ENT course: 1.

Otology- Anatomy & Physiology

exam will beon pathology:diagnosis, symptoms and signs , treatment..

External ear:
contents: Pavilion – elastic cartilage. Concha. Extern acoustic canal (EAC) – Acoustic meatus. Helix and Antehelix. Fossa
triangularis. Tragus and antitragus. Lobulus – no cartilage
External acoustic canal – EAC : Approx. 2,5 cm. Italic “S” shaped . Cartilage external ½.. Bone internal ½. Adherent
tegument . Hair follicles and hair in the external ½ Vascularisation & Inervation of the Pavilion: Arterial – superficial
temporal artery, posterior auricular artery
Limfatic – preauricular, retroauricular and subauricular lymphnodes
Inervation – superficial cervical plexus (S), auriculo-temporal nerve (V), sensitive branch of the Facial nerve
Vascularisation & Inervation of the EAC: same arterial, lymphatic & innervation except : it has brach of the Vagus nerve
(X)

Middle Ear (ME)

contents: Tympanic cavity. Epitympanic Recess.
Eustachian Tube. Mastoid Process
TYMPANIC CAVITY –biconcave lens with 6 walls
-External – Tympanic Membrane (TM) and
attical wall
- Internal – oval window (OW), round window (RO), promontory
-Superior – bone, Medial Cerebral Fossa and temporal lobe
-Inferior – Internal Jugular Vein golf
- Anterior – Eustachian Tube, Temporo-mandibular joint,Carotic Canal
- Posterior –Mastoid process (additus ad antrum)
TYMPANIC membrane: Almost horizontal in new-borns
45° to vertical in adults.. Conical concave inwards
Umbo – the point of maximal concavity. The Gerlach Ligament. The timpano-mallear ligaments ant. and post.
- Superior, Pars flacida = Membrane of SCHRAPNELL, 1/5xS
- Inferior, Pars tensa 4/5xS
Light triangle POLITZER
*more structures of ME Malleus. Incus. Stapes. Chorda timpani nerve
The EUSTACHIAN TUBE : Bone & cartilage united by an istmus,
Opens through contraction of the external peristafiline muscle (deglutition muscle)
Mastoid process Mastoid cells should be pneumatized and layed with mucosa
Mastoid Antrum

Internal Ear (IE) Dug into the temporal bone

-The bony labyrinth Contains perilymph
BONY LABYRINTH Vestibule – formed by Utricula & Sacula, Semicircular canals,
Cochlea
Membranous labyrinth (vesicles and canals) Contains endolymph
COCHLEA: 2 ½ rotations around the Modiolus
Modiolus contains the ROSENTHAL canal and the CORTI spiral ganglion
Scala vestibularis from RW to Helicotrema
Scala timpani from Helicotrema to RW
Helicotrema. Lamina spiralis. Spiral ligament. Basilar membrane
REISSNER membrane. Organ of CORTI . Tectorial membrane

Central acoustic segment: CORTI ganglion (N1) – primary acoustic nuclei.

Intern Acoustic Meatus . Pontocerebellar Angle.Brainstem – secondary acoustic
nuclei (N2).
Superios olivary nucleus, lateral lemniscus, corpus geniculatum mediale
Girus temporalis transversus – area of HESCHL
Vestibulum: Utricule > Saccule. Macula – area of sensory cells.
Macula of Utricle - anterior & inferior.
Macula of Saccule – on the internal wall.
 Receive information on body position and linear movements
Bony semicircular canals – Anterior (ASC), Posterior (PSC), Horizontal (HSC): Contain the membranous canals
Anteriorly –dilated portion – Ampulla. ASC and PSC have a common opening and are at 90° from each-other
HSC is at 30° to the horizontal line.
Membranous semicircular canals: Crista ampullaris. Ampullary Cupula –gelatinous substance that covers the Crista
ampullaris. Receives information on rotational movement.
Central vestibular segment: SCARPA Ganglion from the IAC. Brainstem– 4 vestibular nuclei: external, internal, inferior,
superior. Conexiuni afferent and efferent connexions toȘ. Cerebellum. Oculomotor Nuclei. Dorsal motor nucleus of
vagus. Anterior cornus medularis
Acoustic Function: Mechanical wave with longitudinal propagation (pure tone). Frequency, Amplitude, . Timbre
Acoustic field – 16-20.000 Hz and 1-120 dB. Air Conduction. Bone Conduction. The Eustachian Tube mentains equal
pressure between the ME and the EAC. Air-liquid transmission only 1% of energy – loss of 50dB
Energy recovery mechanisms: Surface difference from TM to RW (100 mm² to 4,5 mm²), lever of the ossicular chain and
phase difference OW-RW

Vestibular Function: Mentains balance. One vestibule provides more impuls – Hipervalent It usually generates a lack of
balance. Utricle – movements forward-backward and up-down, lie down on back or front (dorsal or ventral decubitus).
Saculle – movements lateral, lie down on one side (lateral decubitus).
Semicircular canals – rotation movements

Peripheral vestibular syndrome Central vestibular syndrome

Inner ear or vestibular nerve pathology Brainstem or central nervous system pathology.

Vertigo – ample, rotational, appears as acute, repetitive crisis with Vertigo – less ample, often permanent. Absent or diminished
neurovegetative symptoms (nausea, vomiting). No vertigo between the crisis. neurovegetative symptoms.

Balance disorders – diminished Balance disorders – important

Nystagmus – horizontal or torsional, unidirectional, fatigable if the patient Nystagmus – purely vertical or torsional, uni or bidirectional,
gazes in the direction of the nystagmus. Often associated with tinnitus or permanent (not fatigable). No tinnitus or hypoacusis.
hypoacusis.

Segment or body deviations – harmonic – deviations and falls always to the opposite Segment or body deviations– disharmonic – deviations and falls to the
side of the nystagmus – closing eyes accentuates balance disorders. – often same side of the nystagmus– closing eyes does not accentuate balance
associated with sensori-neural hypoacusis. disorders.
– often associated with neuro-logical signs.

Hipoacusis: Diminished acoustic function. Total loss of hearing– COFOSIS

Clasification: Transmission – affliction of Air Conduction. Sensorineural – affliction of Bone Conduction. Mixed
Mild 15-30 dB. Medium 30-50 dB. Severe 50-70 dB. Profound > 70 dB
Tinnitus: Clasificare\Subjective\ Objective – vascular sounds (bruits), muscular contractions
Otalgia :Otodinia. Reflex otalgia: molars, pharynx, larynx, tonsills, cervical spine, TMJ, parotid gland
Otorrhea: Otolicvorrhea – cerebrospinal liquid (skull base trauma). Serous. Mucous. Muco-Purulent. Purulen.
Sanguinolent
Peripheral vertigo In a vestibular syndrome, one vestibule generates more impulses than the other.
* The nystagmus (rapid movement) is oriented towards the vestibule that generates more impulses.
*Segment and body deviations will be towards the vestibule that generates fewer impulses.
*Each semicircular canal will generate nystagmus in its own plane: Horizontal canal – horizontal nystagmus
Anterior canal – vertical nystagmus. Posterior canal – torsional (diagonal) nystagmus
- Irritative peripheral vestibular syndrome – nystagmus to the afflicted ear, segment and body deviations to the normal
ear.
-Destructive peripheral vestibular syndrome – nystagmus to the normal ear, segment and body deviations to the afflicted
ear.
 2. Otology- malformations
MALFORMATIONS : *Abnormal development of the 1st and 2nd branchial arches
*Pavilion: protruding ears, microtia, macrotia, anotia, congenital fistulae (coloboma auris), acquired malformations
(sportsmen)
1
*EAC: membrane or bone atresia, stenosis 2
.
*ME: malformations, absent or fixed ossicular chain .

1.Microtia left ear, 3rd degree dysplasia of pavilion and EAC atresia

2. Supranumerary tragus (accessory ear) in a 10 year old& adult

3. Malformation of pavilion asociated to EAC atresia 3

4. Total lack of pavilion and EAC agenesis (prosthesis 4

5.treacher-Collins-Franceschetti Syndrome (Dwarf syndrome)
Mother – bird face and epicantus. Daughter – epicantus and microtia
*Exostosis EAC: Especially by exposure to cold water (divers, swimmers)

EXTERNAL EAR TRAUMA

*Pavilion lacerations : surgical treatment, AB (Pseudomonas aeruginosa). Tetanos shot
5
Torn laceration of pavilion after dog bite. (9 year old) and post-op view 6

6. Othematoma :Serous-sanguinolent colection between cartilage and perichondrium

-Hemisferic, ferm, very sensitive. It gets infected or organized.
Puncture-incision and compressive dressing
7. Pavilion pericondritis Permanent deformity of pavilion by thickening of peri-chondrium. Repetitive trauma
7
(sportsmen – rugby, fighting, boxing, judo), othematoma, piercings. Colliflower ear. For acute pericondritis –
antibiotics and incision.
*Pavilion burns: Compressive dressing in the EAC to prevent stenosis
*Frostbite : Spontaneous amputation
*Fractures, Burns, Escoriation of EAC

ME trauma:
1. Tympanic membrane rupture: Acute and immediate pain. Hypoacusis. Tinnitus, vertigo. Bleading or blood clot
in EAC and perforation. Sterile dressing, no instilations!! Tympanoplasty. AB, NSAI
2. Dislocating or fracture of ossicular chain: Incus luxation nicovalei or fracture of stapes crura. Hypoacusis at the
moment of the accident. Surgical treatament – Tympanoplasty
3. Hemotympanum: Blood collection in the tympanic cavity. AB for protection. Spontaneous resorption
4. Barotrauma: Aviators, divers
5. Otalgia, hypoacusis, vertigo
6. Congestion or rupture of TM with intense, hyperemiated vascular network
7. Rest, sedatives, antivertigo medication

INTERNAL ear trauma:

1.Labirynth concussion. In: Cranial trauma, blast, loud noise, barotrauma. Discrete Sensorineural hypoacusis (SNH),
tinnitus. Signs: Vertigo, imbalance dominate the symptoms. Treatment: Rest, sedatives, antivertigo medication.
Disapears in days
2. sound trauma: One time exposure over 120 dB repeatedly over 90dB. SNH, Tinnitus. Audiogrametry – typical
notch at 4000Hz. Progressive and irretrievable. Treatment: Hearing aid
3. Fracture of the temporale bone: Otalgia, bleeding from EAC, otolicvorrhea, facial paralisis VII. Transsmision
Hypoacusis. SNH; vestibular periferal syndrome (destructive). Cranial and cerebral lesions. Treatment: AB,
Cortisone, Simptom treatment, Surgical Treatment
4. Trauma: *Fracture line perpendicular to the temporal bone (through IEC and facial canal)
* Longitudinal fracture line through the temporal bone (through ME, mastoid, tegmen tympani, TM, EAC, mastoid
part of the facial canal)
5. Foreign bodies: Exogenous\Endogenous (cerumen, epidermic)
*Biologic: inert (rise grain, corn, garlic clove etc.) or animated (butterflies, worms, ants etc.)
*Artificial (caps, marbles, toys etc.)
*treatment: Auricular douche, Water stream towards the posterior wall of the EAC

