larynx, pharynx salivary & esophagus, tracheo-bronchology

laryngology anatomy (1)

Anatomy of larynx:
Tubular organ with a variable lumenum, at the superior extremity of trachea and opened inferiorly into the
hypopharynx. Composed: Cartilage + membranes + ligaments. Muscles + mucosa

Muscles of larynx: External – conects L to neighboring organs, fixate, elevate or lower the L.
Internal – phonatory and sphincter functions
-M. Thyro-arittenoid (vocal muscles) – prominent in the lumenum, form the sckeleton of Vocal Cords
- M.Crico-arittenoid posterior (Posticus, CAP) – only glottic opening muscle(abduction)
- M. inter-arittenoid, M.crico-arittenoid lateral (CAL) – adduction, closes glottis, phonatory

Internal Configuration:
-Glottis – between VC. Margins: anterior commisure, free margins of VC, arittenoids and inter-arittenoid fold
- Supraglotic – superior orifice of L (epiglottis, aritteno-epiglottic folds, arittenoids, false vocal cords, ventricle of
MORGAGNI)
- Subglottic – inferior face of VC and mucosa to the inferior margin of cricoid

Vascularization and innervation:

- Arterial: Laryngian sup. and inf. from a. thyroid sup. Laryngian post. from a. thyroid inf.
- Veins follow arteries => IJV
- Lymphatic – poor for the VC and rich subglottic
*Supraglottic => jugulo-carotid superior and middle LN
*Subglottic => prelaryngeal, pretracheal LN => jugulo-carotid
middle and inferior
-Innervation *S: nv.laringeus superior, from X (vagus)
*M: nv. Recurrent laryngeal from X

Respiratory Function Vital Function of L. opens the glottis

to regulate the air flux.
LARINX DYSPNOEA Majore and severe syndrome. Reduction of air flux that passes through L. and has
a laryngeal cause. Respiratory insufficiency of superior laryngeal obstructive cause.
*Causes: Laryngeal Malformations (glottis membrane, juxta-laryngeal cysts) . FB. Larynx Trauma (fracture,
stenosis, hematoma, burns). Acute Inflammations (acute oedema laryngitis, diphteria). BT (papilloma ,polyp) /
MT (cancer). Neuro-motory afflictions (recurrent laryngeal bilateral paralisis in adduction position, laryngeal
spasm)
*MAJOR signs: never missing. Inspiratory bradipnoe. Descending larynx during inhaling. Accentuation of
suprasternal / supraclavicular space
*MINOR signs: Stridor. Accentuation of intercostal/subcostal/substernal space. Voice modification/ caugh.
Extended head during inhaling. Stasis of cervico-facial veins. Paradoxal pulse KÜSSMAUL (decrease of sistolic > 10
mmHg. During inhaling). Respiratory silence
* Treatment: Solving cause. Oxigen therapy. Sedatives that do not depress respiratory centers. Intubation
oro/naso-tracheal. Tracheostomy - classical or extreme emergency
- Indications of tracheotomy : Acute or chronic laryngeal Dyspnoe. Complementary or additional step of
surgery. Diminishing of respiratory dead space for severe pulmonary afflictions or in ventilated patients
(pneumonia, tetanos, intoxications with cu barbituric drungs, severe thoracic lesions)

Phonatory Function:
Social Function of L: Classical mio-elastic theory EWALD –vibration of VC by air column. Neuro-cronaxic theory
HUSSON – vibration determined by central nervous impulse via recurrent nerves. Muco-ondulatory theory
PERELLO – ondulartion of mucosa by contractile modification of VC

DYSPHONIA Phonasthenia - tired speaking voice. Rezasthenia – tired singing voice.

Hoarseness – harsh sound, crepitant, unclear. Aphonia. Diplophonia – bitonal voice. Eunuch voice - teenagers

Sfincter function: Supravital. Protection of respiratory tract. Adductors close glottis. Larynx ascends and is
covered by epiglottis. Cough Reflex with protective role

Cough / expectorating function: Closes glottis and increases pressure in thorax followed by sudden expulsion +
pushes secretions from trachea. Dry cough – laryngitis, tumors. Wet cough– laryngo-tracheo-bronchitis.
Barking cough–subglottic laryngitis, diphteria

Fixating the thorax Closes glottis and increases intrathoracic pressure.Thorax becomes rigid and sustains upper limbs
during effort

Function in blood circulation: Insures variation of endothoracic pressures with a pump effect

Sensitive syndrome Hyperesthesia – acute laryngitis, neurosis, cancero-phobia . Anaesthesia – neurologic, rare.
Severe because if allows food into upper airway . Paresthesia – sensation of FB. Pain – at the greater horn of the
hyoid, accentuated by deglutition, irradiating in the ear
 laryngology malformation (2)
Congenital Malformations:
Agenesis laryngo-tracheo-pulmonary. Atresia with complete imperforation.
Communication between laryngx-trachea-oesophagus. Atresia imperfecta.
Webbed Glottis – diaphragm that unites the VC. Diastema laryngo-tracheo-oesophageal – development defect
of tracheoo-esof. Septum. Absence of epiglottis or shape modifications
Laryngoptosis (fallen larynx). Laringomalacia (floppiness of larynx tissues) – stridor congenital
Thyroid Cartilage opened anteriorly, CV on different levels. Congenital laryngeal Cysts – dyspnoe.
Congenital Hemangioma
*Sd. Cri du chat – deletion of 5p cromosom (5p minus syndrome) – rudimentary larynx, defect of VC adduction during
phonation

Acquired Malformations:
LARYNGOCEL:
Hernia of the MORGAGNI ventricle mucosa via existing paths.
-Internal / external / mixed.
-Sometimes filled with air, increases side in cough or VALSALVA maneuver.
-dysphonia + dyspnoe.
-Extirpation - endoscopic or external approach

LARYNX STENOSIS
Mechanical Trauma with fracture or luxation, surgical or chemical.
Important respiratory and phonatory affliction

LARYNX TRAUMA
1.CLOSED: Concussion and fracture by direct hit (falling, striking) – bicycle handle bars, edge of table, hand, hanging
or indirect (falling with flexed head). submucous hematoma, fracture of cartilage, hematoma, subluxation of
arittenoids
*Clinical: Intense pain, sometimes syncopal (vagal death). Painful dysphonia or aphonia. Odinophagia,
dysphagia. Dry cough. Pain upon palpation of a fixed point. Larynx dyspnoe
I. L. – echimosis, obstruent hematoma, immobilizing VC, reduction of lumen
*Treatment: total vocal rest. AB protection. Tracheostomy if necessary. Cortisone, Codein. Surgical
Recalibration on plastic tube (1-3 months)

Post-traumatic laryngeal Hematoma

2.OPENED:Accidents, aggression, war. cervico-laryngeal wounds. Straight or ridged edges, shrapnel, crush,
subcutaneous emphysema. Shoc, dyspnoe, hemorrhage . dysphonia, dysphagia, cough with foaming, bloody
sputum.
*Treatment: Deshocking, breathing check-up (intubation through mouth or nose, through wound, tracheotomy).
AB. Hemostasis. Tetanos shot. Cleaning and suturing

3.SECONDARY LESIONS Post intubation –glottic oedema

* Treatment with Cortisone, reintubation, tracheotomy. postintubation Granuloma of VC –surgical resection

4. WHIPPLASH OF LARYNX: Vocal Professionals after acute effort. Accentuated dysphonia during speaking.
IL - Echymosis of VC (rupture of vocal muscle). vocal rest, warm aerosols, phoniatric treatment

5.BURNS: Liquids, hot vapors, corrosive substances. signs:pain, larynx spasm with dyspnoe, cough, odinophagia,
dysphagia, Difuse Congestion, oedema, bleeding ulcerations
*Treatment: Vocal rest, calming cough and pain. Instillation or aerosols with Epinephrin, Cortisone. Liquid
food, NG Tube. Tracheotomy if necessary.

