بسم هللا الرحمن الرحيمENT for medical students Dr. Adel Adwan Prepared by: Aya Abukhalil Salah Eldeen Al-Quds university 2010/2011 2 The ear Ear anatomy: Ear is divided into 3 parts: 1. External ear 2. Middle ear 3. Inner ear 1. External ear: Composed of: a. Auricle (Pinna) : It is composed of cartilaginous part (upper 3/4) & fibro fatty part (lobule) Anatomy : b. External auditory canal: S shaped tube extending from the auricle to the tympanic membrane (25 mm). It is pulled backward upward when examining adults and backward downward when examining children. It has two parts: Cartilaginous part (outer one third): it has thick skin that contains piloseboceramen apparatus: hair follicles, sebaceous glands & ceramen glands (that produce wax). In this part there is more incidence of otitis media. Sometimes infected sebaceous glands is found in it. Bony part (inner two thirds): it has thin smooth skin adherent to the bone, so any manipulation or minimal trauma (such as cotton swab) may cause injury. It may contain modified sweat glands that secret yellowish to brown wax (seroma glands). Type of skin in the external auditory canal is keratinized squamous epithelium. It has 2 areas of stenosis: 1. At the end of the cartilaginous part. 2. 0.5 cm lateral to the tympanic membrane. ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen 3 Ink spot test is done to examine the function of the cilia, put ink spot on tympanic membrane, after 5-6 mo will be seen on the external ear. c. Lateral (outer)surface of the tympanic membrane: It is the outer layer of the tympanic membrane which is composed of skin of keratinized squamous epithelium. Tympanic membrane (TM): It is 1 cm in diameter It is formed of 3 layers: - Outer layer (Lateral layer): skin of keratinized squamous epithelium. - Middle layer (B/w the Lateral & Medial): fibrous layer. - Inner layer (Medial layer): respiratory mucosa (Pseudo-stratified squamous ciliated mucosa). Theses 3 layers are found in Pars Tensa (4/5 of the TM, it is easily ruptured because it is tight), but the fibrous layer is absent in Pars Flaccid (1/5 of the TM). TM is obliquely placed, facing downward forward and laterally. Concave laterally and at the depth of concavity is small depression (the Umbo) produced by the tip of the handle of Malleus. It is extremely sensitive to pain and is innervated in its outer surface by supplied by Auriclotemporal nerve and auricular branch of Vagus. We use the pneumatic otoscopy to measure the TM mobility. On otoscopy: hold it like a pencil, pull the Pinna upward backward in adults and straight backward or backward downward in infants: 1. Color: white gray to pale gray. 2. Pars tensa forming the lower 4/5 of the tympanic membrane. 3. Pars flaccid forming the upper 1/5 of the tympanic membrane. 4. Light reflex “Con Flight” from austachian tube. 5. Handle of malleous and umbo on its tip which is the most tense area. 6. Lateral process of the malleus (the short process). 7. Anterior and posterior malleolar folds. 8. - Mobility of the tympanic membrane is in the range of 1 mm, examined by: Pneumatic otoscope Swallowing during examination : swallowing causes negative middle ear pressure & movement of the tympanic membarne Valsalva maneuver during examination Tympanometry: Objective method ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen Incus Stapes . two muscles(stapedius muscle "innervated by nerve to stapedius. Stapes). Mastoid air cells (Air containing cavity in petrous bone of temporal bone). Incus. a branch of mandibular division of trigeminal nerve"). c. E: Umbo. D: manubrium of malleus. Aditus ad antrum (mastoid antrum) : canal between middle ear and mastoid air cells. Adel Adwan . Ossicles: Malleous ENT. d. a branch of facial nerve". Eustachian tube (auditory tube). Middle ear: Composed of middle ear cleft which contains: a. Dr. there is only mucosa lined with Pseudo-stratified columnar ciliated mucosa (respiratory mucosa). B: short process of malleus. Tympanic cavity itself including: ossicles (Malleous. normally there is No skin. two nerves (horizontal and chorda tympani branches of the facial nerve). In the middle ear. b. F:light reflex. The rest are not important ! 2. C: pars tensa. tensor tympani muscle "innervated by tensor tympani nerve.4 A: par flaccid. Levator veli palatini: innervated by pharyngeal plexus mostly vagus nerve. Dr.5 Malleous and incus are derived from the first branchial arch. Incudomalleolar joint between Incus & Malleous. Adel Adwan . Incudostapedial joint between Incus & Stapes. 3. Muscles that open the Eustachian tube: 1. Opening involves cartilaginous portion. ** Function of Eustachian Tube: Protection from nasopharyngeal secretions Clearance of middle ear secretions Ventilation (pressure regulation) of middle ear Physiology of hearing: The middle ear transforms air waves to fluid waves. It has two parts: Proximal 1/3 is bony & distal 2/3 is cartilaginous. Usually closed. Salpingopharyngeus: acts during yawning. innervated by the trigeminal nerve. so any patient with mandibular problem such as mandibular aplasia. 2. Lined with respiratory mucosa & has mucous producing cells and ciliated cells. opens during swallowing. Tensor tympani: innervated by trigeminal nerve. innervated by pharyngeal plexus mostly vagus nerve. 4. you have to suspect middle ear disease or pathology.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . is wider and shorter & straighter than in adults whose Eustachian tube is J shaped. Tensor veli palatini: has the main action. ENT. ** Eustachian tube in children has longer bony portions. Foot plate is attached to the oval window Eustachian Tube (Auditory tube): Connects middle ear and nasopharynx. Stapes is derived from the second branchial arch. 2. There are joints between the ossicles: 1. Inner ear Composed of: a. It is similar to the extracellular fluid (low potassium. 2. Semicircular canals: Anterior (or superior). Adel Adwan .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Vestibule 3.2 otolith organs "utricle & saccule" that are sensitive to linear (or straight-line) accelerations. It consists of 5 distinct end organs: . The vestibular fluids: Perilymph: In the bony labyrinth. consists of: 1.3 semicircular canals that are sensitive to angular accelerations (head rotations) . Utricle and saccule ( in the vestibule): They are sensitive to linear acceleration 3. ENT. The vestibular system It lies in the otic capsule in the petrous portion of the temporal bone.6 3. making 2 3/4 turns around its axis). Lateral (or Horizontal) & Posterior semicircular canals. Bony labyrinth. Cochlea (spiral shaped. Semicircular ducts (in the semicircular canals): They are responsible for angular acceleration. Physiology of hearing: The inner ear transforms fluid waves to electrical waves. consists of: 1. b. 2. Organ of corti (in the cochlea) : The sensory organ of hearing. high sodium). Dr. Membranous labyrinth (which is found inside the bony labyrinth). In respone to depolarization voltage-gated Ca+2 channels are activated allowing for Ca+2 influx and the subsequent liberation of transmitters to produce an action potential. Minute filaments connect the Tip of each sterocilium to the Next longer cilia and finally to kinocilium . Dr. low sodium). Otoliths are mineral and protein particles embedded in the otolith membrane (Calcium Carbonate crystals). When stereocilia bend to the direction of kinocilium. It is continuous with the endolymph of the cochlea. The ciliary bundles of the hair cells project into the overlying gelatinous matrix known as the otolith membrane. it results in opening of K+ channels at the tip of the stereocilia. The otolith organs: Utricle & Saccule ** The sensory organs of the utricle and saccule are the maculae. Each macula consists of hair cells and supporting cells.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . allowing K+ ions to enter and depolarize the hair cell. ENT. and the stereocilia gradually become shorter. Adel Adwan . Macula: It consists of supporting cells and hair cells. It detect and respond to the position of the head with respect to linear acceleration and pull of gravity Each macula contains thousands of hair cells that synapse with sensory endings of vestibular nerve Each hair cell has 60-80 small cilia called stereocilia plus one large cilium called kinocilium The kinocilium is always located in one side. It is secreted by epithelial cells continuously and drains from the inner ear into the venous sinus in the dura mater of the brain. It is similar to the intracellular fluid (high potassium.7 Endolymph: In the membranous labyrinth. In the saccule. forward-backward movement. When the head is upright. bending of stereocilia in the opposite direction (backward to the kinocilium ) reduces the tension on attachments and this closes the ion channels causing receptor hyperpolarization and inhibition of the cell. Stimulated hair cells signal nerve fibers resulting in impulses traveling to the CNS on the vestibular branch of the vestibulocochlear nerve and informing the brain of the head’s new position. left-right movement. the hairs project upward into the gelatinous material. maccula lies in the horizontal plane of the inferior surface of utricle so it determines the orientation of the head in upright position. backward. In the utricle. combination). or to one side. senses motion in the horizontal plane(eg. macula lies in the vertical plane and senses motions in the sagittal plane (eg. ENT.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . When the head bends forward. the hair cells are stimulated as the gelatinous material of the maculae sag in response to gravity causing the hair to bend. up-down movement). Brain responds by sending motor impulses to skeletal muscles to contract/relax to maintain balance. Dr.8 Conversely. Adel Adwan . Adel Adwan . The basal membranes of the hair cells synapse on the sensory neurons of the vestibular nerve. the ampulla. The crista consists of a gelatinous mass. Embedded in the cupula are the cilia of hair cells. Nerve fibers send impulses to the brain – cerebellum Analysis of information allows the brain to predict the consequences of the rapid body movements and signal appropriate skeletal muscle to maintain balance. The ampulla contains a sensory receptor called crista ampullaris. Rapid turns of the head or body stimulate the hair cells of the crista ampullaris. Dr. Crista ampullaris: Detect and respond to angular acceleration & deceleration of the head.9 The semicircular canals Lateral or horizontal. Oriented at right angles to one another. Anterior or superior and Posterior. the cupula.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . The semicircular canals are connected to the utricle at their bases. At the end of each canal is an enlarged chamber. depolarizing the cells. ENT. Appropriate rotation of the head in one direction bends cilia in the opposite. ** The sensory organ of the semicircular duct is crista ampullaris. If the head movement is to the right.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . the cupula in the right horizontal canal is pushed away from the kinocilium. ENT. resulting in opposite changes in their firing rates. Adel Adwan . For example. while those on the other side are hyperpolarized. For example. the hair cells in the canal towards which the head is turning are depolarized. the cupula is pushed toward the kinocilium in the left horizontal canal. which has its hair cells aligned oppositely There are three such pairs: the two pairs of horizontal canals. the orientation of the horizontal canals makes them selectively sensitive to rotation in the horizontal plane. Dr. and the superior canal on each side working with the posterior canal on the other side Head rotation deforms the cupula in opposing directions for the two partners. the result is just the opposite. and the firing rate of the relevant axons in the left vestibular nerve increases. with a concomitant decrease in the firing rate of the related neurons. when the head turns to the left.01 Each semicircular canal works in concert with a partner located on the other side of the head. In contrast. More specifically. Tenderness means otitis extena .