ENT TABLE: MALFORMATIONS:*nasal vascular ,sensitive and sensory syndromes, epistaxis*

DISEASE NAME DIAGNOSIS SYMPTOMS TREATMENT

1.Meningocele\encephalocele Clinical, CT, arteriography Hernia of dura through 1.Removal
dehiscence of cribriform plate of 2. Closure of dura
NF 3.osteoplasty (surgery)
2.Atresia and stenosis of choana -Congenital: difficult to breath and -chronic\ pururenlt secretions surgical
(congenital\ aquired) cyanosis. - can’t breathe
-Rhinoscopy, endoscopy, CT
3.Rhinoscopia (deviated septum) -anterior and posterior Rhinoscopy -pathological when Nasal surgical
-cause: trauma\prolonged -endoscopy obstruction
obstruction\by disease (ex. TB) -CT - low O2 intake
4.Nose Trauma: septal -clinical, CT - can be closed \opened -shock treatment
hematoma(6), classified by Lefort *types: 1.luxation of septal cartilage. -pain, shock, neuroglia, epistaxis, -manual\instrument
2.fracture 3. Orbital compression. chemosis of eyelids, pyramid repositioning bone
4.hematoma displace cone crepitus & -contention (heated)
*most common affects Max. Sinus. movement
5.FB (foreign body) can be by exo\ -clinical, xray, CT -fetid, nasal obstruction, -extraction with special
endogenous causes rhinorreah (muco-purulent) forceps
6. Septal Hematoma (after “ as above (5) -bilateral incision and
4:NasalTrauma) *complications: 1. Perforation. 2. -AB
Abcess (puss). 3. Carvenous sinus -reconstruction
thrombosis (see complications**)
RHINITIS:of nasal epidermis (Chemosis is the swelling (or edema) of the conjunctiva)
tumefied=become swollen.

DISEASE NAME DIAGNOSIS SYMPTOMS TREATMENT

1.Nasal eczema (seborrheic Atopic background -superficial inflammation with vesicles , pustules and -on the lesions:
dermatitis) itching cortisone
-hyperemic skin with crusts and painful lesions with -Nitrate 5%
exaggerated secretions augmentation
2.Vestibul folliculitis -staphylococcus -pain , burning, itching, nose congestion with lobules and -Local AB
(sycosis) infection on facial hair crusts -anti-staphyloccocus
follicles vaccine
3.Carbuncul of nasal --“- as above (staph) -weak organs: immunosuppressed (ex.liver) -general : doesn’t heal
vestibule (boli): -check symptoms -nose: tumefied, congested, sensitive until puss is eliminated
rare but with severe -lips, cheeks, eyelid and nasal wing tumefied -anti-staphyloccocus
complications -inside the vestibule: red prominence with hair , necrotic , vaccine
painful, with puss
4. Thrombophlebitis -“- propagation of -orbital stasis: palpebral tumefaction, chemosis, -massive AB,
(thrombosis of cavernous infection to sinus via exophthalmia, eyeball immobility, amaurosis, -heparine
sinus : see septal angular and orbital -cerebral stasis and edema -anti-inn.
hematoma,sinusitis compli.* veins -alcohol\ice on boil
5. Erysipelas -“-Strep\staph infection -well defined and congested area of N pyramid: butterfly -high dose of AB
with short incubation shape (penicillin and anti
time: bacteriology -fever, malaise, can extend to facial edema staph)
6. Rhinophyma Elderly at risk of Pseudo motor on skin over cartilage, hypertrophic Excision by slicing,
breath acne on pink background then spontaneous
epithelisation
 RHINITIS:1 -acute & 2-7new born(Q:HNS, OR?)
DISEASE NAME DIAGNOSIS SYMPTOMS TREATMENT
1.acute rhinitis -anterior rhinoscopy -favoring factors: cold, pollution, low immune -symptoms treat.: nasal spray,
(common cold, **3 Diag.diff:other viruses, etc.Low immunity, short incubation, fever AI (anti-inflammatory)
phases) -AB- only if needed
2. Gonococcal rhinitis -OR, bacteriological -mucosa: green and ulcerative, upper lip is -cleaning lesion
(during labor infection) swallen, nasal obstruction. -Nitrate % augmentation, AB
3.syphilis congenital Muco-pururelnt, fetid, hand pemphigus ?
4. Hutchinson’s triad Serologic history Interstitial keratitis, sweet teeth , HNS Infection specialist
5. dyphteric rhinits AR anterior rhinoscopy -common in kids aged 2-6 -serotherapy
and xray: white grey -purulent, crusts,lesion on vestibule,pale, -AB
membrane in NF lymphodenopaty
6.measles KOPLICK SIGN (oral -usually in older children
enantema) -epistaxis, otitis media, (sepsis) inflammation
oculo-rhino-pharynx

**acute rhinitis 3 phases:

**acute rhinitis 3 phases: 1. Prodromal phase 2.Cataral phase 3.Mucus phase

symptoms Feverishness, fatigue, torpor, lack of Serous Rhinorrhea, nasal Simptoms become milder.
appetite, head-ache, muscle pain. obstruction, anosmia, closed Mucous secretion. Nasal
In children high fever, dryness of rhinolalia, tearing, malaise Obstruction gradually subsides
nose, throat.
diagnosis Anterior rhinoscopy (AR) – pale, dry AR – intensely congested mucosa, Recovery of smell. Bactarial
mucosa. oedema, profuse secretion . Infection produces muco-
becomes mucous within days. purulent rhinorrhea.