Inflammation of External ear :

1. EAC carbuncle (boil): Inflamation of the hair follicle by Staphilococcus aureus. Signs:Intense otalgia accentuated by
jaw movement, chewing. Hypoacusis. Lymphnodes inflammation. Swelling with central necrosis. Treatment: AB –
Oxacillin 2g/zi, NSAI, local anti-inflammatory and antiseptic. Incision
2.Diffuse otitis externa: Otalgia, serous-purulent otorrhea, lymphnodes sweeling. Signs:Congestion and stenosis of
EAC,Fever, Hypoacusis. Treatment: Daily EAC suction. Anti-inflammatory in the EAC (on mesh).AB, NSAI
3. External ear eczema : Alergic, Dermatologic treatment
-Acute - Pruritus, congestion of tegument, white or yellowish scabs (crust)
-chronic – dry tegument, desquamation, pruritus
4. Otomicosis: Fungal infection of EAC (vegetal parasites) – Aspergillus niger, fumigatus, flavus, Actinomices, Candida
signs:Pruritus, otalgia, auricular fullness, odorless otorrhea, hypoacusis. Diagnosis: Fungal build-up moulded on the
EAC and TM, similar to wet card-board or wet blotting paper. Treatment: Daily suction. Antifungal localy:
Clotrimazolum, Ketoconazolum. Boracic alcohol

3. Otology- ME (middle ear) inflammations

I. OTITIS MEDIA: Inflammation of the ME

Classification: Serous – no infection \ Suppurative –infection \ Acute \ Chronic

Acute Otitis Media (Causes, Pathophysiology, signs and symptoms, treatment and
complications) - YouTube

1.ACUTE SEROUS OTITIS MEDIA : Mostly children. Causes: rinitis, adenoiditis, pharyngitis
*Mechanism: Inflamation of nasal mucosa, rhinopharynx, tonsills => Inflamation and obstruction of Eustachian
tube => The air within the ME is resorbed => negative pressure => exsudative liquid & Tympanic retraction. The ME
mucoasa turns into secretory epithelium.
*Simptoms: Discrete otalgia. Hypoacusis and ear fullness. Autophonia. Sensation of liquid moving inside the
ear. Sometimes mild vertigo. Simptoms of the initial respiratory virus infection: serous rhinorrhea, nasal
obstruction, general malaise
*Diagnosis: Otoscopy. Tympanum congestion, dilated blood vessels on the handle of the
malleus. Liquid level or air bubbles in the liquid. Hypoacusis modiffies during deglutition,
sneezing, nose blowing. Image of acute otitis media, bulging left TM, intensely hiperemic, no
anatomical landmarks. Small perforation in the postero-inferior quadrant with serous liquid
exteriorization.
-Right TM slightly hiperemic, bulging, with dilated vessels around the malleus handle.
No anatomical landmarks
*Positive diagnosis: Clinical and otoscopy. Transmission Hypoacusis in Weber and Rinne
test. Audiogramm. Tympanometry
*Evolution: spontaneous healing in 10-21 days. Can get infected or chronic
*Profilaxis: Curing the rhino-pharyngial causes (adenoidectomy, nasal septum resection, polipectomy).
*Tympanogram. Pressure wave (between +200 şi – 200 daPa) in EAC. Difference between emitted and
reflected energy – impedance. A measure of reactance
- Type A –normal Eustachian function. Equal pressure on 0.
- Type B – flat graphic representation. Massive limitation of
TM movement (liquid in ME, adhesive process, perforation).
- Type C – the graphic peaks in the area of negative pressure
(shifted to the left) – Eustachian disfunction and very low pressure within ME.
* Treatment: Restoring Eustachian permeability (treating the cause) . Nasal Vasoconstriction medication:
Olynth, Rinogut, Vybrocil. Sputum fluidifiant: ACC200, ACC600, Fluimucil. AINS. Valsalva Maneuver, Toynbee
Maneuver, Politzer Maneuver, Otovent balloon

2.CHRONIC SEROUS OTITIS MEDIA: Also known as: otita sero-mucous, mucotympanum, serotympanum, glue-ear
Succedes the acute otitis media by persistence of causes: (adenoids, chronic rinitis, allergic rinitis, chronic sinusitis,
septum deviation, rhinopharynx tumors). Most frequent cause –chronic adenoiditis
* Simptoms: Hypoacusis and autophonia Translucid TM, slightly aspirated, with serous liquid and air bubbles
-Tipically TM Retraction with horizontal malleus handle. Yellowish TM, ground-glass opacity, “oil soaked paper”

*Evolution: Years or decades. Involvement of IE and SNH.

The TM will adhere to the internal wall of the ME (fibro-adhesive otitis).
Retraction pouches of the TM => cholesteatoma
In case of infection => suppurative otitis media
*Positive Diagnosis: Clinical exam. Audiometry. Tympanogramm
* differntial diag.: ME Malformations. Otosclerosis.
Otitis or trauma sequelae . Early signs of rhinopharynx cancer
* Treatment: Removal of obstructive causes. Evacuation of viscous exudate from UM. Tubal
insufflations. Transtimpanal Injections with HHC, Fluidifiers. Diablo type transtimpanal drainage

3. ACUTE SUPPURATIVE OTITIS MEDIA: Warm Abscess of the ME. Produced by pyogenic cocci.
Infection through the Eustachian tube. Sings: Acute inflammation with puss.
Oedema of the mucoasa, ulceration of the mucosa (partial). Puss build-up (under pressure) within the ME.Necrosis
and perforation of TM and even bone.
*Simptoms:
1. Preperforation phase: Pulsating otalgia. Hypoacusis. Autophonia. Fever. Lack of appetite. General
malaise. Intense congestion of the TM. Puss bulging. Sensitive mastoid process. Tinnitus and mild vertigo
*Diagnosis: Audiometry. Mastoid Rx or CTscan – fogging of mastoid cells. Leucocitosis. After 3-4 days –
spontaneous perforation
2. erforation phase Otalgia diminishes spectacularly. Fever diminishes. Hypoacusis accentuates. Purulent
otorrhea. Oedema of the TM, covered in pulsating puss. Spontaneous healing after 3 weeks. Otorrhea
disappears, perforation closes. Can get complicated or chronic – extremely violent germs, small perforation or too
high (non-efficient drainage), weak patient, incorrect treatment. Large perforations to not close.
*Treatment: AB – Augmentin, Claritromicină, Eritromicină. NSAI. Nasal Vasoconstriction. Mucolitics.
Miringotomia . EAC suction. Instilation of AB, antiseptic

4. ACUTE SUPPURATIVE OTITIS MEDIA OF THE NEW-BORN: Special reactivity to infection. Short and wide Eustachian
tube. Horizontal alimentation. Prematurity. Distrofia. Insufficient treatment of upper airway infection.
manifest: agitated, febrile, lack of appetite
latent: up to 8 months. Draws no attention on the ear. First signs – neurotoxic syndrome, cachexia, infectious
syndrome. Slightly modified TM – infection in the attica and antrum, no contact to TM.
* Treatment: Manifest – identical to adult. Latent – surgery (Antrotomy)

5. OTITIS MEDIA IN INFECTIOUS DISEASES

1.FLU (INFLUENZA): Acompagnies and complicates the flu. Fever, malaise, muscle pain, ocular pain, epistaxis.
Otalgia. Mild Hypoacusis . sero-sanguinolent otorrhea. IE affliction – vertigo, SNH. Violet blisters on the TM
and EAC tegument. sero-sanguinolent or normal secretion in ME
*Treatment: NSAI, anti-influenza. AB for protection
2.SCARLET FEVER: ß hemolitic Streptococcus. frequently serious, necrosis and distruction of
ossicular chain.
3. MEASLES:Common germs combined with weak immunity. Simptom treatment
4.DIFTERIA: Rare, propagated from the pharynx. False membranes.
5. TUBERCULOSIS: Bacteria in the Sputum. Multiple TM perforations (sieve). Bone lesions of
the ME. Can cause tearing of the Internal Carotid Artery (ICA) in the bone canal.
6. ZOSTER OTICUS: Afecting the geniculated ganglion of the facial nerve through the varicella
virus (chicken pox). Otalgia. Vesicles in the EAC and concha. Facial Paralisis. Sometimes
involvement of nv. VIII – SNH, vestibular syndrome. Treatment: Cortisone. Antiviral medication: Aciclovir (Zovirax),
Famciclovir, Brivudin. Vitamines NSAI, Antivertigo, sterile dressing, protection AB
7. Mezotimpanitis, tubary otorrhea. Childhood debut. Chronic suppuration of ME. Tubary Mecanism – each
nasal or pharyngeal acute episode generates acute otitis. Usually chronic serous otitis media infected for the same
reasons din aceleaşi cauze (adenoiditis, malformation, septum deviation)

6. CHRONIC SIMPLE SUPPURATIVE OTITIS MEDIA

* Simptoms: Hypoacusis accentuated by age. Otorrhea - mucous/muco-purulent. Central TM perforation.
Congestive ME mucosa during acute episodes. Audiometry –Transmission hypoacusis turns to SNH. Mastoid Rx
or CT scan – diminishing or disappearance of cell pneumatization
* Evolution: Life long, periodic calm and acutization through rinitis, pharyngitis, water in EAC.
* Profilaxis: childhood treatment of infection (adenoiditis) and chronic serous otitis media.
* Treatment: Daily suction. Rezection of polips in ME.
Instilation of AB (Ciplox) and Cortisone, borium acid
Treatment of tubary disfunction: insuflation, Valsalva, nasel dezobtruant, mucolitics
Sistemic AB. Antialergy, Corticoid nasal spray. Prevention of water in EAC
Hearing aid – BAHA
Surgery: Adenoidectomy, septum resection, sinus surgery\ Timpanoplasty with/without antro-
mastoidectomy

7. CHRONIC SUPPURATIVE OTITIS MEDIA WITH CHOLESTEATOMA: Epitimpanitis, purulent otorrhea

**Skin pouch inside the ME – cholesteatoma
* Mecanisms: Epithelial ectodermic embrionary inclusions in the ME (primitive cholesteatoma)
Penetration of EAC epidermis in ME through TM perforation
Intussusception of superior portion of TM into ME by pressure decrease
-Adenoiditis => chronic serous otitis media => retraction pouch of TM through low pressure => increase of pouch
size by accumulating epithelium from EAC => Infection of content => erosion of surrounding bone => complications
-Portions of the matrix become ulcerated and granulations of connective tissue appear => polyps
* Simptoms: Discrete, insidious, from childhood. Discrete hypoacusis. Reduced fetid or sanguinolent
otorrhea. Superior, marginal perforation with puss flowing through it. Whitish lamellas, redish-violet polyps.
* Paraclinical: Audiometry (Transmission hypoacusis). Rx or CTscan – erosion of bony walls of ME and
reduced pneumatization of mastoid cells. “ring and seal”. Antimicrobial susceptibility testing (AST)
* Evolution : Long-term. Alternating periods of acute and chronic
Internal ear affliction by intoxication with bacterial toxins. Vicinity complications
Low tendency of spontaneous healing.
* Profilaxis: Treatment of adenoiditis, tubary disfunction, serous chronic otitis media
* Treatment: Exclusively surgical – radical mastoidectomy and tympanoplasty. Daily suction. Instilation of AB,
local disinfectant Sistemic AB during acute periods.
 4. Otology- complications of otitis
COMPLICATIONS OF OTITIS
Mastoid: Acuteand chronic mastoiditis. Bone: Osteomielitis of the temporal bone. Facial nerve: paralisis.
Labirinth: Labirintitis. Endocranial: extradural, cerebral, cerebellum abscess, otogenic meningitis. Venous: sigmoid
sinus thrombosis. Betzold abscess