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . o Moist keratin debri otitis externa o Moist dirty mass Fungus : Candida albicans. Aspergillus niger (most common one) o Mucoid or mucoperulent discharge Chronic or acute otitis media. Palpate the auricles for: Tenderness Pre or Post auricular swelling or tenderness.00 Ear Examination: Inspect the auricles for: Shape Redness Swelling Ulceration Tumors Fistula Retroauricular skin. Adel Adwan . o Perforated: Central / Marginal. which is S shaped. Preauricular fistua Postauricular fistua : First branchial clet fistula type I which opens in the middle ear & First branchial clet fistula type II which opens in the external auditory canal. o Atrophic retrscted with prominent handle of malleus in long standing negative pressure Secretory or adhesive OM. Dr. by this movement you find out whether there is tenderness or not. Using the Otoscope. inspect the tympanic membrane (Remember the normal land marks!!). o Thick with calcification white in color Myringosclerosis (due to recurrent OM or multiple ear surgeries ). all are normal). Inspect the external canal: Pull the auricle upward backward in adult or backward downward in infants and young children to see the external canal. Aspergillus flavus. OM causes also a reduction in the mobility of the tympanic membrane. Ear discharge: o Brown mass Wax (& can be gold or even black. & examine for the mobility of the tympanic membrane. o Red congested Acute otitis media (OM). ENT. Fibrous polyps.02 o Scanty offensive perulent discharges Cholesteatoma o Clear fluid CSF . Weber's test: place the vibrating tuning fork (512Hz) in the midline on the forehead or upper central incisors. the fork is then immediately placed opposite to the external canal. . Mixed: fibrous-inflammatory polyps. Halo sign : Non specific 2. Inflammatory polyps. 2. How to confirm that it is CSF ? 1. 3. 2. Beta-2 transferrin : Found only in CSF so it is the most accurate & specific one. viral otitis media. o Bleeding trauma.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . The patient may hear: .Better in the normal ear = sensory neural hearing loss. Three types of polyps: 1. tumor. .Equal in both ears = normal. so any inflammation in the middle ear can cause polyp. Dr.Rinne positive: the air conduction is better than bone conduction= normal hearing or sensorineural hearing loss. and traumatic rupture of tympanic membrane. Rinne's test: place the vibrating tuning fork (512 Hz) initially on the mastoid process until sound is no longer heard. Special tests: Tuning fork tests: Weber's test Rinne's test 1. BC > AC = Conducive hearing loss ENT.. Adel Adwan . Glucose level : Non specific 3.Better in the diseased ear = conductive hearing loss. o Serosangious discharge Polyp. AC > BC = Normal or Sensorineural hearing loss - Rinne negative: the bone conduction is better than air conduction = conductive hearing loss. . Polyp: Pediculated portion of edematous mucosa. and the thresholds are recorded on a graph called an audiogram. The testing procedure is repeated at specific frequencies from 250 to 8000 hertz for each ear. . Bone conduction testing is done by placing an oscillator on the mastoid process and measuring threshold at the same frequencies. The unit of sound measurement is decibel (dB). Dr. Adel Adwan .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen > 90 db (profound hearing loss) is an indication for cochlear implantation. The audiogram is a graph depicting hearing thresholds in decibels and frequency in hertz.03 Audiometry: Pure Tone Audiometry (PTA): Subjective method of testing hearing. Degrees of hearing loss: 0-15 dB Normal hearing 16-25 dB Slightly hearing loss 26-40 dB Mild hearing loss 41-55 dB Moderate hearing loss 56-70 dB Moderate-severe hearing loss 71-90 dB Severe hearing loss > 90 dB Profound hearing loss Conductive hearing loss: - Bone Conduction (]) : within normal (0-15 dB) - Air conduction (X): Abnormal - Air-Bone gap > 10 dB Sensorineural hearing loss: - Bone conduction (]): Abnormal - Air conduction (X): Abnormal - Air-Bone gap < 10 dB ENT. It is performed by presenting a pure tone to the ear through an earphone and measuring the lowest intensity in decibels (dB) at which this tone is perceived 50% of the time. This measurement is called threshold. generates a pure tone. and measures the TM mobility in response to the sound at different pressures. TM mobility. Type A tympanogram: represents normal middle ear function. adhesive OM. Normal TM mobility ≈ 0 mm. Tympanogram is the graphic picture that results as the pressure is varied against the TM. atelectatic ear. Eustachian tube function & stapedial reflex. ossicular chain function.04 Mixed hearing loss: - Bone conduction (]): Abnormal - Air conduction (X): Abnormal - Air-Bone gap > 10 dB Tympanometry: Objective method of testing middle ear pressure. Normal middle ear pressure: 0 ± 100 mm H2O. Type B tympanogram: represents restricted tympanic membrane mobility (reduced compliance). The test is performed by inserting the tympanometer probe in the external auditory canal. Dr. chronic OM with perforation. Adel Adwan . Type A curves have normal mobility and pressures and typify normal hearing and sensorineural hearing loss with normally functioning middle ear systems. The instrument changes the pressure in the ear. secretory OM. hemotympanium.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . This curve is very typical of a stiff middle ear system as is seen in acute OM. ENT. Type C curves have normal mobility but it needs higher pressure. Functional assessment of the Eustachian Tube.B.I : e.intact membrane or dry perforation.g: MRI Cholesteatoma protocol to confirm cholesteatoma although it can be seen through the otoscope. Type As tympanogram: represents normal middle ear pressure but reduced mobility suggesting limited mobility of the tympanic membrane and middle ear structure. Dr. commonly seen in fixation of the ossicular chain.R.Valsalva's test.T brain and skull base with or without contrast M. -Tympanometry – for both .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .05 Type C tympanogram: represents significant negative pressure in the middle ear cavity. . Adel Adwan . A. Type Ad tympanogram: represents normal middle ear pressure but hypermobility. ENT. This pattern is indicative of a flaccid tympanic membrane due to disarticulation of the ossicular chain or partial atrophy of the eardrum.R ( Auditory Brainstem Response ) Conventional x-ray mastoids C. needs incision and drainage then pressure to prevent the formation of hematoma again. - It is an emergency. Adel Adwan . - The most common cause is combined. - 2. Otohematoma or aurohematoma: - It is caused by trauma or frost bite. because of the risk of necrosis and cornflower ear. - It is dangerous because cartilage receives its blood supply by perfusion from perichondrium so it results in malnutrition to the cartilage. Furuncle: - It is abscess in the hair follicles or sebaceous glands. - Patients may present with swelling in the retroauricular area or concha. Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . - It is an indication for admission and give antibiotics for gram negative & gram positive bacteria. nasal cartilage or auricule. - It is treated by incision & drainage and antibiotics. - It can be local perichondritis or systemic perichondritis. which may involve laryngeal cartilage. ENT. such as autoimmune perichondritis (so do RF & ANCA). It occurs more commonly in psychotic patients. gram negative bacteria - An emergency. - The most common cause is Staphylococcus aureus. 3. o Systemic perichondritis.06 Diseases of the external ear Diseases of the auricle 1. necrosis and ear deformity (cornflower ear). - It collects between the perichondrium and the cartilage. Perichondritis: - It is inflammation of the perichondrium. - There is dirty moisty foul smelling material. - Treatment: Clearance. give systemic antifungal. 3. put a wick. protection from water exposure & topical antifungal such as nystatine or ketoconazole (This is for the mentioned noninvasive infections). white in Candida. Fungal otitis externa (otomycosis): - Aspergillus species are the commonest cause. earache. Proteus. amphotricine B. Otalgia. - There is keratin containing discharge (whitish moist debri). give systemic antibiotic covering gram negative. difficulty in opening the mouth. - Treatment: Clearance. such as in the immunocompromised patients. Dr. severely stenosed external auditory canal due to edema.07 Acute otitis externa There are 8 types: 1. - Patients present with severe pain. Acute diffuse otitis externa (swimmer disease): - There is a history of water invasion or trauma. - Patients present with hearing loss. E. dryness. coli but can be caused by Staphylococcus aureus. 2. give topical antibiotics (such as quinolones)& corticosteroids for edema. - If invasive fungus. severe pain and tenderness. Herpetic otitis externa (herpes oticus): - It is caused by herpes virus. If not responding to topical treatment. which is a triad of: Vesicles on the tympanic membrane or in the external auditory canal. tinnitus. mainly Aspergillus flavus & Aspergillus niger. - Mostly caused by gram neg. Sometimes we may see the hyphae of the fungus in the external auditory canal. - Presents as a part of ramsay hunt syndrome. yellow in Aspergillus flavus & black in Aspergillus niger. bacteria: Pseudomonas. severe tenderness on examination. Adel Adwan .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . But it can be caused by Candida. Sensori neural hearin loss. ENT. or nystagmus. - Treatment: Clearance. Eczematous otitis externa: - Treatment: Topical corticosteroids and antibiotics 6. - It may lead to osteomyelitis of bone or intracranial complications. - It is usually caused by Gram negative bacteria: Pseudomonas. - Treatment: Cauterization of the granuloma with silver nitrate or topical corticosteroids and antibiotics. topical antibiotics & corticosteroids 5. treatment with high dose dexamethasone as early as possible. Granular myringitis: - It usually occurs after trauma to the lateral layer of the tympanic membrane or after the insertion of ventilation tubes that results in the formation of a granuloma. Myringitis bellousa hemorrhagica: - There is usually a history of URTI. - It is thought to be caused by viral infection or Mycoplasma. - Treatment: Acyclovir 800 mg X 5 times at least for 7 days. 7. 4. ENT. vertigo. Dr. Adel Adwan . 8.08 & may be associated with facial palsy. Seborrhoic otitis externa: - It is infection in the sebaceous glands. patients taking chemotherapy & AIDS. If facial palsy is present. - It affects immunocompromised patients. E. bulla of blood on the tympanic membrane. - Patients present with pain and ear fullness. - Treatment: Macrolides (erythromycin) for 7-14 days.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . coli or Proteus. - Patients present with severe pain. mostly diabetic patients or patients with nephritic syndrome taking steroids. measles or chickenpox. Necrotizing otitis externa (Malignant otits externa): - It is a severe form of acute diffuse otitis externa. - Treatment: Antibiotics for gram negative bacteria. Any diabetic patient with otitis externa should be admitted to the hospital (DM is an indication for admission).Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Dr. Adel Adwan . such as ceftazidime. ENT. meropenim or quinolones (such as ciprofloxacin) at least for 21 days. but may continue to 8 months.09 - Test of choice to detect the presence of osteomyelitis is bone isotope scan. Young age Bottle feeding Pacifier Day care attendance Caretaker smoking Craniofacial anomalies Genetics tendency Allergic disease Immunodeficiency ENT. Nonsuppurative There is No pus b. unilateral secretory OM is nasopharengeal carcinoma until proven otherwise. there is central perforation & is not associated with cholesteatoma. Subacute: 3 weeks-3months (or up to 90 days) a. Suppurative: . 