**general syndromes:
Secretory syndrome Sensitive Sensory syndrome Vascular syndrome epistaxis
syndrome
sympto secretion is usually seromucous Pain projected Ethiology: idiopathic Diagnosis: .clinical .Blood
ms and low quantity to sinus area. juvenile (vascular fragility - Pressure values.
constitutional Coagulogramm. Internal
disease exam. Xray / CT
types 1Pathological:rhinorrhea. 1.Hyposmia \Anosmia – 1.Hyperemia of mucosa – treatment: *Scopus: Stop
2CSF – rhinolicvorrhea. 1.Hyperestesia nasal or neurologic. inflammation . 2.Anemia bleeding. Shock treatment.
3.Serous – acute / allergic. – 2. Hyperosmia – rarely sign of mucosa – local Treatment of cause
4.Mucous – chronic rhinitis inflammation. of disease (medulo – vasoconstriction * General measures: 1.
5.Mucopurulent – acute/chronic 2.Hypoestesia suprarenal tumors). 3.Epistaxis – hemorrhage Calm the patient; patient
sinusitis. – atrophic 3.Parosmia –modified or of NF sited and slightly leaning
6. Sangvinolent – trauma, rhinitis inexistent smells (pregnancy, -can be local (FB, trauma.. forward. 2. Not Swallow
tumors. epilepsy, histeria) etc) or general (blood blood 3.BP measures and
7. Crusty – atrophic rinitis / 4. Caccosmia –fetid – disease) MEDS … 4. vasocons. Is ok,
ozena subjective or objective. can do surgery
 NASAL VASCULAR SYNDROME(further info):
*Anatomicaly: Anterior – most frequent from vascular area of Kisselbach. Posterior – a.sfenopalatine or a.post
ethmoid. Difuse – hemorrhage from numerous small vessels

TREATMENT OF EPISTAXIS (further info):

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)

RHINITIS:chronic specific:

NAME DIAGNOSIS SYMPTOMS TREATMENT

1. syphilis (also in acute) 3 stages: diagnosed by symptomes 1.chancre (blisters,ulcers) ?
2.prolonged innflammation and nasal fissures
3.goma infection with hypertrophic lesions,
profound scaring, „saddle nose”, also at hard
palate
2. sarciodosis: ulcerative Xray at lungs, KWEIM test, HP Red-blue or browm nodules, skin infiltration on High dosage of
pathology (histopathological) from biotopic face, pale amd red granulomas. Affects eyes & steriods
lymph lacrimal g.
3.rhinoscleroma Biopsy, agar culture, HP exam: Secretions and crusts that infiltrate with nodules -AB- rifampicin
(klebiciella, MIKULICZ ceels and ROUSELL that cause nasal obstruction
rhinoscleromatis) corpuscles. And BORDET reaction
4. Leprosy -MITZUDA test - nodular thickening, crusts, fetid, ulcerations diaminodifenilsulfone,
(mycobacterium leparae) TB med

**allergic rhinitis: general info:

 symptoms 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.
types periodical (polinosis). aperiodical (perennial). Infected. Allergic Poliposis – always bilateral. During asthma – allergic
reaction to Aspirin
diagnosis AR – pale or violet, swollen, shinny mucosa. 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

**allergic rhinitis: types:

NAME DIAGNOSIS SYMPTOMS TREATMENT
1.Vasomotor rhinitis AR, testing of -neuro-vascular pathology. Pale, tumefied -antihistamines,sedatives, DNF,elimination
( allergic perennial =all allergen (if negative) mucosa, serus rhinorrhea INT,MNT(?) of irrigative factors, surgery
year)
2. Common chronic AR- congestion of -thick colorless mucus, closed rhinolala, DNF inhalation, nasal cortisone
rhinitis (common cold, has mucosa, fatigue ,pressure, 2ndary to dacryiotitis
3 types: 1.noncomplicated, hypertrophy and &pharyngitis& epiphorus.
2. Micropolyps formation secretions -follows acute infection, favoring factors:
3.hypertrophy turbinate) allergy\systemic disease
3. dry anterior rhinitis AR- pale, dry, thick Dryness, irritation, crusts -oil nasal drops, surgery, inhalation,
(rhinita sicca) mucosa, septum - caused by chemical agents, pollution, meds natural aerosol
perforation
4. atrophic rhinitis -atrophy, unknown Wide NF with yellow green mucus, crusts, Nasal douch (saline, vit.A,sea)
(oezena) cause fetid, atrophic dry mucosa, nasal obstruction, -pushing mucosa to lateral wall with auto\
subjective cocosomia (fetid), extends to hemorrhagic of cartilage or with
larynx and pharynx heterographs of cements , silicone.
-Lautenschlager tech: internal rotation of
nasal wall.
5. nasal TB: clinical & 1.lupus: infection in resistant irganism color -AB: rifampicin, Ixoniazid, etambutol,
4 types: bacteriology change from red to yellow, forms streptomicins
1.Lupus scars,deforms cartilage, NF stenosis
2.tuberculoma: 2. pseudo-tumor, aggressive, with lesions
3.ulcer TB 3.ulcer TB: in patients with pulmonary TB,
4. Bone TB immunosuppressive, increased virulence,
cartilage ulcers
4.forms chronic fistulas

**sinusitis: Gerneal etiology: Very frequent (5% of European population). cause Inflammation of sinus
mucosa . Mostly non-specific. Specific through extension from NF. Polisinusitis / Pansinusitis
 etiology: - Most frequent with Rhinitis. Obstruction of sinus ostium via oedema prevents correct ventilation,
retention of fluid, infection. Can ne with Allergic can be with Accompanies tumors.
major signs: Pain in the head and face area, accentuated by sneezing, bending over, movement. Facial Pressure,
Hipoosmia / Anosmia. Rhinorrhea. Nasal Obstruction, Fever (only for acute),
General diagnosis: virus or by bacteria

** general pahrmacological information:

antiHistamines and corticosteroids are given in allergic reaction treatment (nasal congestion, fever, etc. ) .
antihistamines also have anelgestic role. but only corticosteroids are class of steroids (not antiH). Which they
(steroids) are given for severe pain only (cortisone for example is glucocorticoid and is used as anti-innflammatory
and and antiallergic! NSAIDS are mostly given against pain and fever (example aspirin, advil..) but they are non
steroidal
-never mix steroid drugs with NSAID -lethal. Ok but not recommended to mix NSAIDS with antiH. This
because antihistamines work on brain and NSAIDS on liver. Its very ok to mix steroids with anti H