6. LARYNX FB: Seeds, fish bones, needles, nails. In epiglottis, valleculae (by deglutition), vestibule, ventriculum,
glottis (aspiration).
 *Clinical: Dyspnoe – immediate and rapidly lethal. dyspnoeic effort. Dysphagia. Dysphonia.
-Larynx FB :peanut in glottic space (4 years old patient-up), aspired needle in trachea (15 year old patient)
* Treatment: Ensuring breathing. Tracheotomy, oxygen therapy. Calming pain and cough. Extraction via
natural ways. Maneuver HEIMLICH ensures breathing

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laryngology laryngitis (3)

Acute nonspecific laryngitis:
1.ACUTE CATARHAL LARINGITIS During acute viral inflammation of upper airways +/- infection
*Favorized: smoking, alcohol, pollution, cold, wet, overheated air, intubation, vocal effort
*Hyperemia of mucous, submucous transudate, mucous or muco-purulent exudate.
*Clinical: Hyperesthesis, cough, dysphonia. Fever, frisson, myalgia. IL – difusse congestion of mucosa, yellow
secretion, visible swollen vessels
*Treatment: Absolute vocal rest, antithermic, warm bandage, inhalation, cough medicine, avoiding irritants, AB.

Acute nonspecific laryngitis in children

ACUTE OEDEMATOUS SUBGLOTTIC LARYNGITIS OF THE CHILD Younger than 5-6, severe because of small calliber of L
*Viral Etiology + saprophytic flora
*Favored by: adenoiditis, smallpox, convulsive cough, spasmophilia, cold, wet
*Simptoms: Sudden or insidious dyspnea. Barking cough, clear voice. Evolution towards healing in 7-10 days
but also towards aggravation of dyspnoea – death
*Treatment: Aerosols with Efedrine and Cortisone, O2. Cortisone 10mg/kgc/24h and AB. IOT, Tracheotomy

2.STRIDULOUS LARYNGITIS Discrete inflammation of L. Added spasm

*Cause: rinitis, adenoiditis – secretions run down into L, irritate, produce glottic spasm.
*Crises are dramatic, during night. When adduction muscles relax, breath will start again
*Dg – usually anamnestic
*Treatment Treating naso-pharyngeal infections, Calcium, Vitamines. In crises – splash cold water upwards into
nostrils- reflex yielding of spasm upon contact of water to the NF
3. SUFFOCATING LARYNGO-TRACHEO-BRONCHITIS OF THE SMALL CHILD (CHEVALIER JACKSON)
*Viral, in small children 1-2 year
* Congestive oedema of the airway mucosa, purulent fibrous exudate => fibrous plugs, atelectasis. Severe state,
fever, dyspnoea, cough, difficult expectoration. Evolves to exittus, reserved prognosis
* Treatment: AB high dosis, Cortisone. O2. Proteolytic Enzimes. Bronchia suction

4. OEDEMTOUS LARYINGITIS: Acute laryngitis determined by pyogenic germs with Oedematous lesions post
radiotherapy. Allergic oedema. Oedema in uremia. Predilection for: lingual face of epiglottis, ariteno-epiglottic
folds, in the lax tissue of aritenoids.
* Simptoms: Altered general state, fever. Odinophagia, FB sensation, reflex otalgia, irritative cough. Dysphonia
followed by dyspnea. IL – reddish mucosa, oedema, sometimes gelo-like, reduced lumenum

5. ABSCESS AND PHLEGMONA OF LARYNX (EPIGLOTTIS) High fever, altered septic state, painful dysphagia, LN. Red
oedema of epiglottis +/- obstruction.
* treatment: Admission, AB, surgical opening of collection

6. PERICONDRITIS AND CONDRITIS After epiglottitis, surgery, radiotherapy, long-term intubation . External
Tumefaction, palpable and internal tumefaction.
*treatment:AB, HHC, AINS, drainage. Usualy important sequelle

7. ARTRITIS – painful and important dysphonia

Acute specific laryngitis

1. DIPHTERIA Dysphonia, dyspnoea upon inhaling. Death by asphyxia or toxic shock.
*IL – false membranes obstruating the L. LN . Extraction of membranes, O2, serotherapy, AB. IOT or tracheotomy
– usually necessary

2 .FLU – fever, myalgia, rhinitis

3. MEASLES – catarhal or oedematous subglottic

4. CHICKEN POX – vesicles and superficial ulcerations covered in membranes

5. CONVULSIVE COUGH –catarrhal lesions with broken vessels due to cough effort. Long-term persisting dysphonia.

6. HERPES – vesicles that break easily

7. REUMATISM – monocorditis or arthritis of the aritenoids

Chronic non-specific laryngitis

ETIOPATHOGENESIS:
* Descending Infection (rhinitis, sinusitis, adenoiditis, ozena).
* Ascending Infection (bronchitis, suppuration).
* Respiratory nasal insufficiency – forces oral breath (DSN, allergy, polyposis).
* Environmental – cold, excessive heat, smoking, pollution
* Alimentary habits (cold, spicy, alcohol)
* Forcing the voice
* Endogenous (hepatic, renal, rheumatism, gout)

ANATOMOPATHOLOGICAL :
*Catharal: congestion of mucosa, infiltration of chorion
*Chronic hypertrofic: hyperplasia of epithelium +/- keratinization
 1. Leucoplasia: parakeratosis with moderated akantosis or hyperkeratosis (precancer state)
-Simptoms: Dysphonia – dominant. Cough, tired voice. IL – differs according to clinical type

2. .EVERSION OF THE LARYNGEAL VENTRICLE – mucosa of the ventricle bulges into the lumen

3. PSEUDOMYXOMATOUS LATYNGITIS – great smokers, gelatinous chronic edema of VC

4. RED PACHIDERMIA LARYNGITIS– red, diffuse or islands of thickening of mucosa

5. LEUKOPLASIA – important precancer state, white plaques on VC

6. CONTACT ULCERS OF VC– granulation on arytenoid side of VC, on the opposite side ulceration

7. POSTANESTHESIA GRANULOMA – after prolonged intubation, granulation on the posterior comissure, subglottic

8.VOCAL NODULES – 2 small simetric protrusions on the free margins of the VC 1/3 ant and 2/3 post.

9.REINKE EDEMA – oedema of VC in great smokers, singers

10. OZENA OF LARYNX (LARYNGITIS SICCA)– atrophy of mucosa, dried secretions subglottic with potential
obstruction

11. CHRONIC HYPERKINETIK LARYNGITIS – children

12. PROFESSIONAL LARYNGITIS

Chronic specific laryngitis

TUBERCULOSIS
*Lupus – descending from NF and pharynx. Destructive, not paiful lesions
* Tertiary TB – in patients with pulmonary TB via sputum
* forms: monochorditis, inter-arittenoid, tuberculoma, ulcerative-vegetative

SARCOIDOSIS (BESNIER-BOECK-SCHAUMANN) – dysphonia, irritation of L. Deposits typical for sarcoidosis in L

SYPHILIS – mucous plaques or goma

SCLEROMA and LEPROSY – propagated from pharynx. Obstructive subglottic lesions. Treated with Riphampicine

PEMFIGUS – bubbles that burst and leave painful lesions, especially on epiglottis
 laryngology Paralysis(4)

Neuropathies
1. RECURRENT MONOPLEGIA: Recurrent nerves suffer 3 types of lesions: neuritis, compression, sectioning
* Etiology: trauma, iatrogenic (thyroid surgery, oesophagus, trachea, large vessels, heart), Compression via
tumor (LN, mediastinal, thyroid, oesophagus, aneurisms) Hypertrophy of heart, pulmonary apical lesions
* Clinical: Dysphonia when VC is fixated in abduction (bitonal voice). Dysphonia of singing voice in high pitched
sounds with VC fixed in adduction. IL –VC fixed, atrophic, shorter, arittenoid pushed forward
* Treatment –vocal exercise, injecting silicone into VC (vocal cord)

2. RECURRENT DIPLEGIA
* Sd. GERHARDT – diplegia in adduction – good voice, bad breathing . To do: Cordopexy
* Sd. ZIEMSSEN – diplegia in abduction –normal breathing, bad voice. Frequent food aspiration
* Diplegia in intermediate position

Miopathies: Affliction of larynx internal muscles.