4. cleft palate. Dr.Type 2 (Unsafe type): atticoantral type. 2. Epidemiology: Account for almost 1/3 of the office visit to pediatricians Peak incidence 6-24 month of life More common in boys and in low socioeconomic persons Incidence increased in children with: HIV . trisomy 21 Risks factors: 1. 7. 5. there is marginal or peripheral perforation & is associated with cholesteatoma.Type 1 (Safe type): Tubotympanic type. Chronic: More than 3 months (or more than 90 days) a.21 Diseases of the middle ear Otitis media Definition: Inflammation of the middle ear cleft (( not middle ear cavity)). 8. 2. 6. Classification: 1. . 3. Suppurative There is pus & indicates tympanic membrane perforation. Nonsuppurative :(AKA: Secretory OM / Serous OM/ Exudative OM/ OM with effusion (OME) / Blue ear) ** In adults. Adel Adwan . Acute: less than 3 weeks (or one month roughly) a. 9. b.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Nonsuppurative b. Suppurative 3. Rhinovirus. Decreased mobility is the most important sign. a negative pressure is generated. Air bubbles behind the tympanic membrane. If growth is rapid. normal or hypomobile.20 Pathophysiology Acute otitis media usually arises as a complication of a preceding viral upper respiratory infection (URI). of bluish tympanic membrane: 1. 3. bulging of membrane. D. Microbiology 1. hearing loss. Dr. Influenza viruses.pneumonia 50% H. change colour. the middle ear mucosa absorbs air in the middle ear. a middle ear infection develops. otalgia. Can be with nausea. 2. 80% bacterial: S. 5. Long standing secretary otitis media (SOM).D. Diagnosis Acute OM: Hx: preceding URTI. 5. 3. Shows loss of all normal marks on tympanic membrane. which pulls interstitial fluid into the tube and creates a serous effusion. Parainfluenza. Bluish ear drum. In neaonate: irritability. Tympanic membrane mobility loss. 4.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 3. Adel Adwan . The secretions and inflammation cause a relative obstruction of the eustachian tubes ( eustachian tube dysfunction). Para ganglion tumors: like para carotid tumor (chemodectoma or glomus jugulare tumor "glomus tympanicum"). This effusion of the middle ear provides a fertile media for microbial growth. is the gold standard. Bulging tympanic membrane. poor feeding. If this air is not replaced because of obstruction of the eustachian tube. Normally. Late stages of otosclerosis that gives red reflex (Shwartz’s sign). 2. Exam: pneumotic otoscopy. vomiting and diarrhea. Retraction of tympanic membrane (prominent handle of malleus). 2. Halo’s sign might be positive due to CSF otorrhea detected by B2 transferrin test. Chronic OM with effusion: otoscopy showes: 1. 6. otorrhea. fever.catarrhalis 12% Group A strep 2-4% 20% viral: RSV. 4. vomiting. ENT. tugging at ear. 4.influenzae 25% M. Hemotympanum: it is a skull base fracture until proven otherwise. diarrhea. Air fluid level behind the tympanic membrane. Dehiscence: high jugular bulb. facial paralysis. SNHL or mixed). The most common cause of hearing loss is otitis media. ampicillin. 2nd or 3rd genaration cephalosporin(oral). TM perforation.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . ME pathology. mastoiditis. brain abscess. frequency. IM ceftrixone Acetaminophen and ibuprofen for fever Recurrent AOM Chemoprophylaxis o Sulfisoxazole. cholesteatoma. Intracranial: meningitis. Dr.22 Acute OM Chronic OM with effusion Treatment Acute OM 1st line therapy is amoxicillin (high doze 80-90 mg/kg/ day in 2 divided doses) 2nd line therapy amoxicillin/clavulanic acid. PNC Myringotomy and tube insertion Adenoidectomy OME (OM with effusion) MEE > 3 moths or associated hearing loss. adhesive OM. ENT. amoxicillin. discomfort Antibiotics Antibiotics + steroid o 21% improvement compared to ATB alone o prednisone 1 mg/kg day x 7 days Myringotomy & tympanostomy +/. lateral sinus thrombosis. Adel Adwan . subdural empyema.adenoidectomy Complications: Intratemporal: hearing loss (CHL. extradural abscess. vertigo. labryrinthitis. The most common complication is mastoiditis. Recurrent acute OM: brings to chronic changes in middle ear and tympanic mucosa. Occasionally pain. Nasal decongestant to prevent Eustachian tube dysfunction. 2. Ear protection from water.23 TM perforation Pathogenesis 1. Traumatic perforation. ENT. 2. Prognosis: Central perforation has better prognosis than peripheral perforation. Chronic OM (subtotal perforation) Total perforation Traumatic perforation Symptoms: 1. If not closed after 3 months.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 4. 2. Antibiotic for 7 days is controversial. Recurrent otorhea. Perforation of pars flaccid has worse prognosis than pars tensa. Hearing loss (conductive). Wait for 3 months to close spontaneously (90% of heals spontaneously). 3. although not affecting hearing initially. 5. Treatment: 1. 3. Dr. do tympanoplasty. leading to perforation. Adel Adwan . Perforated lose 20% of its hearing capacity. there is Eustachian tube dysfunction.24 Cholesteatoma: Definition: Chronic O. 2. inner ear. Cholesteatoma is dangerous. ** a & b are more common than c. b. { In the middle ear. invades middle ear and mastoid structures. there is only mucosa lined with Pseudo-stratified squamous ciliated mucosa (respiratory mucosa)}.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Acquired: 3 theories: a. with accumulation of keratin and debris in middle ear and mastoid. Secondary: Migration theory: where there is marginal perforation in the tympanic membrane allowing the skin to enter to the middle ear (migrate). Pathogenesis: Collection of keratin where it is normally not found (epidermis in a wrong place). Treatment: Mastoidectomy ENT. Metaplasia of the respiratory mucosa to keratinized squamous epithelium. c. normally there is No skin. Primary: Retraction pocket theory: In any middle ear pathology. resulting in a negative middle ear pressure causing the tympanic membrane to be pulled medially mostly at the pars flaccid (retraction). Therefore. due to enzymatic activity in the cholesteatoma which causes destruction to the bone leading to facial palsy. Dr. Complications: Slowly destructs ossicles. it needs aggressive treatment ! There are two types: 1. invades CNS. facial canal. Adel Adwan .M. & may eventually reach the brain causing brain abscess. Congenital: Remnant of the neural tube (ectoderm) in the middle ear due to neural tube defect. Adel Adwan .sporadic.hereditary. Letterer-Siwe disease. Treatment: Stapedectomy. suggesting hormonal factor as etiology. 50% . Eosinophilic granuloma. Most frequent between stapes footplate and oval window. Hand-Schuller-Christian disease. Symptoms: Progressive mixed hearing loss.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Pathogenesis: Osteolysis followed by new osteogenesis. Rare in osteogenesis imperfecta (bleu sclera). b. c. ENT. Can be caused by histocytosis X: a. Dr.25 Otosclerosis Normal stapes Otosclerosis Definition: Sclerosis of the joints between the ossicles. 50% . Male: Female 1:2 Undergoes progression during pregnancy. Secretory OM. as gentamycine is vestibulotoxic. Acute mastoiditis. 4. 5. 8. To diagnose otitis media in patients younger than 8 months of age. Myringotomy: It is a surgical procedure in which a small incision is made in the eardrum (the tympanic membrane Indications of myringotomy: 1. Retracted tympanic membrane. ENT. 6. 4.26 Middle ear surgery Myringotomy & Grommets (ventilation tubes): The most common middle ear surgery. In the immunocompromised child. Injection of steroids to treat sudden sensorineuronal hearing loss in patients with DM or HTN (can't use systemic steroids). Eustachian tube dysfunction.g. Acute mastoiditis. Indications of ventilation tubes: 1. 2. Dr. 3. which cause malfunction of the tensor veli palatine muscle). 3. Secretory OM.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 7. ≥ 3 times/6 months or ≥ 4 times/12 months. Adel Adwan . Craniofacial anomalies that predispose to middle ear dysfunction (e. Recurrent OM. Injection of gentamycin to treat vertigo such as in Ménière's disease. cleft Palate. 2. 27 Tympanoplasty +\- ossiculoplasty : Tympanoplasty Grafts used: fascia (temporalis fascia; the mostly used), cartilage, perichondrium, periosteum. *** Skin is NOT used as graft here because it causes cholesteatoma. Goals of surgery: 1. Establish an intact TM. 2. Eradicate middle ear disease and create an air-containing middle ear space. 3. Restore hearing by building a secure connection between the ear drum and the cochlea. Types of tympanoplasty: 1. Type I tympanoplasty is called myringoplasty, and only involves the restoration of the perforated eardrum by grafting. 2. Type II tympanoplasty is used for tympanic membrane perforations with erosion of the malleus. It involves grafting onto the incus or the remains of the malleus. 3. Type III tympanoplasty is indicated for destruction of two ossicles, with the stapes still intact and mobile. It involves placing a graft onto the stapes, and providing protection for the assembly. 4. Type IV tympanoplasty is used for ossicular destruction, which includes all or part of the stapes arch. It involves placing a graft onto or around a mobile stapes footplate. 5. Type V tympanoplasty is used when the footplate of the stapes is fixed. ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen 28 Types of incisions: 1. Retroauricular incision. 2. Endoaural incision. 3. Transmeatal incision: in the external auditory canal, 6 mm from the tympanic membrane. Incision is made from 12 o'clock to 6 o'clock. Refreshment of edges of TM Elevation of tympanomeatal flap Insertion of the graft below the flap Repositioning the tympanomeatal flap ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen 29 Tympanoplasty with ossiculoplasty Incus interposition: Cartilage is taken from the auricle and shaped like the incus, then it is placed between the malleus and stapes. PORP: Partial Ossicular Replacement Prosthesis. Prosthesis is placed between the head of stapes and TM. TORP: Total Ossicular Replacement Prosthesis Prosthesis is placed between the stapes footplate and TM. ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . the ossicles and chorda tympani. Combined approach tympano-mastoidectomy: Stapedectomy Involves removal of the anterior and posterior crura of the stapes. Radical mastoidectomy: involves removal of the mastoid air cells. Modified radical mastoidectomy: involves removal of the mastoid air cells with reconstruction of the TM (Tympanoplasty) and preservation of the ossicles. replacing it with a prosthesis between the incus and footplate and creating fenestrations in the footplate. done for acute mastoiditis. the TM.31 Mastoidectomy Simple mastoidectomy/ Cortical mastoidectomy/ Schwartz mastoidectomy: involves removal of the mastoid air cells only. ENT. Adel Adwan . Dr. autonomic symptoms. or systemic diseases.Brainstem characteristics. Onset: .Sudden onset of vertiginous episodes are often due to inner-ear disease. It reaches 40% in patients older than 40 years. Dr.Vertigo of sudden onset that lasts for minutes can be due to brain or vascular disease. nausea. ear pressure. or tinnitus is also present. vertigo. History - Ask the patient to describe their symptoms by using words other than "dizzy. and systemic diseases. The overall incidence of dizziness. . which is a subtype of dizziness. ENT. and imbalance is 5-10%." Dizziness includes light-headedness.