1.ACUTE MASTOIDITIS Suppurative inflammation of the mastoid during an acute otitis media. 1
Always involves the bone. Most frequent complication of otitis media.
.
* Contributories: Small or high perforation of TM. Aggressive germs. Immunodeficiencies
Ineffective treatment
* Ulcerations of the mucosa and periosteum of the mastoid cells => suppurative osteitis
=> Distruction of bone septum between cells => Mastoid abscess which opens spontaneously
* Simptoms: approx. 3 weeks old Acute otitis media. Pulsating mastoid pain. Abundent Otorrhea.
-Painful mastoid upon palpation, paste-like consistency, tegument hiperemia.
-Retroauricular incision not visible. Pavilion pushed forward. Purulent, pulsating Otorrhea
* diagnosis: Audiogramm: Transmission HypoacusisRx or CTscan – fogging of mastoid cells and lack of inter-cell
septum. CT/RMN
* differntial diagnosis: EAC boil. Difuse otitis externa (the retroauricular incision is still visible). Tumors
* Treatment: Surgery – radical mastoidectomy. Wide spectrum AB. NSIA. Nasal decongestive, Mucolitics,
suction in the EAC

2.CHRONIC MASTOIDITIS: Complication of chronic suppurative otitis media cornice or cholesteatoma with retention
of puss collection inside the cells. Treatment – surgery for cholesteatoma

3.OSTEOMIELITIS OF TEMPORAL BONE: Rare but serious. Severe general state, sepsis. Tumefaction of temporal
bone scuama. Treatment: Surgical – removal of focal infection. Massive AB. Gets complicated frequently with
meningitis – reserved prognosis

4. FACIAL PARALISIS: Complication of otitis media via:

2
- Inflamation of facial nerve with oedema of the nerve in an inextensible canal.
- Exposing the nerve and compression through cholesteatoma. .
*Clinical: Unilateral flaccid paralisis, facial asymmetry.
Deviation of oral commissure to the healthy side. Disappearing wrinckles.
Voluntary movement impossible. Imposibility of eye closure. Deficit in mastication.
*Treatment: Correct treatment of otitis. Emergency surgery of cholesteatoma
- Surgical repair of nerve, neuro-anastomosis facial-hypoglosus, to contralateral facial
- Gold plates in upper eyelid

5.EXTRADURAL ABSCESS :Colection of puss between bone and dura mater.

Frequent complication, early for complications that surpass the dura.
*Clinical: Hemicrania crisis with orbital irradiation. Fever . Meningeal irritation syndrome (neck stiffness, back
pain, difuse headache, hypertensive CSF). Intracranial Hypertension Syndrome IHC
* Positive Dg: CT or intraop.
* differential diag.: Difuse septic meningitis. Cerebral abscess
* Treatment: Exclusivelly surgical – radical mastoidectomy

6.OTOGENIC MENINGITIS: Usually difuse. Generated by cholesteatoma or Acute suppurative otitis media.
* Simptoms: Intense headache, persistent, backpain, altered general state, somnolence. Fever 39-40°C,
photofobia, neck stiffness. Muscle contracture. Miosis, visual impairment, exaggeration of reflexes .
Arythmical HR and breathing.
* Brudzinski’s sign – positive. The triad – headache, vomiting, constipation.
* Evolution – serious, towards exitus through various paralisis and finally brain-stem paralisis.
* Diagnosis: Signs of meningitis in an otitis patient. Lumbar puncture is mandatory – hypertonic CSF, purulent.
Albuminorahia with positive Pandy test. WBC whole or destroyed in the CSF. CT – inflammatory aspect – epiduritis
* Treatment
1. Extreme emergency – massive AB that penetrates the hematoencephalic barrier (Cloramfenicol, 3rd
generation Cephalosporine). If possible – bacterial sencitivity test of CSF
2. Lumbar puncture to evacuate (decrease of hypertonia of CSF)
3. Surgery of otitis
4. Otogenic Destructive Labirintitis right ear
5. Perforation of tegmen tympani
6. Cerebral abscess with massive cerebral oedema masiv (12 year old)

7.CEREBRAL AND CEREBELLUM ABSCESSSuppurative process of the cerebral tissue generated by otitis, almost always
cholesteatoma.
* Simptoms: Debut – easily mistaken with an usual viral infection – headache, mild fever, some behaviour
changes. Latency – few simptoms, 2-3 weeks. Status – BERGMANN triad: ICH syndrome, Infectious syndrome,
neurological syndromes.
* Short evolution, subarahnoid or ventricular drainage => coma, death.
* Positive Dg.: Cholesteatoma with neurological signs or unexplicable infectious syndrome. Ophtalmo and
Neuro exam. CT / MRI
* Treatment – neurosurgery. Otologist drains the infection from middle ear.

8.LATERAL SINUS PHLEBITIS: Usually with acute cholesteatoma.

* Clinical: Sudden debut, sepsis appearance. Fever 40°C with sepsis, massive frisson, tahicardia, earthy facies,
white tongue deposits, oliguria, hepatosplenomegalia (HSM) leucocitosis, anemia, positive hemocultures.
- Posterior rim of the mastoidei, laterocervical, retromandibulary pain.
* Treatment: Opening of the lateral sinus and suction or removal of the thrombus. Internal Jugular Vein (IJV)
ligature beneath the thrombus. Massive AB

9.SEQUELAE OF OTITIS
SIMPLE SEQUELAE: Postotitic Perforation. Interruption of ossicular chain => Transmission hypoacusis (HAT)
- Treatment – miringoplasty or tympanoplasty.

TIMPANOSCLEROSIS: Calcium Impregnation of ME mucosa and blocking of ossicular chain. Follows chronic
suppurative otitis => HAT. Treatment – surgery or hearing aid.

FIBROADHESIVE OTITIS: Permanent tubary obstruction, resorbtion of ME air, sclerosis and retraction of mucosa.
Pouches of viscous liquid. Mixed hypoacusis that evolves in time. Tinnitus. TM attached to the internal wall of
the middle ear, horizontal malleus. Treatment – surgical for early stages. Hearing aid.

5. Otology- inner ear- hearing aids

1.LABYRINTH SYNDROMES: Afflictions of the inner ear. Total – cochleea and vestibule. Disociated – one of the 2
* By cause: Irritative: tinnitus and peripheral vertigo (irritative type)
Destructive: peripheral cochlear SNH and peripheral vertigo (destructive type)
*For cochlea signs are not well defined.

2.NYSTAGMUS: Involuntary, rapid, saccadic eye movement.

- When present without head movement => pathological
- Nistagmus = Nistagmos (a moţăi)
- Head rotation => slow movement of eyes in opposite direction
(vestibular origin) => rapide recovery movement de ratrapaj
(central origin), in in the same direction as head rotation.
-Rapid movement is observable => defines the direction of nystagmus
-Stimulation of a semicircular canal=> Eye movement approx.
in the same plain as the canal

THE MEMBRENOUS :

- Physiological (optokinetic) – normal

 *Vestibular. Cerebellum / Brainstem. Upbeat. Downbeat.
Horizontal. Rotational

3.VERTIGO: A symptom defined by a false sensation of movement .

- Accompanied by nausea and vomiting, profuse sweating and balance disorder creating the vestibular syndrome.
- Commonly by affliction of inner ear. (Vertigo is not fear of hights)
- Dizziness is a feeling of unsteadiness, light-headedness, uneasiness or fatigue and does not imply movement.
- Acrophobia

4.BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV): Most common cause for vertigo.
- Dislocated otoconia inside the SC, most frequently PSC – mobilizes the endolymph without head movement.
- Vertigo exacerbated by certain positions or head movements.
- Dix-Hallpike Maneuver – vertigo without nystagmus is no base for diagnosis.
* Pharmacological: Antivertigo (Dimenhidrinat, Prometazina), antihistamine, vasodilating (Memotal, Pentoxifilin),
Cortisone, Sedatives (Diazepam, Lorazepam)
* Otoconia repositioning maneuvres. Vestibular rehabilitation exercises Brandt-Daroff. Surgical obliteration
of PSC. Usually remitted in 6 months without treatment. May reoccur
* PSC –rotational Nystagmus – Epley Maneuver. ASC – vertical Nystagmus – Deep Head Hanging Maneuver
OSC –horizontal Nystagmus – Lempert (BBQ) Maneuver
*Treatment: EPLEY MANEUVER, LEMPERT (BBQ) MANEUVER, DEEP HEAD HANGING MANEUVER

5.MENIERE’S SYNDROME: Endolymphatic hipertension (Endolymphatic hydrops) – unknown cause.

* Hypothesis: Excessive endolymph production. Low resorption . Altered glycoproteic metabolism.
Immunological affliction of inner ear – through viral infection, allergies, genetic factors, trauma
* Simptoms: Triad: vertigo, tinnitus, SNH . First crisis the most spectacular. Nausea, vomiting, profuse
sweating. Crisis minutes – hours – days – 3 weeks. Difficult to examine in crisis. Irritative vestibular syndrome
with ample nystagmus, horizontal-rotational to the afflicted ear.
-Early stage – SNH typical on low frequencies. Late stage – pantonal SNH. After crisis vertigo disappears,
tinnitus and SNH permanent but improved.
* Treatment: Bed rest, i.v. hidration. Peripheral Vasodilation – Redergin, Pentoxifilin. Psychostimulants and
neurotropic - Memotal . Cortisone . Sedation. changes in dieta: low sodium and caffein

6.VESTIBULAR NEURONITIS / LABYRINTHITIS: Acute, prolonged vestibular syndrome of peripheral origin

* Selective inflammation of nv. vestibularis, probably viral. Selective inflammation of superior part of the labyrinth
(utricle, ASC, OSC)
* Simptoms: Intense vertigo, over hours. Severe for several days, than decreasing over following weeks. Lack
of balance, loss of hearing
* Diagnosis: Anamnesis + exclusion of other causes of vertigo. ENG (Electronistagmography) and MRI rarely used
* Treatment: Vestibular Supresors (Meclizina) – no longer than 1 week in order to prevent inhibation of central
compensation . Sedatives – benzodiazepines. Cortisone i.v.. Neurotropic Vitamines - B1, B6

LUETIC LABYRINTHITIS: Late congenital or secondary sifilis / tertiary acquired. Accentuated hypoacusis, fluctuent.
Annoying tinnitus. Vestibulary syndrome with paroxysmal evolution, peripheral and central.