*Cause: Rheumatism. Vocal Effort. Acute Laryngitis
Generates various degrees of dysphonia and glottis insufficiency
* Treatment: Etiologic. Phoniatric. Tonifying

Associated larynx hemiplegia

*Etiology:
- Affliction exo- and skull base: rhinopharynx cancer, middle ear cancer, glomic tumor of jugular, parathyroid
tumors etc.
-meningeal-radicullary affliction: meningitis (TBC, syphilis), poliradiculoneuritis GUILLON-BARRE, Zoster
-Brain stem lesions : vascular lesions (Sd.WALLENBERG), inflammatory (acute anterior poliomielitis), brain stem
tumors, tumors of cerebellum
*Clinical:
-Sd. AVELLIS: paralysis of hemiveil + hemilarynx + VC (IX, X)
- Sd. SCHMIDT: (X, XI) – hemiplegia of larynx, paralysis of SCM and trapesus
- Sd. JACKSON: sd. Schmidt + paralysis of XII
- Sd. VERNET: sd. SCHMIDT + paralysis of IX – courtain sign
- Sd. COLLET-SICCARD: VERNET + XII
- Sd. VILLARET: COLLET-SICCARD + S cervical (Sd. CLAUDE-BERNARD-HORNER) with exophtalmia, miosis

Larynx Spasms Contraction of various duration of all internal muscles –glottic spasm
*Clinical: Dyspnoea. Agitated, cyanotic, loss of consciousness. Convulsion
* Etiology: Inflammation. FB. Acute adenoiditis in children (stridulous laryngitis). Spasmophylia
* Treatment: etiological, water in NF, tracheotomy
 laryngology tumors(5)

Benigne larynx tumors

LARYNGEAL POLYP : Conjunctive Tumor, angiofibroma, usually in persons that shout a lot.
-clinical:Dysphonia – permanent or intermittent
-Reddish-violet tumor, on the free margin of the VC, as big as a pepper seed
- treatment: Extirpation via surgery (LSS)

LARYNGEAL PAPILOMA: Viral Etiology. Frequent between 2-8 years

-Starts with dysphonia - permanent and progressive
-Dyspnoea -first progressive than permanent
-Berry-shaped masses, reddish, disseminated everywhere on the L mucos
-Treatment: Extirpation of tumoral masses . Distruction via CO2 Laser. Usually recidivating. On puberty
becomes rare and disappears but some cases persist in adults.

Laryngeal Cancer Frequent Tumor. 50% of all ENT cancers and 3% of all malign tumors
-Factors that favorize: Smoking (over 200.000). Alcohol. Pollution. Age > 40
Precancer states (leukoplakia, pachidermia, papilloma in adults). Gender – masculine
-Almost always scuamous cell carcinoms. Infiltrating, vegetative, ulcerated Tumors
-Clinical: Dysphonia- chronic, progressive. Dyspnoea - slowly progressive. Odinophagia irradiating to the ears.
Dysphagia and dry cough. LN with fistulas to the skin. Syalorrhoe(hyper salivation), fetid breath
- Death by: asphyxia, hemorrhage, cachexia or pulmonary metastasis

VC CANCER (GLOTTIC): Dysphonia. Tumor on the VC becomes fixed. Metastasis to the LN - late

VESTIBULO-EPIGLOTTIC CANCER (SUPRAGLOTTIC): Mute clinically for long periods

Odynophagia, dysphonia. Extends to the tongue base, subglottic, glottic. LN meta frequent

TRANSGLOTTIC CANCER: Glottic Cancer that invades the ventricle

SUBGLOTTIC CANCER: produces dyspnea. Extension to VC and trachea

PHARYNGO-LARYNGEAL CANCER: Late manifestations

Odynophagia, dysphonia, dyspnoea, dysphagia. LN meta – early and frequent
- Clinical Debut: Supraglottic – dysphagia, odynophagia
Glottic – dysphonia
Subglottic – dyspnea
- Surgical Treatment: - Cordectomy.
- Fronto-lateral Laryngectomy (one VC and small part of the other) – vertical plane
- Horizontal plane – Epiglottectomy, partial horizontal supraglottic Laryngectomy
- Total Laryngectomy
- Radical neck-dissection
- Palliative Tracheotomy: 60% in 5 years. 95% for cordectomy.
- Radiotherapy completes surgery
-Chemotherapy
-Erigmophonation, Laryngophon, voice prosthesis
 pharyngology anatomy (1)
anatomy:
Pharynx: Tubular Organ at the upper end of the digestive tract
-Constrictor pharyngeal muscles – pharyngeal aponeurosis (fascia) – mucosa
-pharyngeal aponeurosis is inserted on: skull base, pterygoid process, mandible, hyoid bone, thyroid cartilage –
continues with the oesophagus behind the cricoid artilage
- Relations: P(posterior): cervical spine.
S(uperior): sfenoid sinus, basilary process, posterior foramen lacerum
L(ateral): RIOLAN’S bouquet. RIOLAN’S bouquet – muscle and tendon structure inserted on the styloid process
-latero-pharyngeal space divided in two:
1. Prestilian: parotid gland, ECA
2.Retrostilian: vascular and nerve (ICA, IJV, nv.IX,X, XI, XII, S cervical, jugulo-carotid lymphnodes)

Superior part: RHINOPHARYNX, NASOPHARYNX, EPIPHARYNX or CAVUM

-A: choanae.
- L: orifice of the EUSTACHIAN tube, behind it the ROSENMÜLLER fossa and GERLACH‘S tonsil
-S-P: pharingeal tonsil LUSCHKA. Lined with respiratory ciliated pseudostratified columnar epithelium and mucus
glands

Middle part: BUCCOPHARYNX, OROPHARYNX or MEZOPHARYNX

- A: oral cavity via the buccopharyngeal istmus defined by uvula, soft palate, tonsil pillars, tongue.
- L: tonsillar fossa. Tonsils – ovoid proeminent with about 18-20 small depressions (cripts) – canals dug into the
lymph tissue . Tonsils have capsule. Between it and muscle – lax tissue

Inferior part: HYPOPHARYNX or LARYNGOPHARYNX

- A: base of tongue, lingual tonsil, glosso-epyglotic fossa (valeculae) divided by glosso-epyglotic fold
- I: orifice of larynx (glottis)
- L: pyriform fossa, folds of the hypopharynx mucosa that cover the posterior face of the larynx
-Digestive Mucosa, stratified

Vascularisation – Inervation
- ECA(external carotid artery) – ascending pharyngeal, lingual, palatine arteries
- Veins collect into the prepharyngeal plexus
- Lymphatic:
*Rhinopharynx – gg. jugulocarotid superior . In children < 3 years in gg.retropharyngeal GILLETTE
*Oropharynx - gg. Jugulocarotid middle
*Hipopharynx - gg. jugulocarotid middle and inferior
-Inervation:
* M: nv.X for vale and nv.IX for pharyngeal constrictor muscles
* S and Sz: nv.IX (bitter taste at the base of the tongue)
Physiology:
1. Pharyngeal Deglution: second stage of deglutition, reflex
2Phonatory: articulated and singing voice not possible without pharynx that transforms fundamental laryngeal sounds
3. Sensory: only for bitter
4. Defense: via lymphatic tissue at the aero-digestive border
5. Vomiting reflex
6. Digestive pharyngeal syndrome

PHARYNGEAL DYSPHAGIA
-Disruption of 2nd stage of deglutition.
* Impossibility of food bolus passage into the pharynx (paralysis or tumors of the tongue)
* Stagnating bolus in the pharynx (paralysis of pharyngeal muscles in the context of bulbar paralysis or myasthenia)
* Exteriorization of food through the nose = palatine vale insufficiency (paralysis, rupture, malformation)
* Aspiration of food into the airways (anaesthesia of pharinxans laryns)
* Food returns to the oral cavity (regurgitation) in obstruction of pharynx(stenosis, FB, tumors).

Respiratory pharyngeal syndrome

- Nasal obstruction via rhinopharynx obstruction
- Hipertrophy of pharyngeal tonsil LUSCHKA, FB, tumors
- In n.b. life threatening
- Bucco/hypopharynx obstruction provokes acute respiratory insufficiency and is life threatening
- Inflamation with accentuated oedema, post-traumatic, insect bites, QUINCKE’S oedema, angioneurotic oedema,
tumors, large FB

Phonatory pharyngeal syndrome

- CLOSED RHINOLALA (nasal voice) in obstruction of rhinopharynx
- OPENED RHINOLALIA – vale insufficiency – does not close the rhinopharynx. Mostly affected the consonants,
except “m” and “n”
- Obstruction of bucco/hypopharynx does not allow for articulated speech

Sensitive pharyngeal syndrome

- ODINOPHAGIA. Iradiates to the ears and accentuates in deglutition.
- HIPERESTESIA – in inflammation
- HIPOESTESIA – hot food, strong alcohol, nerve damage
- PARESTESIA – chronic inflammation, rarely tumors. Most frequently neurotic – globus hystericus. Sensation of
globe, knot, FB in throat and discharge of secretion posteriorly (postnasal drip).