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . A history of headaches. from other types of dizziness. whereas other symptoms of dizziness may be due to CNS. Patients with peripheral vertigo can usually ambulate during episodes and are consciously aware of their environment. . or a tilting sensation. .Patients with cerebellar disease are frequently unable to ambulate during acute episodes of vertigo. motion intolerance. unsteadiness. Vertigo is defined as an illusion of movement caused by asymmetric input of the vestibular system true vertigo is often due to inner-ear disease.Episodic true vertigo that lasts for seconds and is associated with head or body position changes is probably due to benign paroxysmal positional vertigo (BPPV). especially if cerebrovascular risk factors are present. Adel Adwan .Gradual and ill-defined symptoms are common in CNS. can be associated with migrainerelated dizziness.30 Diseases of the inner ear: Vertigo Epidemiology - Dizziness and vertigo are among the most common symptoms causing patients to visit a physician (as common as back pain and headaches). cardiovascular. Time course: . dysphagia. cardiac. imbalance. or focal weakness. . especially migraine headaches. floating. CNS symptoms: . including diplopia. dysarthria. especially if hearing loss.Vertigo that lasts for hours or days is probably caused by Ménière disease (if associated with hydropic ear symptoms) or vestibular neuronitis (if hydropic ear symptoms are absent). A critical distinction is differentiating vertigo. because they cannot stabilize the eyes during small head tremors.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Examine the neck for range of motion and flexibility. A normal oculocephalic reflex and intact visual acuity with active head movements (dynamic visual acuity) reflect good VOR. Evaluation of the cardiovascular and neurologic systems. motor and sensory modalities and gait. Focused neurologic examination of the cranial nerves. or sensory changes in the cervical C2-C3 or trigeminal distributions usually indicate vestibular neuronitis or recurrent episodes of Ménière disease. The vestibulo-ocular reflex (VOR) It is a reflex eye movement that stabilizes images on the retina during head movement by producing an eye movement in the direction opposite to head movement. Absence of the oculocephalic reflex or a decrease in visual acuity with head movements reflect decreased vestibular function. trauma. The VOR reflex does not depend on visual input and works even in total darkness or when the eyes are closed. the VOR is very important for stabilizing vision: patients whose VOR is impaired find it difficult to read. cold sores. ENT. Examine the ears for visible infection or inflammation of the external or middle ear. head trauma ear diseases. Since slight head movements are present all the time. the eyes move to the left. For example. over-the-counter medications. and recreational drugs (including smoking and alcohol) can help to identify pharmacologically induced syndromes DM. when the head moves to the right. Adel Adwan .32 - - Previous viral illness. HTN. Physical examination - - Supine and standing blood-pressure measurement. Dr. or surgery History of prescription medicines. Test hearing and discrimination by using a tuning fork and by whispering and asking the patient to repeat heard words. thus preserving the image on the center of the visual field. Vestibular examination 1. and vice versa. or any cardiovascular or cerebrovascular disease. herbal medicines. The normal gait is characterized by an erect posture.Examine eye movements for spontaneous nystagmus. . moderately sized steps. first with eyes open. Grade III: When it is evident in all positions of the eyes. and the medial malleoli of the tibia tracing a straight line. i. ENT. on conjugate deviation to one side. must be completely characterized to be correctly interpreted. performing tandem gait. then with eyes closed. The Romberg examination is conducted by asking the patient to stand with the heels together. . 4. or positional. Differentiating peripheral and central nystagmus is a key step. gaze-evoked nystagmus.33 2. . by using Frenzel goggles or infrared video nystagmography). Posture and gait: Ask the patient to repeatedly run the heel from the opposite knee down the shin to the big toe.Nystagmus. Grade II: When in addition. Characterization of nystagmus .Central nystagmus is a purely horizontal or vertical gaze and not suppressed by visual fixation. ask the patient to stand on a high-compliance surface and note any excessive postural sway. Nystagmus is observed under Frenzel glasses after rapid head shaking reflects asymmetric vestibular input. Fixation suppression test: It is important for checking the vestibulocerebellum. Dr. whether spontaneous. Vestibulospinal reflex (VSR) It can be examined with Romberg and gait tests. gaze-induced. posteroanterior or to one side. that is. and ocular motor abnormalities. Watch the patient walking. It also obeys the Alexander law.Peripheral nystagmus is usually rotatory and most evident with removing visual fixation (eg. - Nystagmus is divided into 3 grades: Grade I: Jerky nystagmus is evident only in the direction of the fast phase. and look for incoordination. Adel Adwan .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . A visible nystagmus (right or left) indicates failure of fixation suppression that is always central in origin. Then. the intensity of nystagmus increases with gaze in the direction of the fast phase. it is evident in the primary position. Failure of fixation suppression can be tested by asking the patient to stretch his arms and look at his thumb while being passively rotated (manual rotation of examination chair). These tests provide information about the patient's postural stability when his or her visual and proprioceptive inputs are removed.e. 3. 34 5. Positioning examination The positioning examination (DixHallpike test) is an important component of the vestibular examination to identify BPPV commonly caused by otolith debris (canalith) floating in the semicircular canals (canalithiasis) or adhering to the cupula (cupulolithiasis). The Dix-Hallpike maneuver is performed by guiding the patient rapidly from a sitting position with the head turned 45° to one side to a supine position. BPPV is due to posterior semicircular canal canalithiasis approximately 90% of the time. Typical nystagmus related t posterior semicircular canal benign positioning and its symptoms are delayed by several seconds (latency). They peak in 20-30 seconds and then decay (paroxysmal), with complete resolution of symptoms while the patient maintains the same head position (habituation). Symptoms and reversed nystagmus may occur when the patient is brought back to a sitting position. Therefore, benign positioning nystagmus is latent, paroxysmal, geotropic, reversible, and fatigable. Nystagmus of the less common horizontal semicircular canal canalithiasis form of BPPV is purely horizontal, geotropic (beating toward the down ear), and asymmetric. The direction reverses with the change in head position from one side to the other in the supine position. The intensity of nystagmus is strongest when the head is rotated to the involved side. 6. Caloric test examination Cold or warm water or air is irrigated into the external auditory canal, usually using a syringe. The temperature difference between the body and the injected water creates a convective current in the endolymph of the nearby horizontal semicircular canal. Hot and cold water produce currents in opposite directions and therefore a horizontal nystagmus in opposite directions. In patients with an intact brainstem: If the water is warm (44°C or above) endolymph in the ipsilateral horizontal canal rises, causing an increased rate of firing in the vestibular afferent nerve. This situation mimics a head turn to the ipsilateral side. Both eyes will turn toward the contralateral ear, with horizontal nystagmus to the ipsilateral ear. ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen 35 If the water is cold, relative to body temperature (30°C or below), the endolymph falls within the semicircular canal, decreasing the rate of vestibular afferent firing. The eyes then turn toward the ipsilateral ear, with horizontal nystagmus (quick horizontal eye movements) to the contralateral ear. To remember this: COWS Absent reactive eye movement suggests vestibular weakness of the horizontal semicircular canal of the side being stimulated. Investigations: Electronystagmography(ENG) diagnostic test to record involuntary movements of the eye caused by nystagmus. It can also be used to diagnose the cause of vertigo, dizziness or balance dysfunction by testing the vestibular system. ENG provides an objective assessment of the oculomotor and vestibular systems The test is performed by attaching electrodes around the nose and measuring the movements of the eye in relation to the ground electrode The standard ENG test battery consists of 3 parts: oculomotor evaluation positioning/positional testing caloric stimulation of the vestibular system can be used to record nystagmus during oculomotor tests such as saccades, pursuit and gaze testing, optokinetics and also calorics (bithermal or monothermal). Abnormal oculomotor test results may indicate either systemic or central pathology as opposed to peripheral (vestibular) pathology. The caloric irrigation is the only vestibular test which allow the clinician to test the vestibular organs individually, however, it only tests one of the three semi circular canals - the horizontal canal. While ENG is the most widely used clinical laboratory test to assess vestibular function, normal ENG test results do not necessarily mean that a patient has typical vestibular function. ENG abnormalities can be useful in the diagnosis and localization of site of lesion; however, many abnormalities are nonlocalizing; therefore, the clinical history and otologic examination of the patient are vital in formulating a diagnosis and treatment plan for a patient presenting with dizziness or vertigo. ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen 36 Differential diagnosis of dizziness Cardiovascular causes: - Arrhythmias (fast or slow rate). Orthostatic hypotension. Hypovolemia or anemia. Myocardial ischemia. Structural cardiac or valvular disease. Hypoxia. Vasovagal episode (also neurologic). Neurologic-Otologic causes: Peripheral vestibular causes: - Vestibular neuritis. - Benign Paroxysmal Positional Vertigo (BPPV). - Ménière's disease. Central vestibular causes: - CVA - Vertebrobasilar ischemia. - Cerebellopontine angle mass. - Multiple sclerosis. - Basilar artery migraine. Other Drug effects: - Aminoglycosides. - Anticonvulsants. - Antihypertensives. - Hypoglycemic. - Antipsychotics. - Sedative/hypnotics. - Alcohol. Psychiatric (hyperventilation, anxiety) Thyroid disorders ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen result from a reactivation of herpes simplex virus that affects the patient's vestibular ganglion and vestibular nerves. Less common is undue cervical strain. Adel Adwan . Medications are not effective in the treatment of BPPV. Dr. 2. The common etiology is idiopathic or posttraumatic. The mechanism of BPPV can be due to canalithiasis (otoconia floating in the endolymph) or cupulolithiasis (otoconia adherent to cupula). which is treated with the Lempert or Hamid maneuvers.000 people. The most commonly affected canal is the posterior canal (90% of cases) and. Ménière disease. Semont. possibly because a large spectrum of viruses can cause vestibular neuronitis. Patients are usually ill and cannot perform home or work activities.37 Peripheral vertigo 1. among others). to a lesser extent. ENT. and delayed endolymphatic hydrops are also associated with BPPV. One third of patients have chronic vestibular symptoms and develop BPPV. Other etiologies such as vestibular neuronitis. The most effective treatment is canalith repositioning from the affected canal to the vestibular (using Epley. especially with the Semont maneuver or with neck hyperextension during the Epley maneuver. Lempert. A brief course of antiemetic and vestibular suppressants is usually needed in the acute phase. with an incidence of 170 cases per 100. Vestibular neuritis - - The most common cause of acute vertigo.