NAME DIAGNOSIS SYMPTOMS TREATMENT

1.rhinogeric acute -clinical, AR, xray. Nasal obstruction, rhinorrhea and fever. Unilateral -AB, NSAIDS, cortisone ,puncture for
maxillary sinusitis Palpation-painful pain in canine fossa, dental arch. appear after diriange, sinuscopy, nasal spray and
common rhinitis . aerosol
2. odontogenic Xray, teeth examination Fetid, rhinorrhea, dental pain. -““”””-
acute maxillary (retroalveolar and OPG) propagation: tooth cavity->cyst\apical granuloma +dental treatment
sinusitis with submucus sinus abcess
3. acute frontal Clinical, xray, endoscopy Sometime has photofobia, rare and usually a -“””””-
sinusitis pansinusitis + trepanopuncture (hole)
4. acute ethmoidal AR\endoscopy- has puss in Fronto-orbital pulsating, headache, photophobia, -“”””-
sinusitis middle meatus, xray\CT very rare, has palpebral edema and eye pain
5. acute sphenoid Endoscopy, xray It’s a visual problem with posterior rhinorrhea. But -endonasal sphenoidectomy
sinusitis may go unnoticed with opthalmo.&cerebral comp.
also has retroocular and middle skull pain
6. CHRONIC Clinical, endoscopy, Nasal obstruction, muco-purulent. Pain in affected -AB ,NSAIDS, antihistamins, saline
sinusitis: can xray,CT sinus, pharynx irritation, laryngitis, fetid halitosis douch, aerosol inhalation
propagate to -longer than 3 months (mouth), 3-4 hours oh headache.
mucocele (7) -associated with polyps, -usually 2ndary to long-term ostium obstruction
fibrosis, metaloplasia accumulating secretions accentuate edema.
7.mucocele- CT,MRI: ethmoid, frontal Exophthalmia, mild diplopia, tumefied brain AB,cortisone,surgical

General info Sinusitis diagnosis symptoms types Diff. diagnosis Treatment*

polyposis
No clear cause. Complex simptoms -Hiperplasia with oedema, 1.Allergic, Meningoencefalocel, 1.Conservative:
Main Mechanism – determined by polyps of the mucosa. 2.infectious, Bleeding Polyp of the Glucocorticoids + AntiH
disfunction of ostio- mucosa reaction -Obstruction of NF. 3.solitary (polyp septum, tumors 2.surgery: Polypectomy +
meatal system (low AR – translucid, Rinopharynx inflammation, KILLIAN -unilateral. etmoidectomy + maxillary
drainage and white-grey, closed rhinolalia, snoring. **prognosis: frequently antrostomy (endonasale).
ventilation) –> affected sometimes yellowish, Headache. WOAKES 4.deforming re-occur that needs 3. Radical surgery of
ciliary function –> solitary or multiple, syndrome – deforming juvenile polyposis- radial surgery (3) maxilla (Caldwell-Luc).
irritant substances in tumors. Not painful, juvenile polyposis – “frog WOAKES **prophylaxis:long term 4. FESS (endoscopic sinus
long term conctact to not bleeding. facies” .KILLIAN’s solitary 5. Accompanying nasal coticoid surgery).
mucosa endoscopy. CT choanal Polyp – difficult tumors treatment 5. Specific Desensitisation
deglutition
Sinusitis major complications: in all cases: treat 1st sinusitis cause
ORBITO-OCULAR complications name: DIAGNOSIS SYMPTOMS TREATMENT
1.superficial eyelid fluxation: edema -clinical (with sinusitis) Eyelid edema with\out fistula, fever -if fistula : surgery needed.
NO visual loss involvement, -NO orbit involvemnt -IV NSAIDS& AB, nasal
xray, CT decongestion
2. profound eyelid fluxation : orbital Early stage of orbital abcess* -chemosis (edema of conjuctivis& -“””-
cellulitis -NO visual loss eyelid)
-exophthalmia, low eyeball mobility,
3. orbita abcess: oculo-orbital CT -“””- + Sepsis (=infection), low blood -AB, surgical (orbital
suppuration -NO cornea reflex pressure, amaurosis (=blindness), driange)
midriasis (=pupil dilatation) -endoscopy decompress

4. superosteal – orbial abcess* Clinical, CT Collection between bone and periosteum Surgical driange
of orbita, usually medial and superior
5. nerve affliction: JACCOUD syndrome (nv. II, Petrosfenoid fossa syndrome (nv. III, IV,
Nv. I + III by compression, toxic or III, IV, V, VI) –in posterior Va, VI) – in ethmoid mucocel, ethmoid
infectious nevritis petrosfenoidal sinusitis sinusitis, posterior sinusitis

ENDO-CRANIAL complications DIAGNOSIS SYMPTOMS TREATMENT

name:
1.superior longitudal sinus MRI\CT Frontal &cranial oedema, sepsis, agitation, ICH(headache, -emergency, AB,
thrombophlebitis vomiting), papillary oedema, psychic problem, antiepileptic, heparine,
ophthalmalgia surgery
2.carvenous sinus Eye fundus exam- -purulent meningitis, vein collection with thin walls -high dose of AB,
thrombophlebitis : see in pappilary stasis, between TEMPORAL AND SPHENOID. Drains ophthalmic , cortisone, heparine
epidermis sinusitis hemocultures, facial, sphenoid veins.
lombar puncture, -sepsis, fever, frisson, agitation, insomnia, edema,
MRI exophthalmia, chemosis
3. extra-dural abscess CT, leucocytosis of -puss collection between bone &dura matter, Neurosurgery driange
CSF, late symptoms complication of OSTEOMYELITIS**, neurologic signs , of abscess, AB
convulsions
4. sub-dural abscess CT\MRI Between brain and dura, multipule neurological signs neurosurgery
5. cerebral abscess -“”- Rarw complication,especially of SPHENO\ETHMOID , long -AB, Neurosurgery
term compression of brain-mostly at frontal lobe, driange
sepsis,fever,headache, ICH, neurological signs
6. rhinogeric meningitis Lumbar puncture,CT- -intense headache and persistant fever, drawiness, -lumbar punction for
epiduratitis, cervical pain, BRUDZINSKI’S SIGN positive (involuntary evacuation, surgery, AB
qualitative exam of CSF flexion) high dosage
7. meningeal epiema (puss) Eye fundus exam, CT, -meningeal and infection syndrome ,comatose, -emergency-
EEG neurological signs, toxicoseptic syndrome Neurosurgery, AB, VICU