Sensory pharyngeal syndrome

- DISGUESIS (dis-no, guesis- taste) Mostly in affliction of tongue mucosa

y
 pharyngology malformation (2)
CLEFT PALATE: Isolated Veloschizis ot in severe malformations such as velopalatoschizis or velopalatocheiloschizis

SHORT VALE does not close the rhinopharynx. Difficulty in sucking for n.b. + opened rhinolalia
-Treatment: NG tube feeding or spoon feeding. Sugery at 2 years (urano-staphyloraphia).
Palatine prosthesis (plastic), temporary . Speech therapy
Sometimes the cleft is not apparent (under mucosa). Can be accidentally opened after surgery (adenoidectomy,
tonsillectomy)

LUETA BIFIDA – usually no surgical treatment. Sometimes speech therapy

ECTOPIC THYROIDRound prominence, smooth, red, rich vascularisation, at the base of the tongue, medially, behind
the vallate papillae. This is where the thyreoglotic canal begins (foramen caecum)

ACQUIRED MALFORMATION:
- Vale paralisis (diphteria, brain stem syndromes, affliction of vagus)
- Vale adherent to posterior pharyngeal wall (after surgery, chemical burns, tertiary syphilis scars)
- Vale insufficiency: after surgery (UPPP), tumors, syphilis

EAGLE’S syndrome –long styloid syndrome

-contact to branches of the carotid and irritates the sympathic sheeth of the vessels
- Pain in the region irrigated by ICA, oropharynx with irradiation in the ear
-Sensitivity in tonsil fossa palpation. Pain accentuated by head movement . Odinophagia / Dysphagia

Pharyngeal FB Most frequently food (fish, chicken bones) also Needles, nails, toys, coins, Animated – leeches
Most frequently in oropharynx in the tonsillar crypts. In rhinopharynx by vomiting
In hypopharynx it fixates in the base of the tongue, valeculae or pyriform folds
- Clinical: Odinophagia. FB sensation. Sialorrhea
- Diagnostic: clinical (direct pharyngo-oesophagoscopy). Risk of mucosa lesions and peri-pharyngeal infection
- Treatment: Extraction with forceps via natural access routes. Local anaesthesia with cu Lidocain

PHARYNGEAL TRAUMA
Mecanic: Lesion of mucosa by sharp objects (pencil) \ Lesion of walls – parietal - (knife, glass shard, rasor)
Odinophagia, sanguinolent saliva(blood), dysphagia \ Risk of celulophlegmona through wound
treatment: Liquid or i.v. feeding several days + AB

Termic: Odinophagia, oedema with acute respiratory distress

treatment :Liquid or i.v. feeding several days. Healing in 6-8 days

Chemical: Caustic Agents, base, acid. Corrosive oesophagitis

 Pharyngology: acute pharyngitis (3)
ACUTE NONSPECIFIC TONSILLITIS
1. ACUTE CATARRHAL TONSILLITIS: Respiratory viruses. Difuse, superficial inflammation. Cause: Cold weather,
pollution, cold drinks, promiscuity . Contagious, mostly in collectivities
- Simptoms: Sudden onset, frisson, fever, headache, convulsions in children .
Dryness of throat, odynophagia.
BF – difuse congestion of mucosa, sometime uvula oedema
Promintent vessels and small vesicles on veil
Viral Exam only in epidemics
May get complicated with bacterial infection, acute laryngitis, acute tracheo-bronchitis
- Treatment: Warm dressing on neck, mouth rinse with local disinfectants, cough drops (Tantum, Strepsils,
Trachisept, Bioparox). AINS. Rest . Avoid irritants (spices, alcohol, cold). Increase immunity

2. ACUTE BACTERIAL TONSILLITIS streptococc ß hemolitic, staphilococc, pneumococc, bacilus Friedländer (Klebsiella
pneumoniae), bacilus Pfeiffer (Haemophilus influenzae). Less contagious than viral
- Simptoms: Similar to previous but more severe, altered general state, fever, odynophagia
BF: tumefied tonsils, congested, creamy white-yellow deposits, nonadherent to the crypts
Subangulomandibular, painful lymphnodes
Leucocitosis and neutrophilia + bacterial throat cultures
- Clinical forms:
* Severe: large lymphnodes, uvula oedema, severe gen. state
* Alimentary: with streptococc ß hemolitic transsmited via unboiled cow milk. severe manifestations, often
epistaxis
* Pseudo-membranous: membrans detach easily and do not spread beyond the tonsil
* Ulcerous: very severe, extremely virulent germs and weak immunity
- Treatment: AB antistreptococcus (Penicilina, Eritromicina). Benzatin penicilina (Moldamin).
Rest, admition into Infectious Disease department. Treatment locally

3. PLAUT-VINCENT TONSILLITIS : Ulcero-necrotic, unilateral. Usually in patients with bad oral hygene
- odinophagia – unilateral, moderate, low fever, severe asthenia
- Tonsil ulceration on a dirty base, necrotic, irregular rims
- Dg.dif – syphilis chancre – hard and smooth
- treatment: AB – penicillin. Local

4. ACUTE ADENOIDITIS: Inflamation of the pharyngeal tonsil LUSCHKA

- Ethiology – common flora. Usually after viral infection. Fever and nasal obstruction
BF: muco-purulent secretions flow on the posterior wall of pharynx.
AR: same secretions in NF
PR: tumefaction of pharyngeal tonsil with puss deposits
- Complications: Acute catarrhal or suppurated otitis media \ Stridulous Laringitis \ Retrofaringeal
Adenophlegmon
- Treatment: AB. Nasal dezobstruant. AINS
ACUTE SPECIFIC TONSILLITIS
1. DIPHTERIA Most frequent localization of diphteria. Bacillus KLEBS-LÖEFFLER
- Sourse – diphteria patients and healthy carriers, via saliva, cough or sneeze (PFLÜGGE‘S drops). Incubation 2 – 11
days
- Simptoms: Fever, headache, palor, asthenia, tachycardia. Subangulomandibular lymphnodes
- BF: congested tonsils, covered in yellowish or white-grey spots that join => false membranes (difficult to
dettachand leave a bleeding area). Membranes extend to the veil, pillars, posterior wall, larynx, rhinopharynx, NF,
middle ear.
- Dg confirmed bacteriologically
- treatment: Serum anti-diphteria + Penicillin. Immediate admission.

2. SCARLET FEVER In the invasion phase. Cause: Streptococc ß hemolitic with eritrogenous toxine.
- signs: headache, vomiting, fever, odinophagia, swollen lymphnodes
- BF: tumefied, congested tonsils, intensely congested veil with a clearly demarcated area
- Strawberry tongue
- treatment: Mandatory admission. Penicillin + Local

Strawberry tongue in scarlet fever – color and hyperplasia of the papillae is typical (picture)

3. MEASLES During the catarrhal pre-eruptive period + ocular inflammation (crying facies)
- Oral enanthema appears 1 day before the exanthema –KÖPLIK‘s sign, small white dots on a hyperemic base
beside the 2nd Superior Molar
- It is a catarrhal pharyngitis

4. RUBELA – swollen occipital Lymphnodes is characteristic

5. FLU – fever, myalgia, asthenia

6. HERPES – bundles of vesicles on congested area. They burst and leave superficial painful ulcerations. Extended
Herpes + multiple adenopathy = suspicion of AIDS

7. ZOSTER – similar to herpes but unilateral, accompanied by intense pain

8. THRUSH (CANKER SOARES) –superficial ulcerations. Very painful. Healed in 10-16 days.

Herpes simplex labialis – bundles of vesicles on congested area on upper and lower lip

Herpes labialis upper lip Thrush on tip of tongue

9. QUINCKE’S OEDEMA - in atopic patients (allergies). Risk of asphyxia.

Treatment extreme emergency- Epinephrin 1% i.v., Cortisone, Antihistamin, Tracheotomy if needed

10. TOXIC PHARYNGITIS: Hg, Bi, Au, I, Bromide, P, Pb, Belladonna. Congestion and oedema of pharynx

11. HERPANGINA – vir.Coxsackie A. small vesicles with serous liquid on the veil.)

12. CMV Pharyngitis – ulcerations covered by white deposits on the oral mucosa)
PHARYNGITIS IN BLOOD DISEASES :Blood disease, especially neutropenia provoking, determine pharyngitis.
Ulcerations on the tonsil tissue; Decrease of immunological resistance due to phagocyte activity reduction of
leucocites.