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . A prodromal upper respiratory tract illness may or may not be present Vertigo is without auditory or other CNS symptoms and lasts for several days. but should be withdrawn as soon as possible to facilitate the process of central vestibular compensation (3-5days) Corticosteroids may improve long-term outcomes Early vestibular rehabilitation is important Antiviral medications have not proven helpful. and Hamid maneuvers. Patients may have a residual sensation of disequilibrium between episodes. The most common complication of the Semont or Epley maneuver is the conversion of the posterior canal-horizontal canal BBPV. Benign paroxysmal positioning vertigo (BPPV) - - - Second most common cause of vertigo The typical symptom is brief episodic vertigo upon changing head or body position. the horizontal canal. Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Dr.38 Epley’s maneuver ENT. Adel Adwan . Treatment of migraine-associated vestibulopathy is the same as the treatment of migraine.39 3. 4.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Patients with recurrent symptoms that are steroid responsive may benefit from methotrexate or other steroid-sparing medications. and response to steroids distinguishes this disorder from Ménière disease. infectious. Dr. and hearing loss. tinnitus. These patients should be treated by a rheumatologist. or idiopathic. If ntreated. and it can be used to reduce vestibular symptoms. Corticosteroids. such as shunting the endolymphatic sac. Trigger factors should be eliminated and patients are encouraged to follow common sense diet and lifestyle. Migraine - Common disorder. or lack thereof. with endolymphatic hydrops representing a histological footprint rather than an etiology More than 80% of patients respond to conservative therapy with salt restriction and diuretics. bilateral hearing loss with or without vertigo. Autoimmune inner-ear disease - Typically present with rapidly progressive. affecting 10% of men and 30% of women. of surgery. However. Central dizziness 1. the rapid progression. given orally or intratympanically. Adel Adwan . Vestibular symptoms usually are dissociated from headaches but sometimes can occur as an aura or as part of a headache. can be used to stabilize active disease. The common pathophysiology is disordered fluid homeostasis in the inner ear. Intratympanic gentamicin (chemical labyrinthectomy) is a minimally invasive procedure that emerges as an effective method for treating the disabling vertigo of Ménière disease. The initial onset may be unilateral. ENT. is controversial. bilateral involvement. Ménière disease - - Disorder of the inner ear with typical symptoms of episodic vertigo. The pathophysiology of migraine-associated vestibulopathy is not completely understood. This disease can occur with or without other autoimmune disease or laboratory evidence of a systemic inflammatory disorder Oral and intratympanic corticosteroids are effective in controlling this disease. Bilateral involvement occurs in about 25% of patients. autoimmune. The literature demonstrates wide variation in the effectiveness. About 25% of migraineurs have motion intolerance/sickness as opposed to true vertigo. severe hearing loss and unilateral vestibular paresis are inevitable. The etiology can be hereditary. The role of surgical therapy. Occipital headache precipitated by Valsalva maneuvers. Dr. - Other central causes of dizziness should be excluded: TIA Stroke Multiple sclerosis Tumors and malformations of the posterior fossa: – Vestibular schwannoma (acoustic neuroma) – Arachnoid cysts – Chiari malformation: • occurs in a few adults. • can be excluded by MRI. exertion. It is congenital. or changing position is common. Dizziness may occur with the same precipitants. ENT. but often does not become symptomatic until the age of 20-40 years. Adel Adwan . 2.41 - Prophylactic and abortive medications commonly used in treating migraine should be tailored to patients with vestibular migraine.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . coughing. 2. • It may also occur when a transient conductive hearing loss. 4. is superimposed on a sensorineural hearing loss. 1. Possible causes of SNHL are: 1. it can be due to outer. Mixed hearing loss (MHL) • It may be caused by severe head injury with or without fracture of the skull or temporal bone. Cholesteatoma 4. Ossicular Disarticulation 2. Otitis externa. • patients tend to speak with normal or low volume voice Causes of CHL: Outer ear: 1. Congenital Atresia. Non-organic hearing loss. middle or inner ear disease. Conductive hearing loss (CHL) • It refers to a disruption or mechanical blockage of the movement of sound waves (vibrations) at some point in the hearing system before they reach the inner ear. Sensorineural hearing loss (SNHL). 2. Drugs. • Middle ear structures are intact. 3.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Conductive hearing loss (CHL).40 Hearing loss According to the type. ENT. Otitis Media 2. Hereditary. Sensorineural hearing loss (SNHL) • It implies damage to the sensors or nerve fibers which connect the inner ear to the hearing center in the brain. Occlusion/foreign body such as wax impaction. commonly due to otitis media. Otosclerosis 6. this damage is permanent. Dr. by chronic infection. 2. • Dysfunction of the outer or middle ear. or by one of many genetic disorders. Since damaged nerve fibers do not regenerate or repair themselves like some other parts of the body. Ossicular fixation 5. Middle ear: 1. Types of hearing loss: 1. Adel Adwan . • Middle ear structures are intact. Mixed hearing loss (MHL). 3. 3. TM Perforation 3. it is not considered sudden.42 3. Speech sounds distorted.Meningococcal meningitis. Occurring within 3 days. Criteria for the diagnosis of SSNHL: Idiopathic hearing loss of at least 30 dB. 2. many affected people likely never seek medical attention. SSNHL can occur at any age. Sudden onset SNHL (SSNHL) Definition: Acute unexplained hearing loss. and some infectious diseases such as mumps. Idiopathic : Most common. Elevated biliruben levels (jaundice). 5. Hearing aids may help. zoster.000 people per year . 4. 6. CMV.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 7. Characteristics of SNHL: • • • • • Inappropriately loud voice. Dr. Similar numbers of men and women are affected. Background noise makes listening more difficult. nearly always unilateral. . It's a medical emergency. 8. 2% are bilateral. Infectious. that occurs over less than a 72 hour period. Most cases are idiopathic. and the prognosis depends on the severity of the hearing loss. Tinnitus.Herpesvirus (simplex. Since recovery is often spontaneous. MC patients 43 to 53 yr of age. & is not treated ! Epidemiology: • • • • • The exact incidence of SSNHL is uncertain. CMV). . Over at least 3 audiometric frequencies test. Adel Adwan . Low birth weight caused by prematurity. Permanent damage due to excessive noise. Meningitis. RH incompatibility at birth. Prenatal exposure to Rubella. ** After 14 days. Estimates of incidence typically range from 2 to 20 per 100. ENT. Etiology OF sudden SNHL: 1. varicella. . Associated systemic diseases. . Adel Adwan .Relapsing polychondritis.SLE.Wegener’s granulomatosis. . ENT. Autoimmune disease of the cornea and inner ear. . Aortitis – 10%.Vertebrobasilar insufficiency. Hearing fluctuates with disease exacerbations and remissions. . Cryptococcal meningitis. Mycoplasma. autoantibodies directed against inner ear antigenic protiens. Majority develop bilateral deafness (67%). Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .Sickle cell disease.Vascular disease associated with mitochondriopathy. . HIV.43 - Mumps. .Autoimmune inner ear disease (AIED).Red blood cell deformability. or cross-reacting antibodies — Cogan’s syndrome • • • • • First described by Cogan in 1940. Age of onset 22-29 years. . .Cogan’s syndrome. Syphilis.Polyarteritis nodosa. ◦ ◦ • • Takayasu’s like or medium-sized vessel vasculitis. Autoimmune. pathophysiology: vasculitis of vessels supplying the inner ear. Vascular. pathophysiology: host immune response to the pathologic changes in the membranous labyrinth and subsequent hearing loss 3.Vascular disease/alteration of microcirculation. Rubella. . Toxoplasmosis. . .Ulcerative colitis. .Cardiopulmonary bypass. Presentation – interstitial keratitis(IK) and Meniere’s like episodes of vertigo with Bilateral Rapidly Progessive SNHL (BRPSNHL). 4. . . . An association of genes related to prothrombotic states.Inner ear concussion.Acoustic neuroma. – Presbycusis is sensorineural hearing loss that probably results from a combination of age-related deterioration and cell death in various components of the hearing system and the effects of chronic noise exposure. and increased serum levels of fibrinogen and homocysteine in patients with SSNHL microvascular events as a cause. For example.Temporal bone fracture. . 7.Endocrine disorders: Hypothyroidism . .Medications : Aspirin.Otologic surgery (stapedectomy). . thrombosis. when “shoe.Focal pontine ischemia .” “too.Migraine 6. – Consonant sounds are the most important sounds for speech recognition.” or “new” is spoken. . .” “blue.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . .Meningeal carcinomatosis. many people with presbycusis can hear the “oo” sound. Associated with gradually progressive hearing loss 8. . but most have difficulty recognizing which word has been spoken because they cannot distinguish the consonants. vasospasm.Inner ear decompression sickness.Presbycusis sensory hearing loss (PSHL): Senile hearing loss. ENT.Metastasis to internal auditory canal. Neurologic. cisplatin. erythromycin. . Neoplastic. antibiotics: aminoglycosides.Perilymph fistula. Adel Adwan . antimalarials. . Dr.44 pathophysiology: embolic phenomenon. vancomycin. Traumatic.Multiple sclerosis .” “true.Leukemia. 5.Myeloma.Excessive noise. . Other causes: . loop diuretics. pathophysiology: Traumatic breaks in the membranous labyrinth. . such as chronic exposure to loud music or other sounds.Surgical complication of nonotologic surgery. and hypercoagulable or high viscosity states. Diagnosis: Patients who complain of sudden hearing loss or awaken with new hearing loss. Symptoms of URTIs. ◦ Aural fullness: a sense of air pressure in the middle ear.Better in the normal ear = sensory neural hearing loss. Weber's test: The patient may hear the sound: . Sickle cell disease (African Americans). Physical examination: — Complete Head & Neck exam. it is due to a conductive or sensorineural problem Weber's and Rinne's tests. Rinne's test: + Rinne positive: AC > BC = Normal or Sensorineural hearing loss. 1.Equal in both ears = normal. straining.45 History: Time-course: 1/3 cases upon first awakening in the morning. ◦ Neurologic conditions. ◦ Malignancies. intense noise exposure. Hx of ototoxic drug use. Neurologic exam – cerebellar findings: Romberg Nose to finger. Past medical Hx: ◦ Autoimmune disorders. ◦ Tinnitus.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . ENT. 2. ◦ Hypercoagulable states. Past surgical Hx : stapedectomy or other otologic surgeries. nose blowing. Hx of head trauma. heel to shin Vestibular – Dix-Hallpike test. ◦ Vascular disease. Adel Adwan . Foreign bodies obstructing the canal are sometimes a problem in children. cerumen impaction Cerumen (earwax) accumulation is the most common cause of treatable hearing loss. Associated symptoms: ◦ Vertigo/dizziness: in 1/2 cases. both because of their presence and because of any damage caused during their removal. Hx of flying or diving.Better in the diseased ear = conductive hearing loss. Ears: Rule out effusions. especially in the elderly. . Dr. Weber's & Rinne's tests. cholesteatoma. sneezing. . • Air –Bone gap>10DB MHL — Laboratory testing : — CBC ESR. • Air conduction abnormal. it is mandatory to do MRI with contrast to Rule out: ENT. Adel Adwan . TSH HIV Lyme titer Antigen-specific cellular immune tests – Lymphocyte transformation test (LTT) – Western blot Imaging study: MRI: Any patient presenting with SSNHL. • Air conduction abnormal. Dr.Rinne negative: BC > AC = Conducive hearing loss. Audiogram • Bone conduction within normal. • Air –Bone gap>10dB CHL • Bone conduction abnormal. Subjective method of testing hearing.