Major complications: DIAGNOSIS SYMPTOMS TREATMENT

1. Osteomyelitis** of skull bones: CT Perofrontal and suprafrontal edema progressing to soft tissues, AB (14-21 days), surgical
frontal acute sinusitis intense pain, photophobia, purulent rhinorrhea, severe general osteitis of frontal
state sinusitis (external)
2.sepsis Toxic state of specific metastasis

Sinusitis minor complications: in all cases: treat 1st sinusitis cause

Cysts of upper maxilla DIAGNOSIS SYMPTOMS TREATMENT
1.paradental (redicular) All xray a-symptomatic long time, , granuloma surgical
infection->cyst at LI,CI (central incisor),PM,M
(molar)
2.dentiogerous (coronal) -“”- The dental crown is inside the cyst, affects -“”-, Trepanation,
Canines, the sinus, fever, and infection
3. adamntioma -“”- and clinical puncture Frequent at inferior part of maxilla, -surgical excision, anti-mitotic
(ameloblastoma) potencially malign, therapy, if malign: cobalotherapy
4. mucus cyst (retention -“”- caused by mucus May evolve slowly to mucocele, has FESS surgery
cyst) gland obstruction secretions, affects sinus floor,
5. submucus cyst -“”- & sinuscopy NO secretions, a-symptomatic with facial pain No treatments (no symptoms)

VICINITY (=surrounding) 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)

NOSE TUMORS
BENIGN T: nasal DIAGNOSIS SYMPTOMS TREATMEN
obstruction, muco-
purulent rhinorrhea, rare,
sense of smell disorder
1.osteroma Xray:radio-opque Headache, pressure, ocular deviation, intra-cranial comlication Surgical
2. papilloma biopsy Rare in nose and sinuses, nasal obstruction, epistaxis -“”-
3. bleeding polyp Local angiofibroma in vascularized areas
4. hemangioma and Congenital, 60%in -“”- + crico
lymphangioma girls sticks, rad

Mezenchimal Tumors (rare) – sarcoma, chondrosarcoma, osteosarcoma, lymphoma

* diagnosis: 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

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

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

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

Maxillary pain and nv.suborbitary anaesthesia

III. 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

OTOLOGY :
 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 neurovegetative symptoms.
crisis.

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. To the same
hypoacusis. To opposite side of head rotation direction as head rotation

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

The symptom\syndrome: General info (cause etc) Clinical affects

1. vestibular syndromes: -nystagmus (rapid eye movement) is oriented towards I. nystagmus to the afflicted ear, segment and body
I. Irritative peripheral vestibular the vestibule that generates more impulses deviations to the normal ear.
syndrome - Segment and body deviations will be towards the II. nystagmus to the normal ear, segment and body
vestibule that generates fewer impulses deviations to the afflicted ear.
II. Destructive peripheral
vestibular syndrome
2.labryinthis syndromes: Cause: I: tinnitus and peripheral vertigo Can be total (cochlea and vestibular system) affected or
I. irritative labrynth stndrome II. peripheral cochlear SNH (sudden hearing loss) and dissociated ( 1 of the 2)
II. Destructive labrynth peripheral vertigo
syndrome
3. vertigo nausea and vomiting, profuse sweating and balance Dizziness (unsteadiness) light-headedness, uneasiness or
disorder creating the vestibular syndrome. By middle fatigue and does not imply movement. Acrophobia (fear of
ear heights)
4. luetic labyrinthitis Late congenital or secondary sifilis / tertiary acquired Accentuated hypoacusis, fluctuent. tinnitus
Vestibulary syndrome with paroxysmal evolution,
peripheral and central
5. labyrinthitis meningitis Germ propagation along the meningeal sheath of fever, headache, Severe, bilateral hypoaucusis
nv.VIII.
6.urlian labrynthitis (MUMPS) Complication of epidemic parotiditis. Vascular Only cochlear affliction in one ear Permanent loss of hearing
propagation
7. vestibular schwannoma Benign tumor of nv. VIII, origin in the mielin sheath of Unilateral, progressive loss of hearing, Unilateral tinnitus,
the inferior vestibular nv. Cerebellum symptoms. Small tumors: vertigo, large: sensory
affliction
8. SSC: dehiscence syndrome transmission of sudden pressure change HAT and autophonia, Pulsaring Tinnitus, ear fullness.
Sound/pressure induced Vertigo and nystagmus, Sudden falls. Surgical closure of SSC/ avoid triggers
Sudden falls vertical-rotational nystagmus of healthy
ear
INNER EAR -diseases and syndromes

Peripheral vertigo In a vestibular syndrome, one vestibule generates more impulses than the other.
 -The nystagmus (rapid eye 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:
OSC :Horizontal canal – horizontal nystagmus. ASC: Anterior canal – vertical nystagmus.
PSC : Posterior SEMILUNAR canal – torsional (diagonal) nystagmus

9.OTOTOXICOSIS: Labyrinth affliction via toxic substance.

*etiology (cause):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.
INNER EAR TUMORS:
Signs & symptoms DIAGNOSIS PHASES TREATMENT
ACOUSTIC Benigne Tumor with MRI, -schwannoma, 1.Otologic phase: Developed in IEC. SNH Surgical, neurosurgical,
NEURINOMA = maligne evolution by CT, Eye fundus exam unilateraly, progressive . Vestibular syndrome. approaches:1. retrosigmoid:
VESTIBULAR compression of CNS. Very for papillary stasis (in 2.Oto-neurologic phase: Tumor into the intracranial, intradural.
SCHWANNOMA common. Developed from ICH). Lumbar Pontocerebellar angle and affects the nerves. 1st 2.transtemporal approach –
vestibular beanch of CN 8 puncture sign: cn V anesthesia. CN 7 paralysis, ICH intracranial, extradural.
syndrome. compression 3.Transmastoid approach –
extracranial, extradural