1.ACUTE LEUCOSIS Determines acute ulcero-necrotic bilateral tonsillitis

-signs: Fever, swollen LN and HepatoSplenoMegalia. Ulcerated Gingivitis . Pale mucosa and tegument by anemia
Frequent ulcerations, epistaxis. Leucocites increased dramatically
- dg.: by medular puncture
- treatment: hematological. For pharyngitis AB + Local

2. AGRANULOCITOSIS By affecting the granulocyte series

- treatment: Piramidon, Fenilbutazona, Sulfamide, Antithyroid, Antiepileptic etc.
- signs & symptoms: Brutal onset with extreme general signs. Ulcerations and necrosis of tonsils, bilateral,
extended to pillars, veil, no swollen LN or HSM. Decrease of granulocytes < 1000/mm3
- Evolution mostly lethal. If the patient survives the “granulocyte crisis” (severe infection) he may heal.
* In mielopathies with involvement of the 3 medullary series
1. Irradiation, citostatic, As, benzene, chloramphenicol
2. Ulcero-necrotic bilaterala tonsillitis with anaemia and hemorrhagic syndrome
3. Medulary Transplant

3. MONONUCLEOSIS EBV. Asthenia, headache, fever, odinophagia, dysphagia. ervical, inguinal, axilla
adenopathy + HSM. Diagnosis: PAUL-BUNELL – HANGANUTIU Reaction . Slow healing in 2-3 weeks

AIDS MANIFESTATIONS IN ENT

Primary infection: acute pharyngitis, poliadenopathy, skin eruption
Sd. Limfoadenopathic – superficial polyadenopathy
Buccopharyngeal Candida infection (thrush)
Herpes or zoster infection
KAPOSI’S Sarcoma - violet tumor underneath healthy mucosa on veil, palate, posterior wall, oral mucosa
Cervico-facial Lymphoma
Sensorineural hypoacusis by meningeal or cerebral infection or after treatment (AB
Various common infections (sinusitis, otitis)

STOMATITIS – GLOSITIS

Inflamation of oral and tongue mucosa.

HAIRY LEUKOPLAKIA

BLACK VILLOUS (HAIRY) TONGUE

GEOGRAPHIC TONGUE

CHEILITIS

STOMATITIS
 Pharyngology: chronic pharyngitis (4)
NONSPECIFIC CHRONIC PHARYNGITIS
1.CHRONIC PHARYNGITIS Catarrhal \ Hypertrophic \ Atrophic
-Risk Factors:
Chronic nasal /rhinopharynx obstruction
Acute, repeated, frequent pharyngitis
Chronic nasal /sinus infection/inflammation
Iritants (smoking, alcohol, spicy food, pollution)
Tonsillectomy in a young age
Gastroesophageal reflux
-Simptoms: Dryness, FB sensation, stinging, irritative cough, adherent secretion
- BF: diffuse congestion of mucosa, islands of hypertrophic lymphatic tissue, mucous secretions, atrophy of mucosa
- Pharyngitis in ozena: atrophic, dry mucosa, crusts
Treatment: Treatment of causes. Pharynx disinfectants, Aerosols, sprays , vitamins

Hypertrophic mucosa, granulated look and lymph follicles on posterior wall of the pharynx (picture1)

2. CHRONIC ADENOIDITIS Chronic Inflammation of LUSCHKA tonsil. When hypertrofic = VEGETATIVE ADENOIDS(
Most frequently 3-6 years. In acute unhealed adenoiditis, lymphatic status, cold climate
- Simptoms: Slow onset of nasal obstruction, trouble sleeping, snoring, sleep apnea.
Nasal voice. muco-purulent secretions. Adenoids Facies
Badly implanted teeth, high palatine arch, concave thorax
Tired child, sleepy, attention deficient, poor school results.
Main complication = SEROUS OTITIS MEDIA (picture 2)
- Treatment: Surgical – Adenoidectomy. Breathing exercises

3. CHRONIC TONSILLITIS Chronic Inflammation of tonsils. Consequence of repreated acute tonsillitis, adenoids,
buco-dental inflammation, wet and cold climate, cold drinks.
- Simptoms: Frequent acute bacterial tonsillitis. Pharynx discomfort, asthenia, low fever.
BF: hypertrophic tonsils and pillars. Squzing puss from the crypts (not cazeum)
Kissing tonsils with possible breathing and swallowing impairment
- Treatment – Tonsillectomy

INDICATION OF TONSILLECTOMY: Acute repeated tonsillitis for > 3/ani

- Acute repeated tonsillitis in children >3/year, 3 years in a row
>5/year, 2 years in a row
>6-7/year
- Large hypertrophic tonsils with impairment of phonation, swallowing, breathing
- Unilateral hypertrophy requires biopsy, Tonsillar abscess in history, Infection sources proven by simptoms
and laboratory
- Acute episode of tonsillitis followed by aggravation of chronic renal, cardiac, rheumatism, osteo-articular
pathology. Patients where the chronic tonsillar infection source gives local and regional pathology: pharyngo-
laryngo-tracheo-bronchitis, rhino-sinusitis, ocular
INFECTION SOURCE (FOCUS) inflammatory nonsuppurative disease that involves several organa, limited, in
connection to Streptococcus ß hemolitic type A tonsillitis.
- Clinical: major signs: :Acute Articular Rheumatism. Rheumatism Carditis . Choreea minor (rheumatism)
SYDENHAM. Subcutanous nodules MEYNET. Marginal erithema LEYNER. Rheumatism Purpura.
Acute Glomerulonephritis
Minor signs: Fever, joint pain, tachicardia,. Streptococcus in pharynx. ASLO > 300 (Ac. Anti-
streptolisine O). VSH > 40mm/h. Fibrinogen > 400mg%. PCR present. DUCKETT-JONES Score = 2 major
signs OR 1 major and 2 minor
- Treatment: Penicillin deposit MOLDAMIN 1.200.000 UI/week, 4 weeks in a row, Tonsillectomy

SPECIFIC CHRONIC PHARYNGITIS

1.PHARYNX TUBERCULOSIS
1. Pharyngeal Lupus: Extension of nasal lupus. No pain. Produces important distruction slowly
Characteristic – 3 concomitant lesions: nodule-ulceration – skars
2. Milliar Tuberculosis: Acute Evolution. In sepsis with bacillus KOCH. Milliar image on pulmonary X-ray
Odinophagia, fever, diseminated yellow nodules on congestive fond,
3. Ulcerative-cazeous Tuberculosis :
Infection of pharynx mucosa from the lungs. Extreme pharynx pain. Very difficult alimentation
Extended Ulcerations on grey fond and pale mucosa
4. Latent Tuberculosis: In children. Tonsil Hypertrophy, pale mucosa, cervical lymphnodes. IDR positive
5. Coled Abscess - bone Tuberculosis of the vertebra body (morbus POTT).
Prominent in pharynx and gives obstructive but not inflammatory signs (cold).
Cold Abscess (morbus POTT): CT in axial view, with contrast – bulging of posterior wall of
pharynx and bone destruction of vertebra body

2. PHARYNX SYPHILIS
1. Primary: Ulceration of tonsils, hard rims, well delimited . Subangulomandibular LN
2. Secondary: Corresponds to Treponema pallidum sepsis. 30 days from primary lesion
Lymphatic, diffuse hypertrophy, white plaques on congestive fond
3. Tertiary: Goma. Profound organic affliction. Pseudotumoral – ulcerates and leaves a deep crater
Goma of veil => communication between the oral cavity and rhinopharynx
- Important sequelae: abnormal communication, veil suture to the posterior wall, cvasi-total stenosis of pharynx.