LABYRINTHITIS IN MENINGITIS: Germ propagation along the meningeal sheath of nv.VIII.

Severe signs of meningitis. Severe hearing sequelae, bilateral loss of hearing.

URLIAN LABYRINTHITIS (MUMPS) :Complication of epidemic parotiditis. Vascular propagation.

Only cochlear affliction in one ear. Permanent loss of hearing.

7.VESTIBULAR SCHWANNOMA: Benign tumor of nv. VIII – origin in the mielin sheath of the inferior vestibular nv.
Unilateral, progressive loss of hearing. Unilateral tinnitus. Vertigo especially for small tumors. Lack of balance more
common. Cerebellum symptoms. Nv. Trigeminus involved for large tumors – sensory affliction of face. Headache

8.SSC DEHISCENCE SYNDROME: A new mobile window is created – allows for transmission of sudden pressure change
Sound/pressure induced Vertigo and eye movement HAT and autophonia. Pulsaring Tinnitus, ear fullness.
Sudden falls (drop-attack). vertical-rotational nystagmus to the healthy ear. Surgical closure of SSC/ avoid triggers
9.VESTIBULAR MIGRAINE. PERILYMPHATIC FISTULA. VERTEBRO-BASILAR INSUFFICIENCY.
INFERIOARE CEREBELLUM ARTERY SYNDROME.

10.OTOTOXICOSIS: Labyrinth affliction via toxic substance.

*Endogenous: nephropathy, cirrhosis, diabetes \ Exogenous: industrial (benzene, Pb, As), ototoxic medication
(Genta, Kanamicina, Strepto, Neomicina, Quinine, Aspirine, N Protoxid, Cisplatinum, oral birth control medication).
* Simptoms: Bilateral tinnitus. Bilateral equal SNH. Large loss of acute frequencies. Vertigo and loss of
balance. Typical post-chemotherapy hypoacusis (Cisplatin). Initially (orange) and after treatment (red) with
typical loss of high frequencies.

11.SUDDEN HEARING LOSS: Unilateral SNH with no apparent cause. Usually vasculare or viral.
* Simptoms: Sudden onset. Vertgo rarely
* Treatment: Emergency admission . i.v. – Cortisone, vasodilatory, neurotropic vitamines, sedatives.
Sometimes surgery.

12.OTOSCLEROSIS: Distrophy of bone surrounding the IE (otic capsule). Hereditary disease. Ossification of elastic
ligament surrounding the stapes footplate.
* Simptoms: Onset 15-50 years, progressive hypoacusis. Tinnitus. Tympanogramm shows chain fixation
* Treatment: Surgical – stapedotomy with prosthesis. Hearing aids

13.PRESBIACUSIS: Age hearing loss. Lesions of the hair-cells in the organ of CORTI. After 65 years. The patient has
difficulty understanding, especially on high frequencies. Small lack of balance. SNH bilateral and equal.
* Treatment: Ear cleaning, profilaxis of atherosclerosis. Vasodilatory medication, vitamines. prosthesis

14.HEARING LOSS IN CHILDREN :High occurrence rate. psicho-social development impaired . Bilateral hypoacusis -
Incidence 1-3:1000 n.b.
* Causes: Genetic – congenital or late (over 400 mutations) \ Neonatal \ Postnatal \ Without screening – late
diagnosis – deaf-mute child.
* Screening for risk factors. over 48h ICU. Family history. cranio-facial malformation
* Universal Screening: first 2-3 days. Objectiv methods: acoustic otoemissions OAE
, brain-stem Evoked potentials BERA
* Subjectiv methods: Condition Audiogramm. Tympanogramm
*Treatment: Bilateral prosthesis in the early months. Cochlear implantation. Special schools

15.HEARING AIDS : *Indications for prosthesis:

-Hypoacusis between 30-90 dB, Mandatory bilateral, Healthy patient (psychiatric exam)
*No prosthesis: psychiatric patients. Unilateral hypoacusis. Suppurative ears. Cophosis . BAHA

6. Otology- inner ear- ear tumors

BENIGNE TUMORS OF THE EXTERNAL EAR

 Fairly rare – papiloama, fibroma, lipoma, condroma, keloids, angioma, exostosis, osteoma.

 Hypoacusis via obstruction of EAC

1
Diagnosis – clinical, HP, Dermato Exam

Treatment – surgery.

1.BENIGNE TUMORS OF THE EXTERNAL EAR

2. MALIGNE TUMORS OF EXTERNAL EAR
* Pavilion: Men > 70 ani. Basalioma (exclusively localy malignant) or 2. Carcinoma of EAC
squamous cell carcinoma (invading, metastasis) 2. Basalioma of
treatment: Surgery pavilion (chonca)
* EAC, Radiotherapy or resection of temporal bone – poor results - Severe by early invasion of
bone (before symptoms) - Otorrhea sero-pio-sanguinolent, HAT, Pain a b
- Metastatic lymph-node invasion (squamous cell)
a. Melanoma of pavilion (picture) b. Skin Metastasis laterocervical, contralateral
c. Tongue Metastasis

TUMORS OF THE ME

1.GLOMUS TUMOR OF THE JUGULARY VEIN

From chief cells of the paraganglia (glomus bodies) from the walls of the IJV
*Benigne, vasculare structure and arterio-venous shunts. Erodes the inferior c
*wall of the ME from underneath and breaks into the ME
*HAT and pulsating tinnitus (sincronized with the pulse)
*Penetrates the EAC via TM – red-pinkish polyp. Bleeds easily and severely.
*Evolves to the posterior foramen lacerum – compression on nv. IX,X,XI and endocranial
a.Right ME Glomus tumor. Tip of tumor visibile in postero-inf. Quadrant of TM (*) (picture)
b. CT Axial view of same tumor
c. Massive Glomus of left ME
d.Histological section through ME – occupied totally by glomic tumor (C – cochlea, S – stapes, T - tympanum)

a. aberrant path of Internal Carotid Artery, visible through right TM

(clinically just pulsating tinnitus).

b. CT axial – carotid canal opened paratubary and visible vascular

trajectory in the ME

*Glomus tumor of ME with massive Somatostatin capture on scintigraphy. Dif. diagnosis to other vascular tumors
of ME
*Paraganglioma –posterioar quadrants bulge via red-bluish tumor. Often pulsation can be observed.
*diagnosis: Biopsy. CT / selective arteriography with embolization of branches
* treatment: surgical – many complications\ Radiotherapy does not destroy it but stops the evolution for several
years.

2.RETICULOSIS: Tumors that evolve in the mastoid and exteriorise in the EAC. Mastoiditis symptoms
* Especially in children –eosinophilic granuloma of the ME (histiocytosis X).

3.HANS-SCHULLER-CHRISTIAN disease: mastoid granuloma, exophtalmia, diabetus mellitus by invasion of orbita and
pituitary gland (sella turcica).

4.ABT-LETERER-SIWE disease: maligne variant of reticulosis. diagnosis: Histological. CT for extensive lesions
-treatment: Surgical for localized tumors. Chemo-radiotherapy & Cortisone
5.CANCER OF THE ME: Rare. Following a Chronic Suppurative Otitis. Severe purulent Otorrhea that turns
sanguinolent. paralisys of nv. VII. Aboundent granulation inside the ME – ex.HP. Intolerable Otalgia
* Rapide and serious evolution by invasion of the endocranium
*Treatment similar to EAC cancer.

TUMORS OF THE INTERNAL EAR

1.ACOUSTIC NEURINOMA = VESTIBULAR SCHWANNOMA: Benigne

Tumor with maligne evolution due to compression of central nervous
system. One of most frequent benigne intracranial tumors. Developed
from the vestibular branch of nv. VIII.
1.Otologic phase: Development inside the IEC. HNS unilateraly,
slowly progressive . Vestibular syndrome, especially loss of balance
2. Oto-neurologic phase: Tumor breaks into the Pontocerebellar
angle and affects the nerves. First sign– affecting nv. V with corneal
and regional anaesthesia (oftalmic Va and maxilar Vb branches).
Paralisys VII, ICH syndrome –cerebellum sucked through the occipital
foramen and compression of brainstem
a. Axial MRI-massive vestibular schwannoma in the PCA (picture) b. 3.
Coronal MRI – schwannoma observable in the IEC

3. bilateral vestibular Schwannoma (both PCAs).

Typical aspect of type II neurofibromatosis
* diagnosis: CT with contrast . MRI.
Eye fundus exam for papillary stasis (in ICH). Lumbar puncture
* treatment: 1. Surgical (translabyrinth, retrolabyrinth,
supratemporal). 2. Large tumore – retrosigmoid,
occipital (neurosurgery approach)
3. retrosigmoid approach – intracranial, intradural
4.transtemporal approach – intracranial, extradural
5. Transmastoid approach – extracranial, extradural
 ENT course: 2. Rhinology- Anatomy & Physiology

Anatomy of NASAL PYRAMID:

-Proeminent in the middle of the face – bone, cartilage, fibrous tissue
-Bone skeleton – nasal bone + parts of maxillary bone
-Cartilaginous skeleton –triangular and alar
- Dorsum nasi
*Vascularisation: A.facial and its branches A.dorsum nasi (branch of oftalmic)
- angular vein => V.oftalmic => cavernous sinus
*Inervation: Sensitive – Va & Vb, Motory – VII, Nasal Vestible
-Most anterior part of nasal fossa (NF)
-Layed with epidermis with hairs and gld. Sebaceous
-Cartilaginous skeleton (alar). Limen nasi – the tightest part of the NF

NASAL FOSSA : Between Limen nasi and choane

-6 walls, external the most important. Contain a venous system with cavernous spaces (erectile type)
- Nasal turbinates – bony prominence covered by mucosa. turbinate – head, body, tail.
between turbinate and external wall – meatus. Meatus drains paranasal sinuses and tear ducts
*Inferior – tear ducts.
* Middle – anterior paranasal sinuses (frontal, 4-6 anterior ethmoid cells, maxillary)
*Superior – posterior paranasal sinuses (4-6 celule posterior etmoid cells, sphenoid)
* Medial wall – nasal septum of nasal fossa
*anteriorly -Cartilaginous part
* posteriorly -Bony part –(vomerus + perpendicular lamella of ethmoid bone).
-Covered by adherent mucosa

KISSELBACH’s vascular area – confluence of branches of the anterior ethmoid, posterior ethmoid,
descendant palatine and a.sphenopalatine –1,5 cm. from the entrance of the NF.
a. Important cartilaginous structures projected of the inferior wall of the nasal pyramid (base of nose)
b. Septal subluxation to the left with partial obstruction of the narina picture

* Inferior wall – palatine bone and maxillary spine.