NAME-INNER DIAGNOSIS SYMPTOMS TREATMENT

EAR HEARING
SUDDEN Unilateral SNH is idiopathic . can Sudden onset,rarely vertigo Emergency, cortisone, vitamins, sedatives,
HEARING LOSS be Vascular\viral surgery
MENIERE’S Excessive endolymph production. through viral infection, allergies, genetic factors, Rest, Vasodilation – Redergin, Pentoxifilin.
SYNDROME vestibular syndrome: horizontal- trauma neurotropic – Memotal. Cortisone. Diet,
rotational to the afflicted ear triple: vertigo, tinnitus, SNH. Nausea, vomiting, sedatives
sweating. Irritative
VESTIBULAR Acute, prolonged vestibular inflammation of nv. Vestibularis(8), inflammation Vestibular Supresors (Meclizina), Sedatives,
NEURONITIS / syndrome of peripheral origin. of superior part of the labyrinth (utricle, ASC, Neurotropic Vitamines - B1, B6,. Cortisone
LABYRINTHITI viral. ENG (Electronistagmography) OSC).
S: , MRI Intense vertigo, hypoaucusis
OTOSCLEROSI Hereditary, Ossification of stapes b. progressive hypoacusis, Tinnitus. Surgical – stapedotomy with prosthesis.
S: Tympanogramm shows chain Hearing aids
fixation
PRESBIACUSIS: Lesions of the hair-cells in the organ of CORTI, Ear cleaning, Vasodilatory medication,
Age hearing loss small vertigo, SNH, bilateral and equal prosthesis, vitamins
HEARING LOSS Congenital. cranio-facial High occurrence rate. psicho-social development Cochlear implantation Special school
IN CHILDREN : malformation. acoustic impaired. Bilateral hypoacusis Bilateral prosthesis
otoemissions OAE. Condition
Audiogramm. Tympanogramm
brain-stem Evoked potentials BERA
BENIGN Dix-Hallpike Maneuver – vertigo Most common cause for vertigo, Dislocated PSC : rotational Nystagmus: Epley
PAROXYSMAL without nystagmus is no base for otoconia inside the SC, most frequently PSC – Maneuver.
diagnosis. mobilizes the endolymph without head movement ASC: vertical Nystagmus – Deep Head
POSITIONAL
Hanging Maneuver .
VERTIGO OSC –horizontal Nystagmus – Lempert
(BPPV): (BBQ) Maneuver. Surgical obliteration of
PSC.
INTERNAL ear 1. cranial blast, loud noise 1. Vertigo, SNH (sensoneural hypoaucusis), 1. Rest, sedatives, antivertigo medication
trauma 2. Once: 120 dB ,or repeatedly 90dB tinnitus. 2. Hearing aid
1. Labirynth .Audiogrametry: at 4000Hz. 2. SNH, Tinnitus 3. AB, Cortisone, Simptom treatment,
concussion Progressive ,irretrievable 3. Cranial and cerebral lesions, SNH and Surgical
2. sound trauma: 3. Otalgia, bleeding from EAC, trasmissiotn,
3. Temporal bone otolicvorrhea, facial paralisis VII.
trauma

1.ACUTE SEROUS OTITIS MEDIA 2. CHRONIC SUPPURATIVE (=puss) OTITIS MEDIA 3. CHRONIC SIMPLE
WITH CHOLESTEATOMA: SUPPURATIVE O. MEDIA
Mechanism Outside innflammation-> ET (eustechian tube ) 1.Epithelial ectodermic embrionary inclusions in the ME Evolution: Life long, periodic
& and obstruction->negative pressure->tympanic (primary cholest.)-> 2.Penetration of EAC epidermis in calm and acutization through
retration and secretions from epithelium ME through TM perforation to upper part of ME by rinitis, pharyngitis, water in
Evolution:
- spontaneous healing in 10-21 days. pressure decrease EAC
2. Adenoiditis => chronic serous otitis media =>
retraction of TM through low pressure -> increase of
size by accumulating epithelium from EAC =>
 Infection=> erosion of bone => complications
Simptoms: Otalgia, hypoaucusis, autopjonia, vertigo, Progressing, congenital, Epitimpanitis, purulent otorrhea, Hypoacusis accentuated by
rhinorrhea. Mostly children. Causes: rinitis, marginal perforation with puss, Whitish lamellas, redish- age. Otorrhea. Central TM
adenoiditis, pharyngitis violet polyps perforation
Diagnosis Otoscopy, liquid leverls raise , intese pain Audiometry (Transmission hypoacusis ). Rx\ CTscan – Rx or CT scan: disappearance
erosion of bony walls of ME and reduced pneumatization of cell pneumatization
of mastoid cells. “ring and seal”. Antimicrobial
susceptibility testing (AST)
Positive Otoscopy Transmission Hypoacusis in Weber and Vicinity (near by area) complications, evolution: Audiometry: Transmission
diagnosis: Rinne test. Audiogramm. Tympanometry intoxication with bacterial toxins hypoacusis turns to SNH.
types Can get infected or chronic. Type A: normal Alternating periods of acute & chronic. Low tendency of
pressure on 0. Type B: tympanic membrane cant spontaneous healing
move. Type C: negative pressure , graphic pic
shifter left.
Treatment: Vasoconstrictors (Olynth, Rinogut, Vybrocil), Exclusively surgical: mastoidectomy and tympanoplasty. Hearing aids, mucolytitics,
Sputum fluidifiant, NSAIDS, Valsalva Maneuver, Daily suction, AB, daily suction, resection of
Toynbee Maneuver, Politzer Maneuver, polyps(surgery)
Otovent balloon Adenoidectomy,, anti allery
and corticoid spray
4.ACUTE SUPPURATIVE OTITIS MEDIA- warm abcess 5. CHRONIC SEROUS OTITIS MEDIA
Meachanism 1. Preperforation phase: Pulsating otalgia,Hypoacusis, „otita sero-mucous, mucotympanum, serotympanum”
and evolution Autophonia, Fever. Lack of appetite, General malaise, Intense Most frequent cause –chronic adenoiditis
congestion of the TM. Puss bulging. Sensitive mastoid process, evolution: Years Involvement of IE and SNH.
Tinnitus and mild vertigo The TM adheres to wall of the ME (fibro-adhesive
2. erforation phase Otalgia diminishes spectacularly, NO Fever, otitis).
Hypoacusis accentuates, Purulent otorrhea, Oedema of the Retraction pouches of the TM => cholesteatoma
TM, covered in pulsating puss, Spontaneous healing after 3 In case of infection => suppurative otitis media
weeks.
Simptoms Acute inflammation with puss, edema and ulceration, necrosis & Hypoacusis ,autophonia, with serous liquid and air
perforation to TM bubbles
Produced by pyogenic cocci, through the Eustachian tube Tipically TM Retraction horizontal,Yellowish TM, “oil
soaked paper”