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Diagnostic Testing Audiogram ◦ ◦ Diagnostic and prognostic. • Air conduction abnormal.46 . CRP Chemistry Cholesterol/triglycerides T3/T4. • Air –Bone gap<10DB SNHL • Bone conduction abnormal. Valacyclovir ◦ Vasodilators ◦ Calcium antagonists: Nifedipine ◦ Antioxidants: Vitamin A ◦ Plasmapheresis (in autoimmune cases) ◦ Cochlear implantaion: in bilateral progressive deafness & Profound hearing loss (>90 dB).Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .Prostaglandin .Cyclophosphamide . Age: The average age for those recovering totally was 41. In idiopathic SSNHL. Dr. Multiple sclerosis. Syndromes associated with hearing loss: Alport's syndrome.Steroids .Methotrexate ◦ Diuretics ◦ Antiviral agents: Acyclovir. Ischemic changes. Common cavity syndrome. Age < 15 years & > 60 years: poorer recovery rates. Mondani syndrome: Partial aplasia of cochlea. Audiogram: Patients with profound hearing loss significantly decreased recovery rates. there is a high spontaneous recovery rate (47% to 63%). ENT.47 ◦ ◦ ◦ Cerebellopontine angle tumors (Acoustic neuroma). Associated symptoms: Vertigo: worse outcome. ** 10-19% of acoustic neuroma patients present with SSNHL.8 years. Michel aplasia: Total aplasia of cochlea. better the recovery. ** 1% of SSNHL patients have acoustic neuroma. Adel Adwan . We use: ◦ Anti-inflammatory/immunologic agent as: . Prognosis It is depend on: Time since onset: The sooner the patient was seen and therapy initiated. Treatment: ** SNHL is an emergency !! Treat underlying condition if there is a known cause. Patient may have MI. Auriculotemporal nerve. Patient may have muscle spasm. tympanic branch of glossopharengeal nerve. Sensory innervations of the ear: 1. spondylosis or disc herniation in the neck.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Arnold nerve. It causes referred otalgia of trigeminal origin. peptic ulcer or most commonly. Dr. It causes referred otalgia of cervical origin. Jacobson nerve. laryngitis with hoarseness of voice. It causes referred otalgia of glossopharengeal origin. auricular branch of vagus nerve. Waardenburg syndrome. TMJ problem. a branch of mandibular division of trigeminal nerve. Greater auricular nerve (C2) & Lesser occipital nerve (C3). Adel Adwan . Alexander syndrome. Usher syndrome. 3. Patient may have 4. gingival abscess.48 Goldenhar syndrome. Patient may have dental caries. Referred otalgia Pain referred from structures whose nerve supply also sends branches to the ear. ENT. Treacher collins syndrome. It causes referred otalgia of vagal origin. sinusitis… 2. tip. 3. It needs deep suture if being used for flaps. 2. So. Bony part: forms 2/3 of nose anatomy. ENT. External nose: 1. The skin over the cartilaginous part is very thick because there are sebaceous glands. Dr. The skin over the bony part is very thin due to the absence of sebaceous glands.49 The nose & Paranasal sinuses 1. dorsum. composed of: Upper lateral cartilage. 2. It is composed of: bridge. It is divided into two parts : a. Middle third: From the bridge of the nose to the nasolabial angle (the angle between the columella & philtrum). Cartilaginous part: forms 1/3 of nose anatomy. Lower third: From the nasolabial angle to the chin. Nasal process of frontal bone. located in the middle third of the face with the base at the upper lip and the apex between the orbits (root of the nose).Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Upper third: From the hair line to the bridge of the nose. Lower lateral cartilage. that's why the thin skin is preferred. Adel Adwan . 2 ala nasi & 2 nostrils. hair follicles & sweat glands. The nose: Nose anatomy: ** Face is divided into 3 parts: 1. columella. Ascending (frontal) process of maxilla. 2 lateral surfaces. Nose is a pyramidal structure. composed of: Nasal bone. this thin skin is the one used for flaps rather than the thick skin. hair follicles & sweat glands. During surgery. Posterior wall: Posterior nares/ choana. Lateral wall: 3 turbinates or conchae(three bony projections below each of them lies a meatus). Kiesselbach plexus: 5 arteries. iv. ** Choanal atresia in the pediatric age group is an emergency & has a mortality risk because they are obligate nasal breathers. Adel Adwan .51 b. Anterior wall: Anterior nares/nosetrils. Membraneous part: Columella with skin. . Internal nose: = Nasal cavity proper which extends from nostrils in front to conchae behind. Cartilaginous part (anteriorly): Quadrilateral cartilage which is the most common site of septal deviation. a branch of maxillary artery – Superior labial artery.2 from the internal carotid artery: – Anterior ethmoidal artery – Posterior ethmoidal artery.3 from the external carotid artery: – Sphenopalatine artery. Medial wall: Septum. both branches of ophthalmic artery 3. surgeons should avoid moving the perpendicular plate of ethmoid because of the risk of fracture & causing CSF leak. Bony part (posteriorly): Vomer "backward downward" and perpendicular plate of ethmoid bone "backward upward". It has 6 walls: i. It has 3 parts: 1. a branch of facial artery . The superior and middle turbinates are parts of the ethmoid bone while the inferior turbinate is a separate one. ii. Dr. ENT. 2. a branch of maxillary artery. iii. – Greater palatine artery. it divides the nose into right & left. In the anterior part of the cartilage locates the Little's area that contains the kiesselbach plexus which is the most common site of epistaxis(75-90%).Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . surgeons should avoid excessive movement of the superior and middle turbinates because of the risk of CSF leak. *1 cm posterior to the inferior turbinate lies the pharyngeal orifice of the Eustachian tube behind of which lies a small recess. Above the middle turbinate. v. Floor: formed by the palatine process of the maxilla and the horizontal plate of the palatine bone. The superior meatus receives the openings of the posterior group of sinuses (posterior ethmoidal & sphenoidal sinuses) at the spheno-ethmoidal recess which lies above the superior turbinate. The inferior meatus receives the opening of the nasolacrimal duct which lies 1cm posteriorly to the anterior tip of the inferior turbinate.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . opening of the anterior group of sinuses & middle meatus itself. Dr. Below the middle turbinate. upper and lower lateral cartilages.50 * During surgery. vi. Mucous membranes of the nasal cavity: Respiratory mucosa: Pseudostratified ciliated columnar epithelium. Roof: dorsum of the sphenoid. frontal & anterior ethmoidal sinuses) at the heatus semilunaris. the mucosa is yellowish Olfactory neuroepithelium ENT. nasal bone. the pharyngeal recess or fossa of Rosenmüller which is the most common site of nasopharyngeal carcinoma. ** Osteomeatal Unit (OMU)/ Osteomeatal complex: anterior ethmoid (Bulla ethmoidalis). The middle meatus contains the opening of the anterior group of sinuses (maxillary. cribriform plate of the ethmoid. the mucosa is pinkish Respiratory mucosa. Adel Adwan . look for: Colour of mucous membrane – Normal: smooth glistening reddish white. but CT is much more diagnostic. deviations humb. Internal nose examination. Floor of the nose: because it is the functional area of the nose for breathing. – Chronic rhinitis: congested red non smooth. X-Ray conventional for sinuses and nasal bones in case of trauma. – Clear water discharge: CSF. then with nasal speculum examine the left and right nasal cavities. Adel Adwan . Anterior and posterior Rhinoscopy Nasal Endoscopy Specific diagnostic methods: a) Nasal endoscopy b) Biochemical and immunologic investigation of the secretions c) Cytology and bacteriology d) Allergic investigation e) Biopsy To complete examination of the nose. – Acute rhinitis: congested red smooth. Nasal septum deviation. Amount. Dr. – Fresh blood: epistaxis. Clinical aspects of nasal disease: • • • Nasal obstruction. – Allergic rhinitis: profuse clear mucous discharge with swelling. – Chronic rhinitis: mucoperulent discharge.floor of frontal sinus and maxillary sinuses.52 Nose examination: External nose examination – inspect the skin for swellings. Inferior and middle meatus. – Allergic rhinitis: bluish/ Purple mucosa.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . the naso pharynx should be examined with endoscopy through the nose or with mirror through the mouth. Palpate for tenderness on the bony nose . – Acute rhinitis: profuse amount of mucous or mucopurulent discharge. Inferior and Middle turbinate: Look for congestion or hypertrophy.rise the tip with your finger and look inside the nose to see the skin of vestibule and part of nasal mucosa. color and consistency of secretions – Normal: minimal amount of clear mucous. scars and abnormal colouration. Presence of abnormal growth. Nasal discharge Fetor ENT. – Bloody discharge: tumor (eg: Juvenile angiofibroma)or grannuloma. ulcers. ** Anosmia: Absent sense of smell. propranolol. e. Dr.. • Aplasia of the olfactory bulb (rare). anosmia. in schizophrenia ENT. acquired) Nasal pyramid fracture Septal perforation Nasal polyps Cephalocele / Meningiocele Adenoids (Pharengeal tonsils) Tumors of the nose. hydralazine). polyps.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . paranasal sinuses.g. Parkinson disease.heavy metals.53 • • • • Epistaxis Smell disturbance Facial pain Facial deformity Differential diagnosis of nasal airway obstruction Acute and chronic rhinitis (e.. antidepressants (e.g: Influenza • Radiotherapy (rare) Stimulus conduction and processing • Avulsion of fila olfactoria due to skull base fracture.g. NO. tumor • Scar tissue occluding the olfactory groove • After intranasal surgery Perception: damage to the olfactory epithelium caused by: • Toxic substances SO2.. Transport of odorants • Nasal obstruction Deviated septum • Mucosal swelling. atrophic) Sinusitis Deviated septum (congenital. varnishes • Drugs • Viral infections.. ozone.g. amitriptyline) – Drug abuse: imidazoline derivatives (e. Adel Adwan . reserpine. xylometazoline hydrochloride) Causes of olfactory disturbances: ** Hposomia: Decreased sense of smell. antihypertensive agents (e. diabetes mellitus • Olfactory hallucinations After epileptic seizures. SNHL. allergic. • Injury to olfactory centers: Contusion or hemorrhage due to head injury • Neurodegenerative diseases: Alzheimer disease. • Kallmann syndrome: Hypothalamic hypogonadism. and nasopharynx Foreign bodies (especially in small children) Drugs – Adverse effects: oral contraceptives.g. oxymetazoline hydrochloride. Nasal deformities Deformities of the external nose: Crooked nose Humped nose Saddle nose Broad nose Management: Rhinoplasty Deformities on the internal nose: Nasal septal deviation . following rupture of the vertical epithelial fold between the olfactory groove and the roof of the primary oral cavity (pronasal membrane). Adel Adwan . – Traumatic / Non-traumatic (congenital).Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Dr.70% of the population have nasal septal deviation ! . Classification: – Bony / Cartilaginous. rupture of the oronasal membrane will be absent or incomplete. resulting in the partial (stenosis) or complete closure (atresia) of one or both choanae.Require surgical repair if causing complications. recurrent sinusitis or rhinitis. Classification: Unilateral / Bilateral Bony / Membraneous Complete (atersia) / Incomplete (stenosis) ** Complete bilateral choanal atresia in neonates is an emergency because they are obligate nasal breathers. They develop between the third and seventh embryonic weeks. snoring. 