* Superior wall – os frontalis and cribriform plate of the ethmoid (olfactory area)
* Anterior wall – dorsum nasi and narinas. Posterior wall –choanae (orifice)
Vascularisation: A.sfenopalatine from A.internal maxillary. A.anterior palatine from A.descendant palatine
 A.subcloazonal from A.facial. A. anterior and posterior ethmoidal from the internal carotid system
- Veins drain to the pterigoidal and cavernous plexi
Inervation: Sensitive – Va, Vb. Vegetative – gg.sphenopalatine. Sensory – I
Mucosa: Respiratory ciliated pseudostratified columnar epithelium with numerous glands, lymphatic system and
cavernous spaces
- Olfactory at the cribriform plate, septum and superior turbinate. BOWMANN’s glands secrete lipids and facilitate
olfaction.
- First neuron – SCHULTZE’s cells situated at this level

PARANASAL SINUSES Extensions of nasal cavities into neighbouring bones. Lined with respiratory
ciliated pseudostratified columnar epithelium. The Cilia move towards the drainage orifice.
Vascularisation: A.internal maxillary and A. facial from ICA
-A. anterior ethmoid and post. from ECA. V.oftalmic and V.facial, pterigoidian and faringian plexi

a+ b –anterior sinuses in occipito-mental view (chin-nose-film)- picture

c + d - anterior sinuses in occipito-frontala view (forehead-nose-film)

FUNCTIONS OF THE NOSE:

*Respiratory Function: Physiological breathing only through nose
-6 l/min in rest conditions, 50-70 l/min during effort
- Laminar flow and turbulent flow
-Air suffers 3 modifictions: warming, humidification, purification.
*Nasal cycle: Alternate oedema of nasal mucosa in 2-4 hours cycles.
imagine – oedema of right NF mucosa, especially the INT and MNT
and reduction of left NF oedema
*Olfaction: Weak in humans. Tight connection to taste. Important for
certain jobs: cook, eonologist, perfumer, doctor.
Perceives volatile substances soluble in water and fat. Out of cca. 30000 smells, humans perceive 10000 and
differentiate 200
*Protection function: Temperature and humidity, pH adjustment. lysozyme, protease, interferons – nonspecific
defence . Ig A, M, G –specific defence . Reflex function – connection with lungs, heart, genitals. Phonatory
function – forming certain consonants and timbre of voice

NASAL OBSTRUCTION SYNDROME :

* Clinical: Difficulties in nasal breathing. Oral breathing. Hyposmia, anosmia. Closed Rhinolalia (nasal voice).
* Ethiology: affliction of NF or rhinopharynx

NASAL SECRETORY SYNDROME: Nasal secretion is usually seromucous and low quantity.
* Pathologically – rhinorrhea. CSF – rhinolicvorrhea. Serous – acute / allergic. Mucous – chronic rhinitis
Mucopurulent – acute/chronic sinusitis. Sangvinolent – trauma, tumors. Crusty – atrophic rinitis / ozena

NASAL SENSITIVE SYNDROME Pain projected in the afflicted sinus area. For posterior sinuses in the skull base, retro-
orbitary, occipital. Hyperestesia – inflammation. Hypoestesia – atrophic rhinitis

NASAL SENSORY SYNDROME: Hyposmia or Anosmia – nasal or neurologic. Hyperosmia – rarely sign of disease
(medulo – suprarenal tumors). Parosmia – perceives modified or inexistent smells (pregnancy, epilepsy, histeria)
Caccosmia – perceives a bad smell – subjective or objective.

NASAL VASCULAR SYNDROME: Hyperemia of mucosa – inflammation . Anemia of mucosa – local vasoconstriction
Epistaxis – hemorrhage of NF
*Anatomicaly: Anterior – most frequent from vascular area of Kisselbach. Posterior – a.sfenopalatine or a.post
ethmoid. Difuse – hemorrhage from numerous small vessels
* Ethiology: idiopathic juvenile (vascular fragility - constitutional)
* Local: lesions (nose picking), inflamation acute or chronic (rhinitis, sinusitis), Trauma – nasal and facial, including
thermic or chemical, Nasal foreign bodies (FB), nasal, sinus or rhinopharynx tumors, Exposure to substances
and powders (coccaine).
* General: infection (flu, childhood diseases, typhoid), vascular and Circulatory disease (HTA, arteriosclerosis, heart
disease), blood disease (thrombocytopenic purpura, leukemia, Glanzman disease, von Willebrandt disease),
Coagulopathies (hemophilia, Waldenström disease, fibrine deficiency, vitamine K deficiency, anticoagulant
overdose), Vasopathies (Henoch-Schönlein purpura, Möller-Barlow disease), Chronic hepatic and renal
disease, Intoxications, Endocrine disease (pregnancy – vicarial epistaxis, feocromocitoma), Teleangiectasis
Rendu-Osler

TREATMENT OF EPISTAXIS:
Diagnostics: Anamnesis. Ex.clinical (localisation). Blood Pressure values, Coagulogramm. Internal disease exam.
Xray / CT nose, sinuses, skull base
*Scopus: Stop bleeding. Hemorrhagic Shock treatment. Treatment of cause
* General measures: 1. Calm the patient; patient sited and slightly leaning forward. If this is not possible, the
patient should lay down on his side,
2. Instruct patient not to swallow blood (danger of vomiting and aspiration) but spit it into a kidney tray,
3. Measure BP, HR, Blood work (CBC, Coagulation), 4. BP medication (if necessary),
5. Immediately stop any anticoagulant treatment, 6. i.v. access and hidro-electrolitical balancing,
7. Hemostatic (Adrenostazin®, Etamsilat®, Fitomenadion®),
8. Interdisciplinary consults (Cardiology, Internal Medicine). 9. Clean out the nasal fossa (nose blowing or suction),
10.Apply local vasoconstriction and anesthesia (instillation or nasal gauze stripes),
11.Chemical cautery (AgNO3), electrocautery, criocautery,
12. Anterior nasal packing (gauze stripes, tampons, hemostatic balloon),
13. Bellocq posterior nasal packing (if necessary),
14.As last resort – surgical hemostasis (arterial ligatures, embolization,
Attention! - Nasal packing is always associated with protection antibiotics.

*Special measures: Surgical hemostasis: ligature of ECA, a. internal maxillary a.sfenopalatine, a.ethmoid
Endoscopic ligatures. Embolisation. For hereditary teleangiectasis RENDU-ÖSLER – laser therapy or SAUNDERS
dermoplasty at the septum (free skin graft form the supraclavicle region)

2. Rhinology- malforamtions
NASAL MALFORMATIONS: Face formed by 9 embryological buds => increased frequency of malformation

FACE AND NASAL CLEFT: Oblique – rare. Transversal – from mouth commisure to tragus => Macrostomia.
Medial – hipertelorism, bulldog nose, proboscis, double nose

FISTULAE, CYSTS : Open at the dorsum nasi, glabela, ethmoid region. Bad smelling secretions. Sometimes in the
vestible

DERMOID CYSTS: Contain ectodermic inclusions (tegument cells, hair). From Dorsum nasi to the frontal region

GLIOAMAS: Benigne tumors, solid, developed from birth. Entire length of the nose

MENINGOCELE AND MENINGOENCEPHALOCELE: Hernia of dura and endocranial content through dehiscence of the
cribriform plate into the NF
*Dg: clinical, CT, Arteriography treatment: Removal, closure of dura, osteoplasty

ATRESIA AND STENOSIS OF CHOANA: Congenital or aquired. Surgical treatment. Bilateral – diagnosed
immediately after birth – severe simptoms (acute respiratory insufficiency and cyanosis at birth). May be bony or
membranous
* Simptoms: Imposibility or difficulty of nose breathing. Chronic purulent secretions. Posterior endoscopic
rhinoscopy – stenosis of the left choana atresia of the right
 * Diagnosis: Anterioar and posterior Rhinoscopy. Endoscopy – basic exam. Xray or CT with contrast
* Treatment – surgical

RINOSCOPIA

AQUIRED MALFORMATIONS
- Causes : prolonged nasal obstruction, Trauma, destructive disease (sifillis, TB, cancer, leprosy)
- Deviated nasal septum – almost 90%
- Pathological only when obstruction or poor oxygenation
- Surgical treatment

TRAUMA OF THE NOSE AND SINUSES: Extremely frequent. Closed or opened. The most frequent – maxillary sinus
* Anatomo-pathological types: Luxation of septal cartilage. Fracture (closed of opened). septal Hematoma.
Trauma by orbita compression
* Simptoms: Pain, shock, neurological signs. Epistaxis. Echimosis of eyelids, subcutaneous emphysema.
Deformation, displacement of pyramid and zygoma. Bone crepitus, abnormal bone movement. Nasal Obstruction.
Rinolicvorrhea
* Diagnosis: Clinical. Rx, CT. Ex. Neuro, Oftalmo, Maxillo-Facial
* Treatment: Shock treatment . Manual or instrument repositioning of bones. Contention (internal and
external). Fractured nasal pyramid – nose deviated from median line and oedema of soft tissue.. Xray of fracture
Repositioning of deviated pyramid ( manualy from the outside). Delved pyramid repositioned from the inside
(endonasal) with an elevation instrument

SEPTAL HEMATOMA: After nasal trauma with septum fracture of postoperatively. Bilateral bulging with NF
obstruction. Gets infected => abscess
* Treatment – bilateral incission on different levels and drainage + AB
* Complications – septal perforation, thrombosis of the cavernous sinus
* Simetrical septal Hematoma after septal fracture with intact mucosa and submucosa hemorrhage.
* Septal Abscess – mucoasa with bilateral oedema, hyperemia and exteriorisation of puss
* treatment: reconstruction of nasal wing with cartilage from the pavilion. reconstruction of nasal wing with
cartilage from the pavilion – intraoperative.
-Reconstruction with frontal graft (vascularisation maintained from a. Supraciliar or a. supratrochlearis)
a. Mobilisation of neighbouring tegument and used for lining the NF.
b. frontal graft lowered and detached. It requires cartilage support and composite grafting.
c. frontal defect closed per primam
-Reconstruction with miocutaneous graft from pectoralis major. Very useful for face and neck are. The graft contains
tegument, subcutaneous tissue, fat, part of muscle. It is dissected and repositioned, keeping vascularisation from the
toracoacromial artery

- Reconstruction with scalp graft (Converse graft) – vascularisation from the superficial temporal artery. Its
dimensions favorise total reconstruction of nasal pyramid. To ensure the shape of the pyramid, it should have
support material (rib or pavilion cartilage)

SINUS, MALAR, ORBITA TRAUMA : Multidisciplinary surgery. Osteosinthesis with Tantal wire or plaque

Classification of LeFort: LeFort I – isolated fracture of maxilla on the alveolar line. LeFort II – pyramid fracture of
entire maxilla. LeFort III – detachment of entire facial block from skull base

fractures of frontal basis - Escher classification

Escher I – high
Escher II – medial
Escher III – deep
Escher IV – lateroorbital

a.monocle Hematoma in facial block fracture

b. facial asymmetry by depression of right zygoma

a.

a.facial lateral fracture with displacement

b. blow-out fracture with hernia of orbita through the bony wall – „tear drop” look
c. blow-out fracture (coronal view)