3. PHARYNX CANDIDOSIS Candida albicans has low aggressivity . Patients with immune deficiency .
Favored by long term AB. White spots on congestive fond.
Areas of erythema, brown-black tongue. Oral /pharyngeal discomfort
Bad taste in mouth. Nistatin (Stamicin) + Borax Glicerine topic
Ketoconazol (Nizoral), Diflucan p.o.

Extended lingual Candidosis accompanied by herpes stomato-gingivitis (picture)

 Pharyngology: complications of tonsillitis (5)
COMPLICATIONS OF ACUTE TONSILLITIS
1.ABSCESS OF TONSIL FOSSA Peritonsillar abscess – suppuration of lax cellular tissue around the tonsil
-Most frequent complication of a bacterial tonsillitis. Anterior or posterior
- Clinical: After 2-3 days of evolution of an acute bacterial tonsillitis
Unilateral odinophagia with violent reflex otalgia. Trismus
Fever, poor general state. Tonsillar Voice
Fixed head, slightly flexed to allow saliva flow. Fetid breath
Large subangulomandibular LN. BF: difficult. Bulging of pillar and protrusion of tonsil
-Treatment:
*Puncture – incision of abscess with a thick needle and the LUBET-BARBON forceps- to take out puss
Maneuver repeated daily . AB massive (Penicillin + Gentamicin + Metronidazol). AINS
Disinfectant locally . Liquid feeding. Tonsillectomy 4 weeks after

2. LUDWIG TONSILLITIS (DIFUSE ABSCESS OF THE MOUTH FLOOR): Infiltration with puss, wood consistency of mouth
floor. Diffuse hypertoxic Celullitis. Gas Gangrene. Severe general state

3. RETROPHARYNGEAL ADENOFLEGMONA: New born and child < 3 years. During adenoiditis - disphagia,
breathing problems, nasal obstruction. Bulging of posterior pharyngeal wall with classic Celsus signs present
- Evolution towards spontaneous opening in 7-8 days with flooding of puss into airway => aspirative
bronchopneumonia
-treatment: Incision with scalpel wrapped in tape. Child in ROSE positions and lifted immediately feet up + AB.
Adenoidectomy in 4 weeks

4. LATEROCERVICAL ADENOFLEGMONA: Suppuration of jugulocarotid LN. Infection from tonsillitis.. Abscess

between the great vessels and nerves and SCM
- Simptoms: Laterocervical pain and immobilizing on the afflicted side and rotation towards contralateral side
(torticolis). Severe general state, fever. Painful tumefaction, laterocervical
- Complications: Erosion of large vessels. Trombophlebitis of IJV. Mediastinitis
- Treatment: Surgical opening and draining after diagnostic puncture. AB, AINS

5. LATEROPHARYNGEAL CELULOFLEGMONA Suppuration of cellular tissue from the vascular fossa of the neck,
between the large vessels and pharynx wall.
-Infection from pharynx via lesions of mucosa
-odinophagia, disphagia, altered voice, fever, altered general state
-Bulging of lateral wall of pharynx + external tumefaction
-Opening via pharynx, rarely external approach
- AB for G- and anaerob bacteria

6. SEPSIS: Rare but severe in tonsillitis. Septic fever, severe frisson, pale, HSM, hemocultures positive. Pulmonary,
hepatic, cerebral Abscess
-treatment: Massive AB with sensitivity test from hemoculture. Heparin . Rarely ligature (tie) of IJV
 Pharyngology: tumors (6)
Benigne tumors of pharynx
1.NASOPHARYNX FIBROMA: Almost exclusively in teenage boys. Unknown cause.
-Smooth, pinkish pale, hard, on the rim of the choanae
- HP: angiofibroma with blood vessels without muscle wall
- Grows and expends to neighboring cavities: NF, rhinopharynx, sinus, orbita, zygomatic and pterigo-maxilar fossa,
endocranial
- Simptoms: Chronic nasal obstruction, initially unilateral. Frequent Epistaxis, abundant, with secondary anemia
Transmission Hipoacusis. Cheek deformation, exophtalmia, headache
- Dg: RA+RP, endoscopy, Rx, CT, Angiography (selective arteriography of ECA by SELDINGER catheter and

embolisation). Biopsy strongly NOT indicated !! Nazopharynx fibroma – endoscopy, MRI, Angiography pre and
post-embolisation
- Evolution 5-6 years. Death by anemia or endocranial invasion. If patient reaches sexual maturity, tumor stops
from growth.
- Treatment exclusively surgical with pharynx approach for small ones and lateronasal for large ones.
30-40% recidive rate

2. CHOANAL POLIP – dangles in rhinopharynx. No bleeding. Surgical treatment

3. PAPILOMA : Small white, pink tumors, berry-shaped. Dangle from the uvula and veil. Extirpation with cautery of
scissors

4. HEMANGIOMA Congenital Tumors. Berry-shaped, violee tumors on the mucosa.

Partial Obstruction of pharynx by large tumor
Cautery, sclerotic injection, laser, radiofrequency
Large ones are laborious and prone to accidents and sequelae

5. RANULA

a.Uvula Papiloma (top picture)

b. Pleomorf Adenoms on veil (down)

a.Nasopharynx cyst (left pic)

b. Left choanal Polyp (right pic)
 Maligne tumors of pharynx
RHINOPHARYNX: More frequent after 40. Epithelioma 60%, sarcoama 40%.
- Most frequently from the ROSENMÜLLER fossa.
- Evolution towards the pterigo-maxilar space, anterior foramen lacerum, endocranium
- Forms of onset:
1.Rhinologic: nasal obstruction, rhinorrhea muco-pio-sanguinolent
2. Otologic: catarrhal otitis media
3. Neurologic: neuralgia of nv. V, oculomotor paralisis
4.Lymphnodes: high adenopathy
5. Oftalmologic: amaurosis
- Clinical: RP shows tumor. Palpation of lymphnodes, one or multiple, uni or bilateral, hard, fixed.
Extension to all cranial nerve unilateral – sd. GARCIN
- Paraclinical: Biopsy, CT. Ex neuro, oftalmo
- Treatment: Mostly radiotherapy (Cobalt therapy, Brachitherapy, Curie therapy)
Chemotherapy (Cisplatin, Bleomicine, Methotrexat)
Surgical has reduced indication
-Survival 40-50% after 5 years

1. TONSIL EPITHELIOMA: Ulceration of a hard tonsil, infiltration

- Slow onset, unilateral pharynx discomfort, odinophagia, fetid breath
- Unilateral adenopathy
- Extension to neighbourring structures
- Extirpation of tumor and lymphnodes + Radiotherapy
- Healing 40%

2. TONSIL SARCOMA Increase in volume uni or bilateral, without hardness of carcinoma, followed by ulceration
-Adenopathy more frequent than carcinoma, frequently bilateral
-Evolution typical for lymphoma with extension to local LN groups, sub-diaphragmatic groups and lymphatic
generalization.
- dig.Fine-needle biopsy
-Treatment – radiotherapy

3. CANCER OF VEIL – ulceration on infiltrated fond. Rxtherapy

4. KAPOSI SARCOMA – see manifestation of AIDS in ENT.

5. TONGUE CANCER

6. LIP CARCINOMA AND SARCOMA

HYPOPHARYNX Almost exclusively carcinoma with predilection for the pyriform fold
-Rarely on posterior wall or lingual face of the epiglottis
-Sensation of discomfort /FB upon deglutition
- Fetid breath, odinophagia, sialorrhea, adenopathy
- Disfonia by extension to larynx
- LI: saliva stasis, infiltro-vegetant tumor of the pharynx wall
- Pharyngo-laryngectomy, radical neck dissection, Rx therapy, Chemotherapy. 40% after 5 years survival rate
 Oseopathology(1)

Anatomy of oesophagus
Tubular, membranous organ extended from the edge of cricoid to cardiac sphincter (T11 level)

From superior incisors – OE opening at 15 cm

- cardiac sphincter at 41 cm.
Approx. 26 cm
- 3 sphincters: upper, broncho-aortic, lower (cardiac)
1. Cervical rapport: thyroid, recurrent nerves, trachea
2.Thoracic rapport: bronchi, pulmonary hilum, mediastinal pleura, aorta, heart, peritoneum
3.Vascularization – segmented as is lymphatic drainage
- Innervation – IX, X, Cervical Sympathetic
-Function – taking the bolus to stomach in one peristaltic wave.