Diagnosis Of 1st phase: Audiometry. Rx or CT scan – fogging of mastoid Clinical exam. Audiometry. Tympanogramm
cells. Leucocitosis, After 3-4 days :perforation differential diagnosis:
of 2nd phase: Can get complicated or chronic –violent germs, ME Malformations. Otosclerosis.
perforation (non-efficient drainage), weak patient, Large Otitis or trauma sequelae . Early signs of rhinopharynx
perforations to not close. cancer

treatment AB – Augmentin, Claritromicină, Eritromicină. NSAID. Nasal Evacuation of viscous exudate from UM. Tubal
Vasoconstriction. Mucolitics. Miringotomia . EAC suction. insufflations. Transtimpanal Injections with HHC,
Instilation of AB, antiseptic Fluidifiers. Diablo type transtimpanal drainage
MIDDLE EAR inflammations: otitis media
serous: no infection\ Suppurative: infection\ Acute\Chronic)

6.OTITIS MEDIA IN symptoms Treatment\ extra

INFECTIOUS DISEASES info
Flu Mild hypoacusis, otorrhea (serus),fever, IE affliction: vertigo & SNH, violet blisters on TM NSAIDS, AB
Scarlet fever ß hemolitic Streptococcus. frequently serious, necrosis and distruction of ossicular chain
Measles germs combined with weak immunity Symptoms treat.
Difteria Rare, propagated from the pharynx. False membranes
TB Bacteria in the Sputum, Multiple TM perforations, tearing of ICA(carotid artery) in canal
Zoster oticus Affects ganglion of CN.7 through varicella vitus(chicken pox) , otalgia, vesicles, facial paralysis, Cortisone. Antiviral
smtimes when CN 8 is involved (vestibulus) it causes SNH and vestibular syndrome medication,NSAIDS,
AB
 mezotimpanis tubary otorrhea, Usually chronic serous otitis media, Chronic suppuration of ME

MIDDLE EAR inflammations: otitis media :COMPLICATIONS

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

NAME of DIAGNOSIS SYMPTOMS TREATMENT

COMLICATION
1. ACUTE Audiogramm: Transmission Hypoacusis, CT mastoid pain. Otorrhea, pavilion Surgery :radical mastoidectomy.
MASTOIDITIS fogging of mastoid cells and lack of inter-cell pushed ,purulent. Wide spectrum AB. NSIAD.
septum. Aggressive germs - Ulcer of mucosa of mastoid cells => Mucolitics, suction in the EAC
- diff diag. EAC boli, difuse otitis externa. tumors suppurative osteitis-> loss of bone septum =>
abscess opens
2.FACIAL Via: inflammation of CN.7 with oedema, Facial asymmetry, cant close eye, -emergency for cholestoma, surgery
PARALISIS compression though cholestoma involuntary movements, impaired nerve 7 repair, gold plates for upper
unilateral paralysis mastication eyelid
3.EXTRADURAL CT or intraop. Frequent complication Hemicrania crisis with orbital irradiation, Exclusivelly surgical – radical
ABSCESS: diff. diag.: Difuse septic meningitis. Cerebral fever, Meningeal irritation syndrome(pain), mastoidectomy
Colection of puss abscess Intracranial Hypertension Syndrome IHC
between bone
and dura mater
4.OTOGENIC Lumbar puncture(CSF hypertrophy), Intense headache, persistent, backpain, -massive AB, lumbar puncture,
MENINGITIS: Albuminorahia test, WBC, CT.Generated by altered general state, fever, towards exitus surgery for otitis, Perforation of
inflammation cholesteatoma or Acute suppurative otitis media. through various paralisis and finally brain- tegmen tympani
Brudzinski’s sign, triad :headache, vomiting, stem paralisis, Otogenic Destructive
constipation Labirintitis right ear Perforation of tegmen
tympani
5.CEREBRAL AND almost always cholesteatoma. Frequently BERGMANN triad: ICH syndrome, Neurosurgery, AB.
CEREBELLUM mistaken with viral, Ophtalmo and Neuro exam. Infectious syndrome, neurological
ABSCESS CT / MRI syndromes.

6.LATERAL SINUS Usually with acute cholesteatoma. Sepsis, fever, tachichardia, oliguria, Surgery: Opening of the lateral
PHLEBITIS: lucocytosic, anemia, rerto-mandibular pain sinus and suction or removal of the
thrombus. Massive AB

Complications:
6.SEQUELAE OF OTITIS

SEQUELAE OF symptoms treatment

OTITIS
1.SIMPLE SEQUELAE: Postotitic Perforation, Interruption of ossicular chain => Transmission hypoacusis miringoplasty or tympanoplasty
(HAT)
2.TIMPANOSCLEROSI Calcium Impregnation of ME mucosa and blocking of ossicular chain. Follows chronic surgery or hearing aid.
S: suppurative otitis => HAT.

3.FIBROADHESIVE Permanent tubary obstruction, resorbtion of ME air, sclerosis and retraction of mucosa. surgical for early stages. Hearing
OTITIS: Mixed hypoacusis, tinnitus, aid.
 More complications of O.Media symptoms TREATMENT
7.CHRONIC MASTOIDITIS: Complication of chronic suppurative otitis media cornice or cholesteatoma with surgery for cholesteatoma
retention of puss collection inside the cells.
8. OSTEOMIELITIS OF Rare but serious. Severe general state, sepsis. Tumefaction of temporal bone scuama : Surgical – removal of focal
TEMPORAL BONE Gets complicated frequently with meningitis infection. Massive AB.