*Left lateral facial fracture with displacement of fronto-zygomatic suture + fracture of orbita floor.
* postoperatively (fixation with plates and screws)
*Osteosinthesis (picture) of left infraorbitary arch with plates and screwes. Orbita content maintained cranially with
the retractor.

a.Fracture of anterior and posterior wall of frontal sinus

b.Displacement fracture of posterior wall of sfenoid sinus
c.Pneumoencefalus d. Fracture of floor of the ethmoid sinus

rhinolicvoria- liquid from cerebral fluid drip from nose

FOREIGN BODIES: Exogenous or endogenous (rhinoliths:stones of calcium). Nasal Obstruction (unilateral)

Rhinorrhe muco-purulent, fetid (smell bad)
*Treatment: Extraction with special forceps or hooks.
 3. Rhinology- Rhintitis
INFECTION OF NASAL EPIDERMIS

NASAL ECZEMA (SEBORRHEIC DERMATITIS) : Superficial inflammation of epidermis. Vesicles and pustules on
hyperemic skin, than crusts and painful lesions . Itching, desquamation, burning sensation of the nose and
vestibule. Atopic background and exaggerated secretion. Treatment of lesions, Cortisone
Ag Nitrate 5% on lesions VESTIBULE FOLICULITIS (SYCOSIS)

VESTIBULE FOLICULITIS (SYCOSIS) :Staphilococcicus infection of hair follicle, usually for facial hair. CARBUNCUL OF NASAL
Also present in the nasal vestibule. pain, burning, itching, congestion of nose lobule and crusts. VESTIBULE (BOIL): (SYCOSIS)
Treatment – local, AB ointment, vaccine anti-Staph.

CARBUNCUL OF NASAL VESTIBULE (BOIL): Staph. Infection of the hair follicle. Weak Organisms: Diabetes, liver,
immuno-supressed, tired. Tumefied nose, congested, sensitiv to touch. Tumefaction of superior lip, chick, eyelid,
nasal wing :Inside the vestibule – red proeminence with a hair in the middle. Necrotic and full of puss.. painful.
Generaly does not heal until puss is evacuated. Treatment –local AB or general, vaccine anti-Staph. rare but severe
complications after (after squeezing). nasal boil antibiotic treatment.

a.boil of nasal wing and local hyperemia (LEFT PIC: NO EYE IN)
b. boil of left vestibule with local oedema and lower eyelid oedema via angular vein.

TROMBOFLEBITIS / TROMBOSIS OF CAVERNOUS SINUS: Propagation of infection to sinus via angular and orbital
veins. Signs of orbital stasis: palpebral tumefaction, chemozis, exoftalmia, immobility of eyeball, amaurosis.
Cerebral stasis, Cerebral oedema, coma, death. Treatment: Massive systemic AB , Heparine, Antiinflamatory .Alcohol
isolated Erysipela of nose
or ice packs on boil
(butterfly shaped)

ERYSIPELAS: strepto/staphylococcal Infection of upper dermis with short incubation period (hours-days). Fever.
Malaise. Well defined, congested areas on the pyramid. Butterfly shaped. Dg: simptoms + bacteriology.
treatment: High dose AB (Penicillin, antistaph.) 8-10 days. Erysipelas of face – extended facial oedema and
hyperemia. Gateway – scratch on dorsum nasi.

RINOPHYMA: Pseudotumor of the skin over the cartilage. Elderly patients, at times huge, prevents breathing and
eating. Hipertrofic acne on a pinkish background. Treatment – Excision by sliceing followed by spontaneous
epithelisation.

RHINITIS (INFLAMATION OF NASAL MUCOSA)

ACUTĂ COMMON RINITHIS (COMMON COLD): epidemic, viral (rinovirus) +/- infection with the usual flora of NF
(bacteria). Incubation 2-3 days, short immunity. dif. diag. :Other viruses: mixo, adeno, corona, syncytial
respiratory virus SRV, CFV (chimpanzee flu virus), ASP (African swain pest), some enteroviruses. Favorized by cold,
wet, sudden change of temperature, pollution, decrease of immunity.

ACUTE RHINITIS
1.Prodromal phase: Feverishness, fatigue, torpor, lack of appetite, head-ache, muscle pain. In children high fever,
dryness of nose, throat. Anterior rhinoscopy (AR) – pale, dry mucosa.
2. Cataral phase: Serous Rhinorrhea, nasal obstruction, anosmia, closed rhinolalia, tearing, malaise. AR –
intensely congested mucosa, oedema, profuse secretion . becomes mucous within days.
3. Mucous phase: Simptoms become milder. Mucous secretion. Nasal Obstruction gradually subsides. Recoverry of
smell. Bactarial Infection produces muco-purulent rhinorrhea.
Dg. Dif – allergic rhinitis, vasomotory, acute specific rhinitis. Complications – sinusitis, otitis, tracheobronchitis.
Treatment simptomatic – antithermic medication, antiinflammatory, nasal sprays, inhalation, rest. AB only for
bacterial infection. Increase immunity: sport, avoid smoking, vit.C, vit.A, hygienic measures during epidemics.

COMMON RHINITIS
Simptoms as above with dramatic evolution. Newborns adapt with difficulty to mouth breathing. Nasal Obstruction
prevents child from eating.. Swallowing muco-purulent secretions generates GI tract infections. . Fever,
agitated, torpor, loud breathing with pauses during sleep. Rich muco-purulent Rhinorrhea with nasal erosions.
Complications – adenoiditis, acute otitis, larynx spasm, bronchitis, broncho-pneumonia. Treatment adaptated to
age.

ACUTE STAPHYLOCOCCAL RHINITIS IN NEW-BORNS: Ethiology: staph infection from the mother’s nipple lesions or
mastitis. 3-4 days after birth. Mucopurulent abundent rhinorrhea. Dries up on the upper lip – yellow crusts
similar to lemon or egg yolk. Malaise. Pulmonary complications. Treatment: AB generală and local. Rhinitis
MENINGOCOCCAL, STREPTOCOCCAL

GONOCOCCAL RHINITIS: Mucosa infected during labor. Asociated to gonococcal conjunctivitis. 2-3 days from
birth. Nasal obstruction, muco- purulent greenish rhinorrhea, ulceration of mucosa, swelling of upper lip. Dg –
bacteriological exam from nasal and vaginal secretions, OG exam. AB general and local. Cleaning the lesions.
Profilactic instillation of Protargol or Ag Nitrate after birth.

SYPHILIS: Manifestation of early congenital syphilis. Within 6 weeks. Persistent muco-purulent or sanguinolent
rhinorrhea. Fetid secretions. Deep lesions on upper lip and narina. Pemfigus on hands and feet, skin or mouth
lesions, HepatoSplenoMegalia.. Late Manifestation (after 3 years) – late congenital syphilis.

HUTCHINSON’S Triad: interstitial keratitis, sawteeth, HNS. Dg. – history of disease, serologic testing (Nelson).
Treatment early – infectious disease specialist or venerologist.

DYFTERIC RHINITIS: More frequently between 2-6 years but also possible over 6 months. persistent
serosanguinolent or purulent rhinorrhea, crusts and lesions in the vestibule, submandibular lymphnodes. Pale child,
apathetic, feverish, tahicardic. AR – white-grey membrans in the NF + pharynx. Treatment: AB + serotherapy

MEASLES RHINITIS: Older children. oculo-rhino-pharynx inflammation, mucous rhinorrhea (becomes purulent by
infection with bacteria). Nasal Obstruction. Oral Enantema (Köplick‘s sign). Characteristic Exantema. Facies
“crying”. Repeated epistaxis and acute otitis media.

SCARLET FEVER RHINITIS – after tonsillitis. Purulent

*ALLERGIC RHINITIS: Affliction of mucosa by antigen induced reaction mediated by circulated antibodies. Most
importan – aeroalergens: polen, mites, house dust, hair, profesional, microbes, crioalergens. type I immunologic
disease – anafilaxis. Serous Rhinorrea, nasal obstruction, sneezing. Nasal, pharyngial, ocular Prurit, tearing, facial
tension, hiposmia, anosmia, fever. AR – pale or violet, swollen, shinny mucosa
*Clinical types: periodical (polinosis). aperiodical (perennial). Infected. Allergic Poliposis – always bilateral.
During asthma – allergic reaction to Aspirin
* Diagnosis: Alergologic inquery. Provoqued testing (skin and ocular). IgE dosage . Determining Eosinophilia in
serum and nasal secretion. Rhinomanometry. Allergic rhinitis – whitish mucosSkin test (Prick test). Tests
2,3,4,10,11 are positive (Histamine, Grass, Rie, Birch)
 * Treatment: Eliminating allergen. specific Hiposensibilisation with small Ag dosis, s.c. nonspecific
Hiposensibilsation with la Histamine. Antihistamine medication, Cortisone general/local, cromoglica
(Montelukast), Nasal Vasoconstrictoary sprays. Criocautery / Laser CO2

VASOMOTOR RHINITIS: Allergic perennial rhinitis simptoms. AR – pale, tumefied mucosa, serous rhinorrhea.
Pathogeny –neuro-vascular mechanism. Dg. By exclusion of allergy (negative testing). Treatment: Elimination of
irritative factors, Antihistamine, DNF, sedatives. Surgical: cautery of INT, MNT. Eliminating irritant factors: septum
deviation. Reduction of INT, MNT

COMMON CHRONIC RHINITIS Various Pathogeny. Follows an acute infection. Contributory Factors: Inadequate
Treatment. Allergies. Terrain (Diabetus mellitus, hiperthiroidism, adenoids). Medication, drogs, pollution, cold,
wet. Cardiac, circulatory disease. Fluctuent nasal obstruction. Simptoms: Thick, mucous, colourless rhinorrhea.
Post-nasal drip. Closed Rhinolala. Epiphorus, secondary Dacriocistitis secundară, pharyngitis. fatigue, headache,
cranial pressure. AR(augmented reality ????): congestion of mucosa, hipertrofia of mucosa, secretions between
septum and turbinates.
Evolution: Noncomplicated responds to DNF (dominant negative form ?doesnt follow??)?treatment. The hipertrofic
does not. Forming micropolyps Hipertrophy of turbinate tail.
Dg.dif: Sinusitis, FB, specific rhinitis, adenoiditis, allergy, Wegener’s granulomatosis, tumors.
Treatment: DNF, inhalation, nasal Cortisone. Surgical reduction of turbinates (turbinectomy, cautery, criocautery)

PREGNANCY RHINITIS Nasal Obstruction, congestion of mucosa, rhinorrhea serous/seromucous. Difficult Treatment
because of restrictions

DRY ANTERIOR RHINITIS (RINITA SICCA): Dryness, iritation, crusts. Sometimes small haemorrhage. Cause –
chemical agents, pollution, vasoconstriction medication, postop. AR – pale, dry, thick mucosa or septum perforation.
Oil nasal drops (vit.A), inhalation, natural aerosol. Sometimes surgery to repair damage.