Malformations
CONGENITAL STENOSIS : Dysphagia, cough, vomiting
-Dg: Rx, endoscopic. Dilatations + excision of stenotic tissue (LASER)

TRACHEO-OESOPHAGEAL FISTULA Congenital Communication OE – T. With or without atresia OE or T

-dg. Rx with contrast, oesophagoscopy, bronchoscopy. Treatment: Surgery

HIATAL HERNIA Cardiac sphincter and stomach fundus into thorax via oesophageal hiatus
Mobile – 80% of cases have no symptoms. Fixed para-oesofageal – 50% no symptoms
-signs: Pressure, retrosternal burn, dysphagia, vomiting, GER
- dg :Rx with contrast (in TRENDELENBURG position). Oeso-gastroscopy. Gastropexy (transabdominal)

FB of Oesophagus : Frequent accident especially in children < 3 ani. Cause: Bolus, bones, coins, toys
-Contributory Factors:
*Children – lack of supervision, talking, cough, laughter
*Adults – tachiphagia, inebriation, poor dentition, prosthesis
*Lumenum modifications, diskinesis, stenosis, tumors
*Most frequently in natural sphincters
*Spasm leads to stippling, oedema and si ulceration =>perforation => mediastinitis
- signs: Dysphagia, regurgitation, sialorrhoea
Retrosternal pain – not alarming
Interscapular pain, fever – means perforation – ALARMING
- treatment: Extraction via natural ways or external approach (oesophagotomy, thoracotomy)

Oesophagus Trauma
Bases- deep lesions. Acids –superficial lesions
-Classification *Grd.I – erythema and oedema * Grd.II – erythema, oedema, blisters
*Grd.III – ulcerations *Grd.IV – ulcerations and necrosis
- Evolution:
1. First phase– shock and first symptoms . Congestion, oedem, necrosis. 1-2 weeks
2. Second phase– healing, conjunctive tissue appears, without elastic fibers. Becomes scar in in 3-4 weeks
3. Third phase – false healing, the scarring starts to tighten the lumenum
4. Fourth phase – stenosis + esophagitis above the stenosis via bolus stasis
 * Acute phase: violent and shocking pain in mouth, pharynx, retrosternal, epigastric. Sialorrhoea. hTA,
tachicardia –signs of shock. Intense thirst . Dysphagia. Vomiting with mucosa moulding. Gastric
perforation, mediastinitis, OE-T fistula, eso-bronchic fistula, oeso-pleural fistula, Superior digestive hemorrhage
* Subacute phase:
Latency, the patient improves. Pain progressively subsides. At 2 weeks resumes feeding
*Chronic phase:
Stenosis – dysphagia, sialorrhoe, regurgitation. At 4 weeks dysphagia for solid food. Than for liquids.
Cachexia, dehydrated. Dg – anamnesis, Rx, Endoscopy
Treatment: Deshocking
Neutralizing the caustic agent – water and vinegar/lemon juice for bases
- milk, magnesia usta, albumin water (8 egg whites for 1 l water) for acids
AB, Cortisone
I.V. feeding / NG Tube
Oesophageal stricture dilatation
Oesophagoplasty using the large curvature of stomach (method GAVRILIU) or colon.

Oesophagus Inflammations
ULCERATIVE ESOPHAGITIS: Postmedication – doxycicline, tetracycline, clindamicine, aspirine

GER (reflux): Insufficient cardiac sphincter with mucosa erosion . Retrosternal burn, tension sensation
Accentuated by alcohol, fatty food, smoking. Hemorrhage rarely
- Treatment with antiacids, diet, surgery

Oesophagus Motility Problems

OESOPHAGEAL IDIOPATHIC SPASM Dysphagia, retrosternal pressure, prolonged deglutition. Affliction of
autonomous innervation. Eating in small quantities. Spasmolythic (butilscopolamonium)

ACHALASIS (CARDIOSPASM): Lack of relaxation of lower oesophagus during deglutition. Degeneration of

AUERBACH plexus, hormonal factors, psychic trauma. Food stasis in lower oesophagus, fetid breath, vomiting,
cachexia. Dilatation of lower oesophagus. Extramucous Cardiomiotomy HELLER
-Becomes malignant in 4% after 15-20 years of evolution

Oesophagus Tumors
BENIGNE: Intramural, intraluminal, perioesophageal
-Leiomioma, rabdomioma, fibroma, hemangioma, lipoma, papilloma
-When small – no simptoms. Dysphagia, stenosis, pain, hemorrhage
- Endoscopic ablation, transcervical, transthoracic, transabdominal

MALIGNE: 40% of digestive tract tumors. Non differentiated Carcinoma most frequently
- Sometimes from neighbouring organs – larynx, trachea, thyroid, bronchi, stomach
-Insidious symptoms. Dysphagia, retrosternal fullness, weight loss, vagus irritation (hiccup), cough,
hoarseness, recurrent paralysis, loss of appetite
- Excision en-bloc of lower 1/3 or ½ of oesophagus
-dg By-pass with endoprosthesis or gastrostomy – palliative. Rx-therapy and CHT palliative
- Low survival rate – 10% at 5 years with surgery - 0-5% without
 Salivary glands pathology(1)
Annexes of the oral cavity. Main glands – parotid, submandibulary, sublingual, Accesory
- Histologic Unit –salivary acini (epithelial secretory cells that open in the lumenum)
- Channels -> intralobulary -> interlobulary -> main duct
- Parotid –serous secretion. Submandibularely / Sublingual – sero-mucous
1000 – 1500 ml / 24h

Methods of investigation
* Clinical: shape, consistency, volume, pain, modification of secretion, dysphagia, trismus
*Rx – sialography, tomodensitometry, ultrasound
*Scintigraphy with Tc99
*Endoscopy
*Microbiological exam
*Citodiagnosis of saliva or via puncture
*Biopsia

Secretion modifications
HIPOSIALIA: Transient in emotional states, fever, diabetes . Persistent - drugs (Plegomazin, Levomepromazina)
Post-irradiation

SIALORRHEA: Causes: buco-pharingeal, oesophageal, gastric, intestinal, hepatic. Facial Neuralgia, cerebral tumors,
high doses of Cortisone

Inflammation of salivary glands

1.ACUTE SUPPURATED PAROTIDITIS: - Catharal: Dryness of mouth, retro-mandibulary and maseterine
tumefaction, pain, pushing of ear lobe upwards. Dough consistency, painful. STENON duct congested.
Opalescent saliva.
- Gangrenous: rare. May destroy the facial nerve
- Suppurated: Altered general state, intense, pulsatile pain, irradiates in
neighbouring regions. Edematous diffuse Tumefaction. Congested Tegument. Trismus. Congested STENON
duct, tumefied, opened. Pressure on gland will expose puss. Reversible facial Paralisis
-Treatment:
Sialogoga – stimulation of secretion. AB. Incision for abscess

2. EPIDEMIC PAROTIDITIS: Paramyxovirus that provokes local epidemic. Incubation 10 – 20 days. Immunity for life
(usually). Signs: Tumefaction of parotid, hyperemia of STENON, nonpurulent saliva. Pavilion pushed outwards
75% bilateral. Virus neurotropic – may destroy nv.VIII and generate HNS
-treatment: AINS, pain medication, liquid food, Ig antiurlian

3. NONSPECIFIC CHRONIC PAROTIDITIS :Enlarged gland, congestive ostium, opened, murky saliva, fibrine plugs and
puss. Normal Tegument. Dryness of mouth, parotid pain (moderate). Oral hygiene. Stimulation of
secretion. Treatment: AB and HHC endocanaliculary

