sarcoma
 Lymphomas–B cell type
 Burkitt lymphoma
3. Oral cavity and oropharynx
 atrophic or hypertrophic forms of candidiasis.
 Infection of oropharynx, hypopharynx, oesophagus. They cause difficulty and
painful swallowing.
 Herpetic lesions of palate, buccal mucosa, lips or
gums.
 Giant aphthous ulcers
 Adenotonsillar hypertrophy.
 Generalized lymphadenopathy
 Kaposi sarcoma of palate
 Non-Hodgkin lymphoma of tonsil or tongue
 Hairy leukoplakia
  Gingivitis
4. Larynx
 Laryngitis
 Kaposi sarcoma
 Non-Hodgkin lymphoma
5.Salivary Glands
 Parotitis
 Xerostomia
 Diffuse parotid enlargement
 Lymphoepithelial cysts of parotid.
 Kaposi sarcoma
 Non-Hodgkin lymphoma
6. Neck
 Lymphadenopathy.
 toxoplasmosis or non-Hodgkin or Hodgkin lymphoma

CHEMOTHERAPY OF HIV INFECTION:

There are four major classes of antiretroviral drugs:

1. Nucleoside reverse transcriptase inhibitors
 Zidovudine
 Didanosine
 Zalcitabine
 Stavudine
 Lamivudine
2. Non-nucleoside reverse transcriptase inhibitors
 Delavirdine
 Nevirapine
 Efavirenz
 Tenofovir (nucleotide analogue)
3. Protease inhibitors
 Saquinavir
 Ritonavir
 Indinavir
4. Fusion inhibitors
 Enfuvirtide
 CLINICAL METHODS IN ENT

HISTORY TAKING

1. History of present illness.

2. History of past illness.
3. Personal history
4. Family history
General Setup and Position of Patient:

 Semi-dark room
 Patient seated on a stool or chair opposite to the examiner
 Bull’s eye lamp(at the level of patient’s left shoulder) and head mirror/head light
used

I. EXAMINATION OF EAR

Symptomatology:

1. Hearing loss.
2. Tinnitus.
3. Dizziness or vertigo.
4. Ear discharge.
5. Ear ache.
6. Itching in the ear.
7. Deformity of the pinna.
8. Swelling around the ear.

Examination of ear:
A. Physical Examination:
1. Pinna and surrounding area
 Size(microtia/macrotia)
 Shape(cauliflower ear)
 Redness(furuncle)
 Swelling(abcess/heamatoma)
 Vesicles(herpes zoster)
 Scars/ulceration
 Raised temperature(perichondritis)
2. External auditory canal
 Without a speculum:
 # Pinna pulled upwards and backwards; tragus pulled forwards
# Examine for size, contents and swelling
 With a speculum:
# Look for wax, debris, discharge, polyp, granulations, exostosis,
neoplasm, sagging of posterosuperior area (in coalescent mastoiditis)
3. Tympanic membrane
 Colour: Red (acute otitis media);
Blue (haemotympanum);
Chalky plaque (Tympanosclerosis)
 Position: Retracting(m/c in attic) – tubal occlusion, adhesive otitis
media
Bulging – acute otitis media, heamotympanum
 Surface: Vesicles(herpes zoster/myringitis bullosa)
Perforation (ASOM/CSOM) - Central/attic/marginal
 Mobility: Normal-mobile
Fluids or adhesions in middle ear-restricted mobility
Atrophic segments-hypermobile
4. Middle ear – Examine for middle ear mucosa and in-growth of squamous
epithelium(In the presence of perforation)
5. Mastoid – Swelling/Obliteration of retroauricular groove/fistula/scar
# Mastoid irregularities ironed out in periosteal inflammation
(subperiosteal abscess)
# Tenderness elicited at three sites:
Over the antrum; over the tip; part between tip and antrum
6. Eustachian tube – Function of tube tested by VALSALVA MANOEUVRE(In
perforation, air is felt to escape from the ear when patient tries to blow with
mouse and nose closed)
7. Facial nerve and other cranial nerves – ASOM, CSOM, herpes zoster oticus,
trauma, tumours.
B. Functional Examination:
1. Auditory function - Voice tests and Tuning fork tests
2. Vestibular function – Spontaneous nystagmus, Fistula test and Positional tests

II. EXAMINATION OF NOSE AND PARANASAL SINUSES

Symptomatology:

1. Nasal obstruction.
2. Nasal discharge.
3. Postnasal drip.
4. Sneezing.
5. Epistaxis.
6. Headache or facial pain.
7. Swelling or deformity.
8. Disturbances of smell.
9. Snoring.
10. Change in voice (hyper- or hyponasality).