ATROPHIC RHINITIS (OZENA): Atrophy of mucosa and structure of the turbinate. Unknown cause
Simptoms: Wide NF, full of yellowish-green crusts, fetid. Atrophic Mucosa, dry. Nasal Obstruction - paradox.
Subjective Cacosmia, in time becomes objective. Extends to pharynx and larynx.
Treatment: Nasal douche (saline, vit.A, sea water). Pushing the mucosa to the lateral wall with autografts or
homografts of cartilage, bone cement or heterografts of silicons, acrilate. Internal Rotation of the nasal wall towards
the septum (Lautenschläger‘s technique).

NASAL TUBERCULOSIS Several clinical types:

1. Nasal Lupus :TB infection in a resistant organism. Reddish Nodules in vestibule, turbinates, septum. Turn
yellowish, ulcerate and form vicious scars. Deform the cartilage and give NF stenosis.
2. Tuberculoma Pseudo-tumor. Aggressive bacillus. Productive lesions.
3. Ulcer Tuberculosis In patients with pulmonary TB, weak immunologic terrain. Increased virulence.
Destructive ulcerations in the cartilage.
4. Nasal bone Tuberculosis: Forms chronic fistulas. Diagnosis: clinical, bacteriologic, bioptic
Treatment: Rifampicine, Izoniazid, Etambutol, Pirazinamida, Streptomicine.

NASAL SIFILIS Std.I – chancre. Std.II – prolonged inflammation with nasal fissures. Mucous yellowish plates on
a congested base. Std.III – goma. Hipertrofic Lesions that ulcerate and leave a crater. Disastrous scarring,
collapse of nasal pyramid – “saddle nose”. Goma of the hard palate - communication to the oral cavity.
* Saddle nose – typical for congenital syphilis

SARCOIDOSIS (BESNIER-BOECK-SCHAUMANN DISEASE): Red-bluish or brownish Nodules, skin infiltration on nose

and face. nasal, pharyngial, laryngeal, tracheal Mucoasa with pale red granulations. Afects the eyes, salivary and
lacrimal glands. Uncertain Pathology. Dg: pulmonaru Xray, KWEIM’s test. HP from bioptic lymphnodes.
Treatment: Steroids in high dosis

RHINOSCLEROMA: Klebsiella rhinoscleromatis (FRISCH bacillus). Atypical Rhinitis. Secretions and crusts. Than
infiltrates with nodules that obstrate NF (sclerotic hypertrophy of mucosa). Dg: biopsy and HP exam (MIKULICZ’s cells
and ROUSELL’s corpuscles), FRISCH’s bacillus, BORDET-GENGOU reaction, cultures on agar-agar.
Treatment: Rifampicine
LEPROSY: Mycobacterium leprae (HANSEN’s bacilllus). Nodular thickening of vestibule, crusts, fetid secretions,
ulcerations, lion facies. . thermo-analgesic Dissociation. MITZUDA’s test. Treatment - Diaminodifenilsulfone
and tuberculostatic (TB treatment)

4. Rhinology- Sinusitis
SINUSITIS General info: Very frequent (5% of European population). Inflammation of sinus mucosa . Very rare
without rhinitis. Mostly non-specific. Specific through extension from NF. Polisinusitis / Pansinusitis
* Ethiology: - Most frequent – Rhinitis. Obstruction of sinus ostium via oedema prevents correct ventilation,
retention of fluid, infection. - Allergic - Accompanies tumors.
- Dentary – apical abscess premolar II, molar I. - Traumatic – direct sau by nasal packing
- Accompanies tumors. - Hematogen – immunodepressed
* Agents: Viruses (Rhinovirus, coronavirus), Bacteria: Pneumococcus, Staphilococcus, Streptococcus,
Haemophilus influenzae, E.coli, Moraxella catharalis, anaerob (dentary), Micotic.
*Anatomo-pathology: serous, purulent, osteitic, ulcero-necrotic, osteomielitic, cazeous, with
polyps.
* Major signs: Pain in the head and face area, accentuated by sneezing, bending over, movement,.
Facial Pressure, Hipoosmia / Anosmia, anterior or posterior, unilateral / bilateral Rhinorrhea,
Nasal Obstruction, Fever (only for acute),
* Minor signs: headache, Fever (other than acute), Halitosis, fatigue, apathy, depression, lack of appetite
Dental pain, Cough, Otalgia / ear pressure,

*Diagnosis: AR – congestion and oedema of mucosa. Rhinorrhea, Nasal Endoscopy, Xray in different views,
CT, MRI, Sinus ultrasound, Puncture / irrigation, Sinusoscopy, exploration of sinus, irigation –
biopsy, Bacteriological exam of nasal secretion

RHINOGENIC ACUTE MAXILLARY SINUSITIS Most frequent. Usually after common rhinitis. Unilateral pain in the
canine fossa, jugal region, lower eyelid, dental arch. Purulent unilateral Rhinorrhea. Nasal Obstruction. Fever.

*Diagnosis: Clinical exam (AR, Endoscopy).

Palpation of canine fossa – painful. Image:
Xray. or CT.

* Treatment: Antibiotics , NSAI. Cortisone local

or oral.
Puncture –drainage through the inferior meatus
or Sinusoscopy, Nasal spray / Aerosol

ODONTOGENIC ACUTE MAXILLARY SINUSITIS Starts from a cavity. Evolves into a cyst or apical granuloma and
submucous sinus abscess. Associated to fetid rhinorrhea and acute dental pain. Exam of mouth and teeth, XRay
retroalveolary and panoramic. Treatment similar to previous + dental treatment.

ACUTE FRONTAL SINUSITIS Relatively rare. Usually in a pansinusitis. Supraorbital pain, accentuated by bending
over, nose blowing, palpation of supraorbital fossa. sometimes photophobia. Diagnosis - anemnesis, clinical,
endoscopy, image. Treatment – Medicine + Trepanopuncture

ACUTE ETHMOID SINUSITIS Extremely rare as isolated. frontoorbital pulsating headache + photophobia.
Palpebral oedema and pain with eye movement. AR or endoscopy – puss in the middle meatus. XRay or CT for
diagnosis
ACUTE SPHENOID SINUSITIS Rarely as isolated form. May go unnoticed. Oftalmologic and cerebral complications.
retroocular pain and pain in the middle of the skull. Posterior Rhinorrhea and post-nasal drip. Visual acuity
problems. Diagnosis – endoscopy and imagery. Treatment – endonasal Sphenoidotomy

CHRONIC SINUSITIS Inflammation / infection of sinus mucosa secondary to long term obstruction of ostium.
Acumulating secretion accentuates oedema. Longer than 3 months. Associates significant histological
modifications: polyps, fibrosis, metaplasia.
* Simptoms: Nasal Obstruction and muco/purulent rhinorrhea . Light pain in the area of the affected sinus.
Pharynx Irritation. Re-occuring Laryngitis with acute disphonis in the morning. Fetid halitosis Headache in the
morning (3-4 hours).
* Diagnosis: Anamnesis, clinical. Endoscopy. Imagery (Rx, CT).

* Treatment: Same combination of AB, antiinflamatory, decongestive and antihistamine medication as in acute.
Saline douche. Aerosol / inhalation. Surgical Treatment : Middle turbinate surgery. Septoplasty. Polypectomy.
surgery – CALDWELL-LUC technique. FESS (ablation of mucosa blocking the ostiumul and keeping endosinus mucosa
– fixing ventilation and drainage of sinus

MUCOCEL (PIOCEL) Obstruction of sinus – retention of puss. Tumefaction of the are, crepitation on palpation,
displacement on eye, limitation of eye movement, visual problems– atrophy of nv. II and amaurosis. Dg: clinical +
imagery. Trat: extirpation and creating a wide communication ostium with the NF

NASAL POLIPOSIS Complex simptoms determined by mucosa reaction to certain factors. Hiperplasia with
oedema, polyps of the mucosa. No clear cause. Main Mechanism – disfunction of ostio-meatal system (low
drainage and ventilation) –> affected ciliary function –> irritant substances in long term conctact to mucosa.
* Ethiology: Genetic predisposition. Chronic inflammation of mucosa (rhinitis and chronic sinusitis).
Late reaction in allergic rhinitis . Accompanies nasal tumors (by stasis).
FERNAND-VIDAL-LERMOYEZ Syndrome – triad:

polyposis, asthma, Aspirine allergy.

* Simptoms Obstruction of NF, hipo/anosmia, epiphora, rhinorrhea. Rinopharynx inflammation, closed
rhinolalia, snoring. Post-nasal drip. Headache. WOAKES syndrome – deforming juvenile polyposis – “frog
facies” . KILLIAN’s solitary choanal Polyp – difficult deglutition
* Diagnosis: AR – translucid, white-grey, sometimes yellowish, solitary or multiple, tumors. Not painful, not
 bleeding. Rigide or flexible endoscopy. Imagery (CT).
* Clinical types: Allergic Poliposis Infectious during sinusitis. Solitary polyp KILLIAN, unilateral.
Deforming juvenile Poliposis WOAKES. Accompagnying tumors
*Dg.dif: Meningoencefalocel (Rx or CT). Bleeding Polyp of the septum. Nasal Tumors
* Treatment:
- Conservative: Glucocorticoids local or general + Antihistamine – sometimes total remission.
- Polypectomy + etmoidectomy + maxillary antrostomy (endonasale).
- Radical surgery of maxilla (Caldwell-Luc).
- FESS (endoscopic sinus surgery).
- Specific Desensitisation.
* Reserved Prognosis – frequent recurrence even with radical. Sinus surgery (unclear ethiology). Profilaxis –
long term nasal corticoid treatment.

5. Rhinology- Complications Of Sinusitis

Circumstances: Increased virulence of bacteria, Increased resistance of bacteria, Contributory anatomical

conditions, Immunological deficiency, Ignorring possible complications, Lack of treatment (long term sinusitis).
Usually in acute sinusitis.

Classification: Major - orbito-ocular - endocranial - osteomyelitis of skull bones - sepsis

Minor – cysts of the upper maxilla - vicinity complications - extension to other sinuses
- chronicity of an acute sinusitis
Mucocel

MAJOR COMPLICATIONS OF SINUSITIS

ORBITO-OCULAR COMPLICATIONS Usually in ethmoid or frontal sinusitis. Also in pansinusitis.

Classification of orbito-ocular complications

1. Superficial eyelid fluxion

Clinical: - eyelid oedema +/- fistula, - no orbita involvment, - mobile eyeball, - no visual acuity
impairment, - no exoftalmia, - fever
Diagnosis: - clinical (within sinusitis) - no involvement of eyeball or visual acuity - imagery (CT)
Treatment: - AB i.v - NSAI i.v. - nasal decongestant - fistula --> surgical drainage

2. Profound eyelid fluxion, also known as orbita cellulitis. Difuse Inflammation of orbita fat, early stage of Orbita
abscess.
Clinical – red oedema of eyelid. - chemozis (oedema of the palpebral conjunctiva). - hypomobility of
eyeball - exophtalmia - visual acuity maintained

3. Orbita abscess (oculo-orbitar suppuration), Also known as oculo-orbitar suppuration. Evolution of an orbita
cellulitis.
Clinical : - sepsis. - chemozis, exophtalmia, amaurosis. - midriasis, no cornea reflex
Diagnosis : CT scan
Treatment Antibiotics (no collection on CT). Surgical (collection pe CT) – drainage and orbita decompression
 (endoscopy or external approach). Orbita Abscess and retrobulbar collection with deviation of eyebulb (picture)

4. Subperiostal orbita abscess Collection between bone and periosteum of orbita. Usually medialy and superior
Diagnosis – clinical and imagery. Surgical Drainage Any ocular complication requires also Treatment of the
sinus cause.