4. SPECIFIC CHRONIC PAROTIDITIS

TUBERCULOSIS –purulent saliva, cazeum in Stenon duct
SYPHILIS
ACTINOMICOSIS – limited and painful tumefaction, puss with yellow granulations
SALIVARY LITHIASIS: Most frequently submaxillary. Calcium carbonate and phosphate stones. Usually in
WHARTON duct. Signs: Salivary Colic during meals, pain, tumefaction, waves of saliva. Bidigital Palpation – stone
dg. Extirpation – endoscopic or by dissecting the channel
Sialosis-Alteration of gland parenchyma + enlargement or, less frequently, atrophy of gland + secretion problems.
1. SJÖGREN’S SYNDROME: Triple simptomatology – salivare, ocular, articular. More frequent in women > 40-50
years
-autoimmune reaction determines atrophy of parenchyma, Xerostomia – dryness of upper airways mucosa
- Tumefaction of parotid bilaterally . Atrophy of glands in severe cases
-Dry Keratoconjunctivitis, chronic arthropaty, rheumatoid purpura, periarthritis nodoasa, sclerodermy
- Artificial tears, artificial saliva
-Stimulation of saliva secretion – pilocarpine chlorhidrate
- Immunosuppresion and Cortisone high dose

2. MIKULICZ DISEASE: Simetrical Hypertrophy of salivary and lacrimal glands with decrease or dissappearence of
secretion. Dryness of mouth and conjunctiva The Sd. MIKULICZ associates LN.
-treatment: Cortisone in moderate dosis over long periods

3. SARCOIDOSIS: Nodular skin lesions , on veil, tonsils, pharynx. Bone, LN, pulmonary lesions
-Bilateral tumefaction, not painful of parotid, submandibular glands
- Decreased salivary Secretion
- Cortisone Treatment

Benign salivary tumors : 80% parotid, 10% submaxillary, 10% rest

1. PLEOMORPHIC ADENOMA: Mixed Tumor – epithelial and mesenchima
-Initially small nodules, well delimited, elastic, mobile. Gradually increases and deforms the area
- More frequent in women
- dgSialography – image of “ball squeezed in hand”. Scintigraphy with Tc99 – mute area
-Evolves slowly. Malign transformation – sudden acceleration of growth, irregular surface and consistency, facial
paralysis, pain, LN, altered general state
- Treatment only surgical – Parotidectomy with preservation of facial nerve / Submaxillectomy

2. CYST-ADENOLYMPHOMA (WARTHIN TUMOR): Localization on inferior pole of parotid

- More frequent in men > 40
- Simptoms similar to previous
- Subtotal Parotidectomy with preservation of facial nerve
- Does not recidivate

Malign salivary tumors ¼ of salivary tumors

Signs of malignancy: Rapid growth or in surges. Pain . Hard infiltration. Adherent to deep layers.
LN Metastasis. Facial Paralisis

1. ADENOID CYST CARCINOMA: Most frequent. Originates in the channels and ducts
-Early pain. Infiltrating the skin.
- Early Paralisis.
- Metastasis – lung, bone, skin, brain
- Total Parotidectomy without preserving the facial nerve + Rx-therapy

2. ADENOCARCINOMA: More frequent in parotid.

- Less aggressive type – predominant neuro-secretory. Aggressive type – predominant muco-epidermoid
- Characteristic – LN
- Total Parotidectomy without preserving the facial nerve + radical neck dissestion + Rx-therapy + CHT

3. EPIDERMOID CARCINOMA / NONDIF. CARCINOM: Increased malign potential.

- Especially in elderly patients
- Radical surgery + radical neck dissection + Rx-therapy + CHT
 Tracheo-bronchology: anatomy-physiology (1)
Trachea
Continuation of larynx from which picks up many afflictions. Attached to the cricoid cartilage
- In adults 10-13 cm. from 16-20 cartilage rings (horse-shoe shaped)
-Posteriorly - membranous and in contact to oesophagus
-The tracheal spur at the level of C6 vertebra, the origin of the 2 primitive bronchias
- The main right Bronchia 17° angle to the vertical; 35° angle on the left
- Cartilage rings become complete at the level of the bronchi and in bronchioles disappears completely

Vascularisation: Superior and inferior thyroid arteries

The tracheal spur and the bronchi – bronchial artery from the aorta
Lymphatic - cervical nodes connected to thoracic nodes
Innervation – nv. X and cervical Sympathetic chain

Physiology :Mucociliary apparatus moves towards the larynx to eliminate secretions.

Warming, humidifying and purifying inspired air (starting in the nose)
In the trachea air is at 36°C regardless of ambient (around\surround)
Temperature is decreased in case of oral breathing
Humidity of air is 99%

Tracheo-bronchology: malformations (2)

Megatrachea, Megabronchi, Congenital Stenosis, Congenital Bronchiectasis

KARTAGENER’S – bronchiectasis, sinusitis with or without polyposis, situs inversus

Produces: irritative cough, large quantity of sputum, Hippocratic fingers (clubbed fingers)

Foreign bodies: Severe Accident, especially in children.

-Organic FB – dangerous since they increase their size in moisture (beans, rice), decompose in irritative oils (nuts,
peanuts, seeds) or irritate mucosa mechanically (bone, teeth, corn)

Inorganic FB – better tolerated (nails, screws, toys)

- Pathogenesis: Aspiration most frequently. Calcification of residual sputum => bronchial stones
Cazeum secretion in TB. Ascaris
Aspiration during eating, playing, loughter, coughing, sneezing.
-More frequently in the right bronchia at the trachea spur. Sometimes they end up in the main bronchia.
- Symptoms:
* Severe : Agitated, dyspnoe accentuated by inhaling or cough. Cyanosis of cephalic extremities
Rapid death by asphyxia (cant breath) or syncope (fainting)
* Moderately severe cases – acute phase of 30 min
- clinical exam:
Asymmetry of thoracic movements. Pulmonary rhonchi
Respiratory silence or diminishing of Vesicular Murmur of the afflicted lobe
Rx for opaque FB (foreign body), atelectasis of a lobe, pulmonary emphysema (collapse alveoli), signs of
pneumonia (old FB)
HOLZNECHT Sign– mediastinum shifts to the side of a bronchial stenosis during inhaling
- Dg:
Anamnesis, description of accident. Clinical . Rx + Bronchoscopy
- Dg.dif: Dyphteria, TB(tuberculosis), pneumonia. Laryngeal Spasm. Convulsive cough. Tumors , laryngeal
stenosis
- Treatment – tracheobronchoscopy with extraction
 Trauma of Trachea and Bronchi
Increasingly frequent: driving accidents, sports, aggression
-Simptoms: Dyspnoe, suffocation sensation
Lesions of large vessels
Vicinity ((=close to the area)) infections
Hemoptysis, subcutaneous emphysema
Pneumothorax, atelectasis (lung collapse)
- Dg: Anamnesis, auscultation, RX, CT, Bronchoscopy
- Treatment: Tracheotomy emergency. Suture of wound. Recalibration of lumenum.
Lobectomy for ruptured bronchia

Tracheo-bronchology: stenosis tumors (3)

ACUTE STENOSIS (narrow) : Inspiratory Stridor, irritating cough. Cyanosis, lack of air sensation
- Dg: rigid bronchoscopy with therapeutic role
- Dg. dif: laryngeal stenosis, aspirated FB (foreign body) , pulmonary embolus, pulmonary oedema, asthma
- Treatment: bronchoscopy, AB, AINS (NSAID nonsteroidal anti-inflammatories) , HHC, Tracheotomy

CHRONIC STENOSIS : Permanent Dyspnoe, accentuates periodically during acute infections

Causes: prolonged intubation, incorrect tracheotomy, intratracheal tumors, bronchial tumors,
tracheomalacia ( soft trachea), nonspecific infections, pulmonary radiotherapy
- Treatment: resection and reconstruction of trachea

BENIGNE & MALIGNE Adenoma, fibroma, chondroma (cranial) , lipoma, amyloid tumors, neurinoma,
hemangioma, papyloma, pleomorphic (parotid gland tumor) adenoma
-signs:Cough seizures, dyspnoe ( shortness of breath) aggravated gradually
-Haemoptisis (coughing up of blood.)
- Treatment –tumor ablation, endoscopic or external approach

MALIGNE

Histology - squamous cell carcinoma (SCC, 45%), adenoid cystic carcinoma (ACC, 16%), carcinoma not specified or
undifferentiated (12%), small cell carcinoma (10%), adenocarcinoma (6%), large cell carcinoma (4%) and sarcoma
(4%)