Examination of Nose:
1. Examination of external nose
(a) Skin:
 Inflammation(furuncle, septal abscess)
 Scars(operation/trauma)
 Sinus(congenital dermoid)
 Swelling(dermoid or glioma)
 Neoplasm(bcc/scc)
(b) Osteocartilaginous framework (deviated or twisted nose / hump /
depressed bridge / bifid or pointed tip / destruction of nose – trauma,
syphilis, cancer)
(c) Palpate to find raised temperature, fixity of skin, thickening of soft tissues,
tenderness, fluctutation or crepitation.
2. Examination of vestibule
 Tilt the tip of the nose upwards
 Examine for furuncle, fissure, crusting, dislocated caudal end of septum,
tumours.
3. Anterior rhinoscopy
 Thudicum or Vienna speculum is used
 Examine for nasal passage, septum, floor of nose, roof and lateral wall
 Colour of mucosa, size of turbinates, discharge and presence of mass are
noted
 Probe test done to ascertain the site of attachment, consistency,
mobility and sensitiveness of the mass
4. Posterior rhinoscopy
 Posterior rhinoscopic mirror is used
 Touching the posterior third of tongue is avoided to prevent gag reflex
 Examine for,
# Choanal polyp or atresia
# Hypertrophy of posterior ends of inferior turbinate
# Discharge in middle meatus
5. Functional examination of nose
 (a) Patency of nose
 Spatula test
 Cotton-wool test
(b) Sense of smell (common substances used are clove oil, peppermint, coffee
and essence of rose)
Note: Ammonia is not used to test the sense of smell (as it stimulates CN V)

Examination of Paranasal sinuses:

1. Maxillary sinus
 Examine to elicit tenderness by pressure over the canine fossa
 Transillumination done by placing a light source centrally in mouth and
closing the lips : a crescent of light in the inferior fornix and glow in the
pupil(equally bright on both sides)
2. Frontal sinus
 Tenderness elicited by pressure with a finger on its anterior wall above the
medial part of eyebrow,
(or) by pressing upwards on its floor above the medial canthus
 Transillumination : light source in the superomedial angle of the orbit and
observing the transmission of light from the anterior wall of the sinus (it is
compared on both sides)
3. Ethmoid sinus
 Tenderness elicited by gentle pressure applied on the medial wall of orbit
just behind the root of the nose (e.g. In acute ethmoiditis)
 Probe test done to assess the consistency and friability of any mass.
4. Sphenoid sinus
 Difficult to examine under normal conditions (anterior wall seen in
atrophic rhinitis)

Note: Anterior and Posterior Rhinoscopy done to examine for discharge, crusts, polyp
or growth.
Note: X-rays preferred over transillumination in all cases.

III. EXAMINATION OF NASOPHARYNX

Symptomatology:
1. Nasal obstruction
2. Postnasal discharge
3. Epistaxis
4. Hearing impairment (tubal block)
5. Cranial nerve palsies
6. Enlargement of lymph nodes in the neck

Examination of Nasopharynx:
1. Anterior rhinoscopy (facilitated by decongestion of nasal and turbinal mucosa
with vasoconstrictors)
2. Posterior rhinoscopy
 Discharge
 Crusting: Atrophic rhinitis or nasopharyngitis
 Mass:
(i) Smooth pale mass—antrochoanal polyp.
(ii) Pink lobulated mass—angiofibroma.
(iii) Irregular bleeding mass—carcinoma.
(iv) Smooth swelling in the roof—Thornwaldt’s cyst or abscess.
(v) Irregular mass with radiating folds - adenoids.
(vi) Irregular mass filling the lower part of choana - mulberry
hypertrophy of inferior turbinate.
 Bleeding
3. Other methods
(a) Digital examination (adenoids, antrochoanal polyp can be examined)
(b) Endoscopy (rigid nasal endoscope or flexible nasopharyngoscope can be used)
(c) Retraction of soft palate with catheters and mirror examination (reserved for
difficult cases)
4. Cranial nerves: Malignancy of nasopharynx can involve any of the CN II to XII,
more often CN IX, X and XI.
5. Cervical lymph nodes (lymph nodes commonly involved in nasopharyngeal
malignancy are upper internal jugular and those along the accessory nerve in the
posterior triangle of the neck)

IV. EXAMINATION OF ORAL CAVITY

Symptomatology:

1. Pain
2. Disturbance of salivation
3. Disturbance of taste
4. Trismus
5. Lesion of oral cavity

Examination of oral cavity:

1. Lips – Look for any swellings, vesicles, ulcers, crusts, scars and clefts
2. Buccal mucosa(ask the patient to open the mouth and retract the tongue with a
tongue depressor)
# Change in colour
# Change in surface appearance-(ulceration / vesicles / bullae/ striae / scars
/ erythroplakia / leucoplakia / pigmentation / atrophic change of the mucosa /
swelling or growth)
3. Gums and teeth
(a) Red and swollen gums - Gingivitis.
(b) Ulcerated gums covered with a membrane - Viral ulcers/Vincent
infections.
(c) Hyperplasia – Pregnancy/phenytoin
(d) Growths – Benign/malignant neoplasms.
(e) Loose teeth – Maxillary/mandibular growth, periodontitis.
(f) Carious infected tooth - Upper = maxillary sinusitis and Lower =
Ludwig’s angina.
(g) Malocclusion – Fractures/TMJ abnormalities
4. Hard palate
(a) Cleft palate: Congenital
(b) Oronasal fistula: Trauma/syphilis
(c) High-arched palate: Mouth breathers
(d) Bulge: Tumours of palate, nose or antrum
(e) Bony growth in midline: Torus palatinus
(f) Mass or ulcer: Cancer
5. Anterior two-thirds of tongue:
Examine the natural tongue position, protrusion, movements. Also examine
the tip, dorsum, lateral borders and undersurface.
(a) Large size –
Macroglossia/haemangioma/lymphangioma/cretinism/oedema/ abscess.
(b) Inability to protrude - Congenital ankyloglossia/painful ulcer/abscess
(c) Deviation on protrusion – CN XII paralysis
(d) Bald tongue – Iron deficiency anaemia/median rhomboid glossitis
(e) Fissures. Congenital (Melkersson syndrome)/syphilitic (non-healing).
(f) Ulcers - Aphthous traumatic/malignant/syphilitic/tubercular.
(g) White thick patch or plaque - Leucoplakia.
(h) Proliferative growth - Malignancy.
6. Floor of mouth: Frenulum / opening of submandibular duct / ulcer / Swelling
7. Retromolar trigone: Look for inflammation d/t impaction of last molar or
malignancy
V. EXAMINATION OF OROPHARYNX

Symptomatology:

1. Sore throat
2. Odynophagia
3. Dysphagia
4. Change in voice
5. Ear ache
6. Snoring
7. Halitosis
8. Hearing loss
9. Abnormal appearance

Examination of Oropharynx:
Ask the patient to open his mouth and use a tongue depressor to displace the
tongue; Laryngeal mirror used to examine the base of the tongue.
1. Tonsils:
(a) Presence/absence
(b) Size – large/small
(c) Symmetry – Unilateral/bilateral enlargement
(d) Crypts:
# Follicular tonsillitis – yellow spots at the openings
# Keratosis – white excrescences
(e) Membrane – Diphtheria/Vincent’s angina/membranous tonsillitis
(f) Ulcer – Ulcerating tonsillolith/TB
(g) Mass – Cystic/pedunculated/proliferative
(h) Bulge – Peritonsillitis/parapharyngeal abscess

Note: Pressure on anterior pillar express cheesy material from crypts

(normal) or frank fluid pus (septic tonsil)
Note: Palpation of tonsil – done to know the consistency (hard:
Malignancy/tonsillolith)
Note: Pulsation in tonsillar area – internal carotid artery aneurysm
2. Pillars: Acute tonsillitis ( Uniform congestion of pillars, tonsils and pharyngeal
mucosa )
3. Soft palate: Redness/bulge/swelling
 Peritonsillar abscess: Uvula becomes edematous and displaced to
opposite side
  Vagal paralysis: Deviation of soft palate to the healthy side, when the
patient says “Aah”
 Curtain effect: Paralysed posterior pharyngeal wall muscles moves like
a sliding curtain to the healthy side, when the patient says “Aah”
 Bifid Uvula: Submucous cleft palate/Nigeria(practice of amputation of
uvula during childhood)
4. Posterior pharyngeal wall:
 Granular pharyngitis: lymphoid nodules
 Sinusitis: purulent discharge
 Chronic sinusitis: hypertrophy of lateral pharyngeal wall behind the
posterior pillar
 Atrophic pharyngitis: thin glazed mucosa and crusting
5. Base of tongue and Valleculae:
(a) Indirect laryngoscopy: look for colour of mucosa, ulceration, swelling
(b) Palpation of Base of tongue: to know the extent of the deeper infiltrating
tumour of tongue

VI. EXAMINATION OF LARYNX AND LARYNGOPHARYNX

Symptomatology:

1. Disorders of voice
2. Respiratory obstruction
3. Cough and expectoration
4. Repeated clearing of throat
5. Pain in throat
6. Dysphagia
7. Mass in the neck

Examination of larynx and laryngopharynx:

1. External examination of larynx
(a) Redness of skin
(b) Bulge or swelling
(c) Widening of larynx
(d) Surgical emphysema
(e) Change in contour or displacement of laryngeal structrues
(f) Movements of larynx
2. Indirect laryngoscopy: Used to examine the structure of oropharynx, larynx and
laryngopharynx
3. Flexible or rigid fibreoptic endoscopy:
 (a) Flexible endoscopy: A flexible rhinolaryngoscope is used when
# there is presence of anatomical abnormalities
# the patient is intolerant to mirror
(b) Rigid endoscopy: A rigid fibreoptic telescope is used (Local anaesthesia
required for patients with an active gag reflex)
4. Assessment of voice:
The quality of voice of the patient is noted, when he is speaking (hoarse,
rough, breathy, bitonal, dysphonic, whispered or feeble)
5. Assessment of cervical lymph nodes

VII. LYMPH NODES OF THE HEAD AND NECK

Examination of Neck nodes:

 Stand at the back of the patient
 Neck is slightly flexed to achieve relaxation of muscles

1. Upper horizontal chain (submental, submandibular, parotid, facial,

postauricular and occipital nodes)
2. External jugular chain (superficial to sternomastoid)
3. Internal jugular chain (upper, middle and lower groups)
4. Spinal accessory chain.
5. Transverse cervical chain.
6. Anterior jugular chain.
7. Juxtavisceral chain (Prelaryngeal, pretracheal and paratracheal nodes)

Note the following points regarding the palpable lymph nodes,

1. Location of nodes.
2. Number of nodes.
3. Size.
4. Consistency. (Metastatic nodes are hard;
Lymphoma nodes are firm and rubbery;
Hyperplastic nodes are soft.)
5. Discrete or matted nodes.
6. Tenderness. (Inflammatory nodes are tender.)
7. Fixity to overlying skin or deeper structures. (Mobility should be checked both
in the vertical and horizontal planes.)
 SOME IMAGING TECHNIQUES IN ENT

Aim of Imaging Techniques:

Imaging helps doctors to detect the spatial extent of disease, anatomical danger
area and help in planning of surgery, precise an appropriate treatment.

IMAGING TECHNIQUES:

1) Computer Tomography Scan(CT)

2) Magnetic Resonance Imaging(MRI)

3) Positron Emission Tomography Scan

4) Ultrasonagraphy

5) Digital Volume Tomography

Computer Tomography Scan(CT)

 Cross-Sectional imaging
 most popular imaging techniques
 useful for the diagnosis of cancer
 Its advantage over x-ray was that it eliminates the overlap structures that happen
in x-ray.
Advantage:

 Highly accurate.
 Painless procedure.
 Provides real time imaging and helps doctor to view 3d images.
Disadvantage

 Large expose of radiation.

 Sometimes before scan patients receive a dose of contrast material, containing
iodine. Some people are allergic to this and experience its side effects.
 ^CT image of nose

^CT scan of neck sagital view ^CT showing significant subglottic stenosis
CT scan images of Ear
CT scan AT EAR AT NECK AT NOSE
(Petrous & Mastoid part of
Temporal bone)
Done for  Hearing loss, Evalution of Sinuses
 Face palsy, head and neck During chances of
 Including acquired lesion nose cancer
diseases –especially
inflammatory traumatic,
and
 Neoplastic processes of
inner, middle and outer
ear
 To determine the Extent
of bony destruction in
disease like
cholesteatoma, mastoid,
and tumors.

Magnetic Resonance Imaging(MRI)

 Provide a very detailed diagnostic picture.

 Method of choice to assess anomalies of inner ear diseases.
 Mainly used during the pre and post-operative tumor imaging.
 Particularly in the ear disease, cholesteatoma, MRI and other specialized form of
MRI scans play very important role as scans can avoid the second look surgery.
Advantage

fast, painless and non-invasive

do not use ionizing radiation.

Disadvantage

No harmful effects.

Should not be done in first 12 weeks of pregnancy.

Metal implants like cochlear and pace makers may be affected by magnetic field.
^normal ear anatomy in MRI

Positron Emission Tomography Scan

 Type of nuclear medicine imaging.

 Examine the chemical activity in patient’s body
 Provides unique and exact information , including details of both function and
anatomic structure of body
 Plays an important role in diagnosing laryngeal and hypo pharyngeal cancers.

^PET of brain

With the help of PET nowadays, parkinsonism disease is detected at earlier stag

Ultrasonagraphy

 Ultrasound otolaryngology is quite useful because clinical findings can be

misleading.
 It is a valuable tool for diagnosing of Peritonsiller abscess and in the assessment
of neck masses and for throat problem such as throat cancer, increased lymph
nodes, and thyroid problems. ( Remember, where there is a mass ,Our 1st
thought come in mind for investigation is ultra sound)
 ^Ultrasound of Thyroid

Digital Volume Tomography

 One of kind of CBCT, Cone beam computed tomography
 Similar to computed tomography
 High spatial resolution and low ionize radiation and reduced metal effect.
 It is mainly used by dentist.
 The role of DVT in otolaryngology is not much, it is mainly used during nasal none
fracture, lateral, anterior skull base, and paranasal sinus.