30% of people. affecting app. ENT. Choanal atresia Embryology of choanal atresia The choanae are the posterior openings that connect the nasal cavities with the nasopharynx.54 Nasal diseases ** The most common nasal mucosal disease is Allergic rhinitis. such as: nasal obstruction.If this process is disturbed. – S-shape. . – Saddle nose.Snuff takers.Rhinolith Systemic causes: . Adel Adwan . .Neglected foreign body. . .Traumatic: surgery / Pick ulcer.Other vasculitis syndromes. – Fracture of cribriform plate and CSF leak.Chrome ulcer: affects workers in chrome factories. ENT.SLE. . – Adhesions. . Dr. Septal perforation Etiology: Local causes: . – SMR: Submucosal Resection.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .Wegener's granulomatosis.55 Types of deviation: – C-shape with sharp angle. – Retrobulbar hematoma. – C-shape. Complications of surgery: – Perforation. Management: – Septoplasty. picking.Idiopathic. Von willebrand disease. Tell the Patient to firmly grasp and pinch his entire nose between the thumb and fingers for at least 10 minutes. Leukemia. - Bleeding above middle turbinate. ** Hypertension is NOT a cause of epistaxis. Liver failure. leaning forward to reduce venous pressure. - Bleeding posteriorly. pneumonia. Trotter position: Place patient in an upright position. . ENT. mostly due to ethmoidal artery. .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . such as. but epistaxis is more severe and more prolonged in hypertensive patients and they need admission. Adel Adwan . Dr.Compress the soft outer portion of the nose against the midline septum for about 5-10 minutes continuously. accounting for 75-90% of cases. .Traumatic: Surgery.Neoplastic: Any tumor can cause epistaxis but angiofibroma is the most one. Hemophilia. Christmas disease (Hemophilia B).Inflammatory: Any acute rhinitis can cause epistaxis. Moreover. foreign body… . Management: 1.56 Epistaxis Causes: Local causes: . Systemic causes: . whooping cough. there is a theory that seeing the blood coming out of the nose causes an increase in blood pressure ! Sites of bleeding: - The most common site of bleeding is Little's area Kiesselbach's plexus.Environmental: especially coldness and dryness. mostly due to sphenopalatine artery. Retro columellar vein is the most common site of bleeding when the cause is increased venous pressure.Increased venous pressure: such as in right-sided HF. Vitamin K deficiency. .Blood and blood vessels disease: Any cause of bleeding tendency. 6. Dr.Closed.57 2.Palpation. 4.Intranasal inspection. Management: if there is NO edema. . Adel Adwan . Embolization: using angiography 8. 3. Anterior packing: Gauze packing inside the nose for anterior epistaxis. . Nasal bone fractures: Classification: .Inspection. . ENT.Radiographic evaluation. 7. Posterior packing: for 24-48 hours for posterior epistaxis 5.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . do nasal bone reduction. . Ligation of the arteries. Cauterization: using silver nitrate. Diagnosis: .Open. Application of ice. SMR: for recurrent epistaxis from little's area. Glucose level : Non specific 3. Inflammations of the external nose & nasal cavity Vestibulitis: Purulent inflammation of the hair follicles. the patient should be admitted and started on IV ATB.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Dr. Adel Adwan .58 if there is edema. saddle nose or septal perforation. ** Look for septal hematoma. Beta-2 transferrin : Found only in CSF so it is the most accurate & specific one. How to confirm that this is CSF ? 1. It is caused by Streptococci or staphylococci so it is treated with ATB covering gram +ve. CSF leak The most common site for CSF leak is through fractured cribriform plate. It is an emergency because of its location in the dangerous triangle and the risk of retrograde transmission of the infection through the valveless emissary veins into the cavernous sinus. then do nasal bone reduction. So. However. why is it an emergency?! Cartilage receives its blood supply from the perichondrium. Halo sign : Non specific 2. ENT. so the presence of the hematoma deprives the cartilage from its blood supply leading to necrosis. it should be evacuated by incision and drainage. if furuncle (abscess) was formed. wait for 1-2 weeks. mostly caused by viral infection. Hoarseness occurs due to post nasal drip causing chronic laryngitis. – Fungal infections: Aspergillosis. - Allergic rhinitis: Etiology: Triggered by an immediate IgE-mediated reaction (type 1 hypersensitivity reaction). – Sarcoidosis . ENT. Simple: Either inflammatory or allergic.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 2. Management: Treat the underlying cause (such as septal deviation. They also complain of frequent throat clearing and occasional hoarseness. – Rhinoscleroma. It is the most prevalent infectious disease. Neoplastic.g. Symptoms: Patients present clinically with obstructed nasal breathing and a mucous nasal discharge. - Nonspecific chronic rhinitis: Etiology: Can develop due to anatomic changes (e. and itching of the nose and eyes (conjunctivitis). septal spur) or other lesions of the nasal cavity (polyps. Adel Adwan . Environmental factors such as sustained extreme temperatures or air pollutants can also bring on this condition. such as inverted papilloma which has a high risk of recurrence and 15% risk of malignancy transformation. It may lead to nasal polyps. ** Nasal polyps: 1. a watery nasal discharge. polyp…)..59 Rhinitis: . Mucormycosis ..Acute (simple) rhinitis: Infectious rhinitis or common cold. Rhinosporidiosis. – Wegener granulomatosis (Wegener disease). Symptoms: The clinical manifestations include obstructed nasal breathing and sneezing attacks. classified as seasonal (hay fever) or perennial according to the presence of the allergen in the environment. marked septal deviation. but can be caused by bacterial infection. tumors) and nasopharynx (adenoids). Eliminate environmental treiggers/ factors. – Actinomycosis – Syphilis. Dr. - Specific chronic rhinitis: – Tuberculosis. It resembles allergic rhinitis in its clinical features. rauwolfia alkaloids. - Hormonal rhinitis: It occurs mostly during pregnancy (estrogen-dependent rhinitis). or less specifically to emotional stress. Dr. - Rhinitis caseosa It occurs post acute rhinosinusitis. beta-blockers. They can be differentiated by taking a smear. oral contraceptive use. it affects workers in dry atmospheres. - Atrophic rhinitis: It is a chronic form of rhinitis. which gives supply to nasal mucosa. - Rhinitis Medicamentosa It is caused by long-term use of decongestant nosal drops. It can also result from the use of certain antihypertensive drugs (e. Secondary due to excessive use of nosal drops. - Vasomotor rhinitis: It is a combination of nasal rhinorrhea. Symptoms are related to a temperature change. drug abuse (cocaine). It is treated with sinus wash out. the consumption of hot liquid or alcohol. Adel Adwan . ACEI). It is characterized by a cheesy material which is secreted from the sinuses to the nasal cavity. characterized by dryness of the nasal mucosa & very bad nasal odor. which cause medical polypectomy as they help in decreasing the polyps size. which shows eosinophils in allergic rhinitis but not in vasomotor rhinitis. - Rhinitis sicca It is a form of atrophic rhinitis. ** The greater superficial petrosal nerve is a parasympathetic nerve which causes increased secretion (rhinorrhea) & vasaodilataion (congestion) in the nasal mucosa.61 Management: Anti-histamines Local corticosteroids. sneezing & nasal obstruction with unknown etiology.. or less specifically to emotional stress. tegretol (carbamazepine) & other drugs.g. Iatrogenic causes include a botched septoplasty or an excessive turbinate reduction (conchotomy). but there is no evidence that the patient has been previously sensitized. the consumption of hot liquid or alcohol. Pathogenesis: ** The greater superficial petrosal nerve (which arises from facial nerve) meets the deep petrosal nerve (which arises from superior cervical plexus) in the pterigopalatine fossa to form the nerve of pterigoid canal (vidian nerve). ENT. It can be: Primary due to fibrosis in submucosal tissue and endarteritis in terminal arterioles of the nose causing dryness and crustation leading to bad nasal odor.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Symptoms are related to a temperature change. or previous radiotherapy for nasal and sinus tumors. ** Vasomotor rhinitis is thought to result from neurovascular autonomic disturbances in regulating the tonus of the nasal mucosal vessels. . It is done for allergic rhinitis.Severe uncontrolled epistaxis. Dr. ENT.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . It is done for septal deviation. Conchotomy (turbinotomy) It involves removal of the mucosal surface of the turbinate. it is important to avoid excessive manipulation of the middle turbinate and perpendicular plate of ethmoid to avoid CSF leak. Septoplasty It involves correction of the deviated septal part. Turbinate surgery SMD (Submucosal diathermy) It involves cauterization of the turbinate causing fibrosis and shrinkage. CO2 laser ** During surgery. but now it is treated the same as allergic rhinitis.Septal deviation. which results in over stimulation of the parasympathetic input. Management: It was used to be treated with vidian neurectomy. It is done for: . Turbinoplasty/ SMR of the turbinate Coblation Using a combination of laser and ultrasound. Nasal surgey Septum surgery SMR (Submucosal Resection) of the nasal septum: It involves extensive removal of deviated cartilaginous part. One of its complications is atrophic rhinitis.60 ** The deep petrosal nerve is a sympathetic nerve which causes decreased secretion & vasodilatation in the nasal mucosa. Adel Adwan . .Lie within the ethmoid bone.Pyramidal in shape. .62 2. Frontal sinues: . The anterior group of sinuses opens into the middle meatus at the hiatus semilunaris. Dr. ** Osteomeatal Unit (OMU)/ Osteomeatal complex: anterior ethmoid. middle. Sphenoidal sinuses: . 2. 3. However. This anatomical relationship explains the pathophysiology of sinusitis of dental origin. ** Maxillary sinus is the most frequently to get infected but the ethmoidal sinus is the most important one. The paranasal sinuses Anatomy: Anterior group: Maxillary Sinuses. called ethmoidal labyrinth.Lie within the frontal bone. Anterior Ethmoidal Sinuses. . ENT. Posterior Ethmoidal Sinuses. so its inflammation and enlargement causes obstruction to the anterior group of sinuses which open into the middle meatus at the hiatus semilunaris.Lie within the maxilla.The roof is formed by floor of orbit. . 4.Lie within the body of the sphenoid.2 in number.Anterior. separated by a bony septum. either after extraction in the presence of thin maxillary sinus floor or due to apical granuloma or abscess. ** The sinuses have small orifices (ostia) that open into the nasal meati.The floor is related to the roots of the premolar and molar teeth. . Maxillary sinuses: . .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . the posterior group of sinuses opens into the superior meatus at the spheno-ethmoidal recess which lies above the superior turbinate.2 in number. This is because the bulla ethmoidalis "the largest anterior ethmoidal air cell" lies above the hiatus semilunaris. posterior ethmoidal sinuses. 1. opening of the anterior group of sinuses & middle meatus itself. which is caused by anaerobes and occurs most commonly due to 2nd & 3rd molars.2 in number. . Ethmoidal sinuses: . Frontal Sinuses. Adel Adwan . Posterior group: Sphenoidal Sinuses. Development of paranasal sinuses: - Ethmoid sinuses are present and the only pneumatized at birth.63 This picture shows the bulla ethmoidalis and its relationship to the hiatus semilunaris. and become completely developed at adolescence. 