MIDDLE EAR TUMORS:

DIAGNOSIS SYMPTOMS TREATMENT
1.GLOMUS Histological section -Benigne, vasculare structure and arterio-venous shunts->Erodes the surgical – many complications\
TUMOR OF THE through ME – inferior wall of the ME-> and breaks into the ME Radiotherapy does not destroy it but
JUGULARY occupied totally by -HAT and pulsating tinnitus (sincronized with the pulse) stops the evolution for several years.
VEIN= From chief glomic tumor (C – - Penetrates the EAC via TM – red-pinkish polyp. Bleeds easily and
cells of the cochlea, S – stapes, severely
paraganglia (glomus T - tympanum) - Evolves to the posterior foramen lacerum – compression on nv. IX,X,XI
bodies) from the and endocranial
walls of the IJV
2.ABT-LETERER- Histological. CT maligne variant of reticulosis Surgical for localized tumors.
SIWE for extensive lesions Chemo-radiotherapy & Cortisone
3.CANCER OF paralisys of nv. VII Rare. Following a Chronic Suppurative Otitis. Severe purulent Otorrhea similar to EAC cancer.
THE ME (FACIAL), that turns sanguinolent, Aboundent granulation inside the ME, Intolerable (SURGERYMOSTLY) :Surgery ,
Otalgia, Rapide and serious evolution by invasion of the endocranium (radiotherapy has poor results)

SYMPTOMS
4.RETICULOSIS: Tumors that evolve in the mastoid and exteriorise in the EAC. Mastoiditis symptoms. Especially in childre
granuloma of the ME (histiocytosis X).
5.HANS-SCHULLER- mastoid granuloma, exophtalmia, diabetus mellitus by invasion of orbita and pituitary gland (sella turcica).
CHRISTIAN

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

Malformations and trauma:

EXTERNAL EAR TRAUMA

Pavilion lacerations Pavilion pericondritis Pavilion burns, othematoma

forsbite, fracture
Symptoms manent deformity of pavilion by thickening of Frostbite : Serous-sanguinolent colection between
 peri-chondrium. Repetitive trauma Spontaneous cartilage and perichondrium. Hemisferic,
(sportsmen ), othematoma, piercings. amputation ferm, very sensitive. It gets infected or
Colliflower ear. organized
treatment surgical treatment, AB For acute–antibiotics and incision. burns: Puncture-incision and compressive dressing
(Pseudomonas aeruginosa Compressive

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:

name Signs and symprtoms treatmnet

Labirynth concussion. Discrete Sensorineural hypoacusis (SNH), tinnitus. Vertigo, imbalance. Rest, sedatives, antivertigo
medication. Disapears in days

sound trauma: 1 time exposure over 120 dB repeatedly over 90dB. SNH, Tinnitus. Audiogrametry – Hearing aid
typical notch at 4000Hz. Progressive and irretrievable
Fracture of the temporale Otalgia, bleeding from EAC, otolicvorrhea, facial paralisis VII. Transsmision AB, Cortisone, Simptom treatment,
bone Hypoacusis. SNH; vestibular periferal syndrome (destructive). Cranial and cerebral Surgical Treatment
lesions
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)
Foreign bodies: Exogenous\Endogenous (cerumen, epidermic). Biologic: inert ,or animated. Artificial Auricular douche, Water stream
(caps). towards the posterior wall of the EAC

Laryngology:
-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

Aquired: symptoms diagnosis treatment

SECONDARY LESIONS glottic oedema (post intubation) Cortisone, reintubation, tracheotomy
Granuloma of VC –surgical resection.
WHIPPLASH OF Vocal Professionals after acute IL - Echymosis of VC (rupture of vocal muscle vocal rest, warm aerosols, phoniatric
LARYNX: effort. Accentuated dysphonia treatment
during speaking
BURNS Liquids, hot vapors, corrosive pain, larynx spasm with dyspnoe, cough, Vocal rest, calming cough and pain.
substances odinophagia, dysphagia, Difuse Congestion, Instillation or aerosols with Epinephrin,
oedema, bleeding ulcerations Cortisone. Liquid food, NG Tube.
Tracheotomy
LARYNX FB: Seeds, fish bones, needles, nails. Dyspnoe – immediate and rapidly lethal. Ensuring breathing. Tracheotomy, oxygen
In epiglottis, valleculae (by dyspnoeic effort. Dysphagia. Dysphonia. therapy. Calming pain and cough.
deglutition), vestibule, -Larynx FB :peanut in glottic space (4 years old Extraction via natural ways. Maneuver
ventriculum, glottis (aspiration). patient-up), aspired needle in trachea HEIMLICH ensures breathing

Acquired Malformations:
LARYNGOCEL: LARYNX STENOSIS
Hernia of the MORGAGNI ventricle mucosa via existing paths. Mechanical Trauma with fracture or luxation, surgical
-Internal / external / mixed. or chemical.
-Sometimes filled with air, increases side in cough or VALSALVA Important respiratory and phonatory affliction
maneuver.
-dysphonia + dyspnoe.
-Extirpation - endoscopic or external approach

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

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

name symptoms diagnosis treatment
1.ACUTE OEDEMATOUS insidious dyspnea.Barking cough, Favored by: adenoiditis, smallpox, Aerosols with Efedrine and Cortisone, O2.
SUBGLOTTIC LARYNGITIS OF clear voice convulsive cough, spasmophilia, cold, Cortisone 10mg/kgc/24h and AB. IOT,
THE wet. Viral Etiology + saprophytic flora Tracheotomy
2. .STRIDULOUS LARYNGITIS inflammation of L. Added spasm. rinitis, adenoiditis – secretions run Treating naso-pharyngeal infections,
When adduction muscles relax, down into L, irritate, produce glottic Calcium, Vitamines. In crises – splash cold
breath will start again spasm. Usually anamnesis water upwards into nostrils- reflex yielding
of spasm upon contact of water to the N
3.SUFFOCATING LARYNGO- Viral, in small children 1-2 year. Congestive oedema of the airway AB high dosis, Cortisone. O2. Proteolytic
TRACHEO-BRONCHITIS OF evere state, fever, dyspnoea, cough, mucosa, purulent fibrous exudate => Enzimes. Bronchia suction
THE SMALL CHILD difficult expectoration. fibrous plugs, atelectasis.Evolves to
(CHEVALIER JACKSON) exittus, reserved prognosis
4.OEDEMTOUS LARYINGITIS: by pyogenic germs with Oedema in uremia. inophagia, FB
Oedematous lesions post sensation, reflex otalgia, irritative
radiotherapy. Allergic oedema. cough. Dysphonia followed by
Altered general state, fever dyspnea. IL – reddish mucosa, oedema,
sometimes gelo-like, reduced lumenum
ABSCESS AND PHLEGMONA High fever, altered septic state, Admission, AB, surgical opening of
OF LARYNX (EPIGLOTTIS painful dysphagia, LN. Red oedema collection
of epiglottis +/- obstruction
PERICONDRITIS AND After epiglottitis, surgery, AB, HHC, AINS, drainage. Usualy
CONDRITIS radiotherapy, long-term intubation . important sequelle
External Tumefaction, palpable and
internal tumefaction.
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