5. Nerve affliction. Nv. I + III by compression, toxic or infectious nevritis petrosfenoidal Jaccoud syndrome (nv. II,
III, IV, V, VI) –in posterior sinusitis Petrosfenoid fossa syndrome (nv. III, IV, Va, VI) – in ethmoid mucocel, ethmoid
sinusitis, posterior sinusitis

ENDOCRANIAL COMPLICATIONS Classification of endocranial complications

1. Superior longitudinal sinus Thromboflebitis
* Clinical: - Signs of sinusitis always present, - Large frontal oedema, - Masive cranial oedema, - Signs of ICH:
headache, vomiting, papillary oedema, psychiatric problems, - sepsis, - Agitation, - Ophtalmoplegia.
* Dg.poz - MRI / angioMRI or CT (may be inconclusive)
* Treatment : emergency. AB massive + Antioedema medication. - sometimes Antiepileptic medication,
- heparine (debatable) - surgical (resection of osteo-myelitis lesions and drainage of sinus

2. Cavernous sinus Thromboflebitis : Collection of veins with very thin wall, between the temporal and sphenoid
bones. Drains facial, oftalmic, middle cerebral and sfenoid veins
* Clinical: sepsis, fever, frisson, agitation, insomnia, torpor, eyelid oedema extended to entire face, exophtalmia,
chemozis, ophtalmoplegia
* Dg.poz. eye fundus exam – papillary stasis. Hemocultures. lombar puncture –purulent meningitis. angioMRI
confirms Dg.
* Treatment: AB high dose (Antibiotics resistance test). Cortisone. Heparine

3. Extradural Abscess: Collection of puss between bone and dura mater. Direct complication of osteomyelitis of the
frontal bones.
* Clinical: - late simptoms, as it becomes large, aggravating sinusitis,
obtundation, neurological signs (specific to the affected lobe), convulsions
* Dg.poz. : CT + Leucocitosis of CSF
* Treatment: Drainage (neurosurgical) of abscess. Surgical for sinusitis. AB i.v. massive

4. Subdural Abscess: Between dura and brain tissue. Multiple neurological signs.
* Dg.poz. – imagery
* Treatment neurosurgery

5. Cerebral Abscess Rare complication. Especially in sfenoid or ethmoid sinusitis with aggressive germs or weak
immunity patients. Long term latency until signs of cerebral compession. Most frequent in the frontal lobe.
* Clinical: - sepsis, fever, headache, - ICH (vomiting), behavioural changes, neurological signs,
sinus suppuration signs.
*Dg.poz. – imagistic (CT/RMN)
*Treatment: - AB i.v. emergency. neurosurgical drainage. surgical treatment of sinusitis (mixted team)
6. Rhinogenic Meningitis (picture: from right frontal sinus)

Today more frequently latent, masked by antibiotherapy.

*Clinical: - intense headache, persistent, fever 39-40°C. drowsiness, cervical pain,
photophobia
Brudzinski’s sign positive (involuntary flexion of thighs and knees upon flexing the
head)
*Dg.poz. :lumbar punction (hypertonic purulent liquid) + qualitative exam of CSF. CT -
inflammatory aspect of dura – epiduritis
Treatment: extreme emergency – AB . massive (passes the blood-brain barrier) and AB
resistance test form CSF. lumbar punction for evacuation (decrease of hipertonic CSF).
surgical for sinusitis - Mandatory

7.Meningeal Empiema Severe clinical manifestation – associates meningeal syndrome and infectious syndrome
* Clinical: - obnubilated, sometimes commatose . neurological signs. toxicoseptic syndrome
* Dg.poz. – eye fundus exam – large papillary oedema (counter-indication of lumbar punction)
CT sets diagnosis and localization . EEG profoundly modified
* Treatment: neurosurgical of extreme emergency. AB massive. ICU. surgery of sinus. Prognostic
depending on early treatment. . Frequent Sequelle – epilepsy

OSTEOMYELITIS OF SKULL BONES: Frequent complication of acute frontal sinusitis

* Clinical: - prefrontal and supraorbitary oedema progressing towards soft tissue. intense pain, photophobia.
accentuating purulent rhinorrhea. severe general status
* Dg.poz. – CT (lysis of frontal cortical bone)
* Treatment: - AB i.v. massiv, up to 14 – 21 days. surgical for osteitis and frontal sinusitis (external approach).

Picture: Frontal soft tumefaction, consistency of dough, with secondary facial

oedema, especialy eyelids bilaterally

RHINOGENIC SEPTICEMIA Toxicoseptic state with septic methastasis.

* Treatment - extreme emergency to maintain vital functions (ICU). Sinus surgery after full recovery.

CYSTS OF THE UPPER MAXILLA- Classification of maxillary cysts

1. Paradental cyst (radiculodental) Evolution of a granuloma into a cyst by mild, long term infection. In the
vestibule (lateral incisive), floor of NF (central incisive), maxillary sinus (premolar, molar). Asimptomatic long term.
Puncture shows serous yellowish liquid. May get infected or may diform the cheeck..
Xray for diagnosis. Surgical Treatment.

2. Dentigerous cyst (coronodental): Dental crown inside the cyst. Most frequent on canine. Develops towards NF,
sinus, vestibule, hard palate. If infected – fever, pain
* Treatment : trepanation . surgery of sinusitis (for fistulas)

3. Adamantioma (ameloblastoma) Disembrioplazia of dental origin, potentialy malign. More frequent in the
inferior maxilla. Exteriorised and invades neighbouring structure (maxilla, ethmoid, orbita, NF)
* Diagnosis: Xray + Puncture of sinus
* Treatment : complete extirpation with excision into healthy tissue +/- Prosthesis . malignisation – Cobaltotherapy
and . anti-mitotic postop.

4. Mucous cyst (retention cyst): By obstruction of an orifice of a mucous gland. Secretion productive. May evolve
into a mucocel. Localised on the sinus floor in the alveolary region. Evolve slowly until filling the sinus.
Evacuation by puncture or surgery (FESS)

5. Submucous cyst: Do not produce secretions, no wall. May be latent, asimptomatic or may associate facial pain.
* Dg. XRay, sinusoscopy.
* Don’t require Treatment if asimptomatic.

VICINITY COMPLICATIONS –Classification of vicinity complications

1.Extension to other sinuses (polisinusitis, pansinusitis)
2. Rino-faringo-laringo-tracheo-bronchitis – descendent
3.Chronic tonsillitis (maintains vicinity infection)
4.Dacriocistitis, Conjunctivitis
5. Tubary Disfunctions (serous or suppurated otitis media)
6. Vestibular Rinitis (inflammation of nasal vestibule)

Chronicisation of an acute sinusitis

Mucocel: Cyst-like benigne tumor developed from the sinus mucosa.
-Own membrane and mucous, sterile content. Most frequent fronto-ethmoid.
-Ethiology – congenital or aquired (agent that stimulates mucus secretion – craniofacial trauma, surgery, chronic
sinus inflammation)
-Clinical: - progressive exophtalmia - mild diplopia, no chemozis - headachee, hyposmia - hemispheric
tumefaction, compressibile, not painful - crepitation like “ping-pong ball”
-Dg.poz. – CT axial and coronal, MRI
Frontal Mucocel - hemisferic frontal Tumefaction

Frontal Mucocel that displaces the eyeball caudaly.

Maxillary mucocel – cranial displacement of orbita content

Ethmoid mucocel – lateral displacement of orbita content

Sfenoid Mucocel

Treatment : AB şi Cortisone i.v for acute cases

-Surgical – marsupialization by endoscopy (sometimes external approach for massive extension)
-Treatment - surgical of polyposis. Posterior part of maxillary sinus . maxillary tuberisity

6. Rhinology- tumors
BENIGN TUMORS: Relatively rare. Nasal Obstruction. muco-purulent rhinorrhea. Smell sense disorders.
1. OSTEOMA
Especially frontal and ethmoid. Signs: headache, pressure, ocular deviation, intracranial complications
*Dg – accidental in random XRay. Treatment surgical.
a.Osteoma in XRay – radioopaque tumor in the anterior ethmoid cells (left picture)
b. same image on CT (well defined shape)

2.PAPILOMA Rarely in nose and sinuses. Potentially maligne.

signs:Nasal Obstruction. Reoccuring Epistaxis.. Dg. by biopsy
treatment:Surgical excision. In maligne cases – radiotherapy resistent

3.BLEEDING SEPTAL POLYP Localized Angiofibroma in the vascular area

4.HEMANGIOMA AND LIMFANGIOMA Congenital. 60% in girls

*Treatment at 3-4 years, surgical – laser, criocautery, dissolving with inactive Mg sticks. Radiotherapy may be
efficient but produces deforming skars and danger of malignancy.

MALIGNE NASAL TUMORS

Exterior of nose – bazalioma, epidermal carcinoma, melanoma.
* Keratoacantoma – benign tumor hard to differentiate from a scuamous carcinoma
* Senile Keratoma, Xeroderma pigmetosum – precancer states
*Inside the nasal fossa – epithelial carcinoma, adenoid-cystic carcinoma, adenocarcinoma

Basalioma of nasal pyramid (basal cell Carcinoma) (picture)

Squamous cell Carcinoma (clockwise in picture)

a.Preoperative b. Postoperative + plastic surgery with frontal flap c. After flap detachment
d. Final result
Mezenchimal Tumors (rare) – sarcoma, chondrosarcoma, osteosarcoma, lymphoma
HISTIOCITOSIS X and rabdomiosarcoma – most frequently in children
* Simptoms: Progresive nasal obstruction, purulent or sanguinolent rhinorrhea, epistaxis,
nasal & orbita deformity, cervical adenopathy.
* Treatment: Surgical. radiotherapy (cobaltotherapy, curietherapy, linear accelerator).
Paliativ - citostatic

SUPRASTRUCTURE From ethmoid, invade NF. Signs: Nasal obstruction, mucopurulent

rhinorrhea, epistaxis. Invades orbita – exophtalmia, blindness. Invade endocranialy – death

MESOSTRUCTURE: From maxillary sinus. Late simptoms. Deforms cheek .

Maxillary pain and nv.suborbitary anaesthesia

INFRASTRUCTURE Evolves into the mouth. Teeth pushed from alveolae and tumor
buds appear. Deformed palatine arch. Treatment: Surgical. Radiotherapy or chemotherapy . Healing ratio at 5
years - 37%