.1.DIPHTERIA Most frequent localization. Fever, headache, palor, asthenia, tachycardia. Serum anti-diphteria + Penicillin.
diphteria patients and healthy Subangulomandibular lymphnodes. congested tonsils, Immediate admission
carriers, via saliva, cough or covered in yellowish or white-grey spots that join =>
sneeze (PFLÜGGE‘S drops). false membranes (difficult to dettachand leave a
Incubation 2 – 11 days bleeding area) Membranes extend to the veil, pillars,
posterior wall, larynx, rhinopharynx, NF
2. SCARLET Cause: Streptococc ß hemolitic headache, vomiting, fever, odinophagia, swollen Mandatory admission. Penicillin
 FEVER (see otitis with eritrogenous toxine lymphnodes. Strawberry tongue
media)
3. MEASLES 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 2 nd 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 superficial ulcerations. Very painful. Healed in 10-16 days. Herpes simplex labialis – bundles of vesicles on congested area on upper
SOARES) and lower lip
9. QUINCKE’S in atopic patients (allergies). Risk of asphyxia. Treatment extreme emergency- Epinephrin 1% i.v., Cortisone, Antihistamin,
OEDEMA Tracheotomy if needed
10. TOXIC Hg, Bi, Au, I, Bromide, P, Pb, Belladonna. Congestion and oedema of pharynx
PHARYNGITIS
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)

Acute specific tonsillitis

ACUTE NONSPECIFIC TONSILLITIS

symptoms Cause and diagnsois treatmeant
ACUTE Respiratory viruses Difuse, superficial Cause:Cold weather, pollution, cold drinks, promiscuity Warm dressing on neck,
CATARRHAL inflammation. Sudden onset, frisson, dig: Viral Exam only in epidemics mouth rinse with local
TONSILLITIS fever, headache, convulsions in disinfectants, cough drops.
children Dry throat, odynophagia NSAIDS. rest
ACUTE Less contagious than viral. more Cause: bacterial, Leucocitosis and neutrophilia + bacterial throat : AB antistreptococcus
BACTERIAL severe than above. fever, cultures. Forms: (Penicilina, Eritromicina).
TONSILLITIS odynophagia. tumefied tonsils, 1. Severe: large lymphnodes, uvula oedema, severe gen. state. Benzatin penicilina
congested, creamy white-yellow 2.Alimentary: with streptococc ß hemolitic transsmited via unboiled (Moldamin). Rest, admition
deposits, nonadherent to the crypts. cow milk. severe manifestations, often epistaxis into Infectious Disease
Subangulomandibular, painful 3. Pseudo-membranous: membrans detach easily and do not spread department. Treatment
lymphnodes beyond the tonsil locally
4. Ulcerous: very severe, extremely virulent germs and weak immunity
3. PLAUT- : Ulcero-necrotic, unilateral. Tonsil Cause: Usually in patients with bad oral hygene : AB – penicillin.
VINCENT ulceration on a dirty base, necrotic,
TONSILLITIS irregular rims odinophagia –
unilateral, moderate, low fever,
severe asthenia
ACUTE Inflamation of the pharyngeal tonsil Cause: common flora. Usually after viral infection AB. Nasal dezobstruant.
ADENOIDITIS: LUSCHKA. muco-purulent secretions complications: Acute catarrhal or suppurated otitis media \ AINS
flow on the posterior wall of pharynx. Stridulous Laringitis \ Retrofaringeal Adenophlegmon
tumefaction of pharyngeal tonsil with
puss deposits

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: or hyperkeratosis (precancer state).Dysphonia. Cough, tired voice

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

NONSPECIFIC CHRONIC PHARYNGITIS

name symptoms Cause and diag. Treatment

1.CHRONIC PHARYNGITIS Chronic nasal /rhinopharynx obstruction, Iritants (smoking, alcohol, spicy food, Pharynx disinfectants,
Catarrhal\Hypertrophic \ Dryness, FB sensation, stinging, irritative pollution). Gastroesophageal reflux Aerosols, sprays , vitamins
Atrophic cough, adherent secretion. Pharyngitis in
ozena: atrophic, dry mucosa, crusts
2. CHRONIC ADENOIDITIS When hypertrofic = VEGETATIVE Inflammation of LUSCHKA tonsil. Surgical –
ADENOIDS. nasal obstruction, trouble Main complication = SEROUS OTITIS MEDIA Adenoidectomy.
sleeping, snoring, sleep apnea. muco- Breathing exersize
purulent secretions. Adenoids Facies Tired
child, sleepy,
3. CHRONIC TONSILLITIS acute bacterial tonsillitis. asthenia, low Cause: repreated acute tonsillitis, adenoids, Tonsillectomy
fever. Kissing tonsils with possible buco-dental inflammation, wet and cold
breathing and swallowing impairment climate, cold drinks
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

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

Chronic specific pharyngitis

1.PHARYNX TUBERCULOSIS

1.PHARYNX TUBERCULOSIS:
1. Pharyngeal Lupus: No pain. Produces important distruction slowly. 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: children. Tonsil Hypertrophy, pale mucosa, cervical lymphnodes. IDR positive
5. Coled Abscess bone Tuberculosis of the vertebra body (morbus POTT). not inflammatory signs
(cold) CT in axial view, with contrast – bulging of posterior

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.