2. rhinosinusitis is now the preferred term for this condition. ENT. The maxillary presents at birth and become pneumatized at 4 years of age. Act as resonance to the voice. The frontal sinuses begin to develop at 7 years of age. Protect the eye. 3. Adel Adwan . The sphenoid sinuses are present by 5 years of age.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Sinusitis: Definition: Sinusitis is characterized by inflammation of the lining of the paranasal sinuses. Function of paranasal sinuses: 1. Dr. Because the nasal mucosa is simultaneously involved and because sinusitis rarely occurs without concurrent rhinitis. Reduce the weight of the skull. sphenoidal and frontal sinuses become developed completely at 18 years of age. ** Maxillary. 64 Pathophysiology: The sinuses are lined by respiratory epithelium mucosa. Cystic fibrosis. 3. ciliary function and quality of mucosa. leukemia .Adenoid hypertrophy . The common cold: major predisposing factor at all ages. Dr. neutropenics. Sinusitis 2. diabetics. Immotile cilia syndrome. Risk factors: 1. - * The most important pathological process: Mucosal edema resulting from a viral rhinosinusitis obstruction of natural ostia hypooxygenation acidosis vasodilation increased secretion by goblet cells ciliary dysfunction with poor mucous quality retention of secretion and predisposition to bacterial infection.Turbinate hypertrophy . 9. Nasal polyps.Foreign body .Cystic fibrosis . 7. Immunodeficiency.g.Wegener's granulomatosis . HIV infection. Etiolgy: Ostial obstruction: Inflammation . 2. 10. Tumor. Superficial viscous layer and underlying serous layers.URTI .Septal deviation .Allergy Mechanical .Congenital abnormalities i. Nasogastric or nasotracheal intubation. Rhinitis Anything that blocks mucus from exiting the sinuses predisposes them to inflammation. 5.Tumors .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen Triad of: 1. cleft palate Non-ostial obstruction Immune .Immunosuppressed patients (e.Lymphoma.Polyps . 8. 6.e. Nasal foreign body. Situs invertus .Immotile cilia syndrome (Kartagener's) ENT. Cold air. Normal function depends on patent ostia. HIV) Systemic . Bronchiectasis 3. 4. Adel Adwan . 3.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .g. Mucor. Adel Adwan . > 3 month.Facial pain/ pressure .Purulent/ discolored nasal discharge .Facial fractures Bacteria causing sinusitis include: 1. 1-3 months..Fever ENT. 2. which is often caused by gram-negative bacteria (Klebsiella and Pseudomonas). Sinusitis in neutropenic and immunocompromised persons may be caused by Aspergillus and the Zygomycetes (e. S.Facial fullness/ congestion . Invasive: it is usually caused by Mucor. influenzae Maroxella catarrhali Less commonly: S.65 Direct extension Dental . ** Fungal sinusitis is divided into: 1.Infection Trauma . it has a very high mortality rate because it causes destruction and necrosis to the bone and may reach the brain. Non-invasive Classification: According to duration: Acute Subacute Chronic < 1 month. Dr.Nasal obstruction . Acute suppurative sinusitis Definition: Acute infection and inflammation of the paranasal sinuses. Clinical diagnosis requiring at least 2 major symptoms or 1 major symptom and 2 minor symptoms Major symptoms . Rhizopus). and anaerobes. other streptococci. Antibiotic therapy predisposes to infection with antibiotic-resistant organisms.Hypodmia/ anosmia . Indwelling nasogastric and nasotracheal tubes predispose to nosocomial sinusitis. It occurs in immunocompromised patients 2. 4. aureus. pneumoniae Nontypable H. 66 Minor symptoms . sub-periorbital abscess or intracranial) spread – Pitt's Puffy tumor. hyposmia Signs more suggestive of a bacterial etiology are erythematous nasal mucosa. Moderate symptoms that worsen or persist beyond 5 days: institute an intranasal corticosteroid spray and continue for 14 days if symptomatic relief is noted within 48 hours. mucopurulent discharge.Fatigue .Dental pain . but viral is still more common Maxillary sinus most commonly affected Must rule out fungal causes (mucormycosis) in immunocompromised hosts (especially if painless. Severe symptoms that worsen or persist beyond 5 days and refractory to intranasal corticosteroid (INCS): Augmentin (Drug of choice) or clarithromycin therapy ± INCS ± referral to a specialist or if there is a late complication.Viral (most common): rhinovirus. catarrhalis. consider a bacterial etiology. H. bacterial Children are more prone to a bacterial etiology than adults. bloodless mucosa on examination) Organisms: . anaerobes (dental) Clinical features: Sudden onset: Nasal blockage/ congestion and/or Nasal discharge/ posterior nasal drip ± facial pain or pressure.Ear pressure/ fullness Etiology: Viral vs.Cough . pus originating from the middle meatus and the presence of nasal polyps of a deviated septum Acute viral rhinosinusitis lasts < 10 days. influenza. pneumoniae (35%). Symptoms improving within 5 days: symptomatic relief "such as decongestant" and expectant management. Dr.Headache . influenzae (35%). If symptoms increase after 5 days or last longer than 10 days. M. ENT.Halitosis . Adel Adwan .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Management: Anterior rhinoscopy x-ray/ CT scan not recommended unless complications are suspected (i.e. parainfluenza . Surgery if medical therapy fails: 1.Bacterial: S. FESS: Opening of the entire osteomeatal complex in order to facilitate drainage while sparing the sinus mucosa. decreased acuity) Pott’s puffy tumors Characterized by an osteomyelitis of the frontal bone with frontal breakthrough. The infection can also spread inwards. Subperiosteal frontal bone abscess (Pott's Puffy tumor) b. immobile globe.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . ptosis. Periorbital cellulitis b. Complications: Consider hospitalization if any of the following are suspected: 1. This results in a swelling on the forehead. Orbital apex syndrome (as "a" above plus neuritis. Neurologic a. Dr. Orbital (Chandler's classification) a. ENT. Orbital abscess e.67 2. Cavernous sinus thrombosis (The most important sign is pulsating proptosis) 2. Osteomyelitis 4. Adel Adwan . Antral washout: Irrigation of the maxillary sinus through its natural ostium or through a puncture of the inferior meatus (but 1 cm distance is maintained to avoid causing injury to the nasolacrimal duct which opens into the inferior meatus and consequently leading to nasolacrimal duct stenosis causing excessive tearing "epiphora"). Although it can affect all ages. papilledema. Superior orbital fissure syndrome (CN III/IV/VI palsy. Meningitis b. Abscess 3. leading to an intracranial abscess. it is mostly found among teenagers and adolescents. Bony a. Subperiosteal abscess d. Intracranial a. Orbital cellulitis c. V1 hypoesthesia) b. dilated pupils. anaerobes .Chronic inflammatory disorder e. Caldwel view (Occipitofrontal view): Shows frontal. Best for maxillary sinuses. difficult to perform in children and is not reliable. Diagnosis: Cultures of the nasal mucosa in not useful. S. Conventional Radiographs. Dr. 4 views: 1. antifungals and immunotherapy.Fungal: Aspergillus Clinical features: (similar to acute. anterior ethmoidal sinuses & via the mouth. cystic fibrosis. Sinus aspirate culture is the most accurate diagnostic method but is not practical or necessary. Adel Adwan . sphenoidal sinuses & sella turcica.Underlying dental disease . maxillary & anterior ethmoidal sinuses.aureus. wegener's Organisms: . Best for frontal sinuses. catarrhalis. 3. but less sever) Chronic nasal obstruction Purulent nasal discharge Pain over sinus or headache Halitosis Yellow-brown post-nasal discharge Chronic cough Maxillary dental pain Sinobronchial syndrome: Post nasal drip in chronic sinusitis causing lower respiratory tract symptoms such as chronic cough ** Allergic fungal rhinosinusitis is a chronic sinusitis affecting mostly young.Allergic fungal rhinosinusitis .Bacterial: S. influenza. H.g.g. Etiology: Can result from any of the following: . Lateral soft tissue view: Shows adenoids. pneumonia.g.Untreated nasal allergy . ENT. Treatment options include FESS ± intranasal topical steroids. atopic individuals. deviated septum (predisposing factor) . Water's view (Occipitomental view): "with opened mouth" Shows maxillary sinuses.68 Chronic sinusitis Definition: Inflammation of the paranasal sinuses lasting > 3 months.Inadequate treatment of acute sinusitis .Anatomic abnormality e. immunocompetent. S.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . the sphenoidal sinuses. frontal sinuses. Transillumination: show evidence of fluid. 2.pyogenes.Ciliary disorder e. M. Kartagener's . MRI Treatment: Antibiotics for 3 to 6 weeks for infectious etiology Augmentin (40-50 mg/kg/day). Mucosal thickening. but it is not specific for sinusitis. it may occur in simple rhinitis. amoxicillin is the best in children (80-90 mg/kg/day). CT: The gold standard for sinuses. Flagyl TM Topical nasal steroid. Signs of sinusitis on X ray: 1. macrolide (clarithromycin).Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 4. Submentovertical view (bucket-handle): Shows ethmoidal sinuses. Dr. Sinus opacity or clouding 3. Air-fluid level 2. Mucocele (frontal and ethmoid) ENT. Polyps 2. clindamycin. fluoroquinolone (levofloxacin).69 Lateral soft tissue view of the neck and upper thoracic region is ordered if there is suspicion of foreign body. Adel Adwan . saline therapy Surgery if medical therapy fails or fungal sinusitis Removal of all diseased soft tissue and bone. post-op drainage and obliteration of pre-existing sinus cavity FESS Complications: 1. 2. Dr. extends from base of the skull down to level of cervical spine C7. It is continuous with the oral cavity through the faucial isthmus. It is lined with mucosa and is divided into three parts: 1. The oral cavity: Anatomy: The oral cavity is bounded anteriorly by the lips. Adel Adwan . Anteriorly open in the nose. 2. It is divided into 2 parts: 1. the lateral wall containing ENT. c. and superiorly by the hard and soft palates. The epithelial lining is respiratory ciliated and stratified squamous epithelium. The tongue. with transitional epithelium area. posteriorly by the anterior faucial archs. Draining ducts of the sublingual gland:8-20 excretory ducts called the ducts of Rivinus and the largest duct is the sublingual duct (of Bartholin) which joins the submandibular duct to drain through the sublingual caruncles located on both sides of lingual frenulum. inferiorly by the floor of the mouth. The alveolar precesses. Oropharynx: extends from the level of soft palate down to the upper edge of the epiglottis. It contains the pharyngeal tonsil (adenoid).Contains: a. The stensen's duct(parotid gland duct) opposite to the second upper molar tooth. Vestibule: . b.Between the lips and teeth.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . inferiorly open in the oropharynx. The pharynx: Anatomy: It is long muscular tube about 12cm in length. b. ** The epithelial lining of the oral cavity consists of nonkeratinzed stratified squamous epithelium with subepithelial collections of minor salivary glands.71 The oral cavity & Pharynx 1. Wharton's ducts of submandibular glands. laterally the Eustachian tube open on either side. Nasopharynx: extends from the base of skull down to the level of soft palate. contains: a. 2. Its posterior wall is in front the second and third cervical vertebrae. Oral cavity proper: . Adel Adwan . The epithelial lining consist of nonkeratinized stratified squamus epithelium. Dr. After the age of 10-12 years. Hypopharynx or laryngopharynx: extends from the upper edge of the epiglottis superiorly to the lower edge of cricoid cartilage. so no Not covered by capsule. they atrophy. ENT. there risk of recurrence post removal is a risk of recurrence post removal. The tonsillar fossa lies between two (anterior & posterior)pillars. 3. The anterior pillar is formed by the palatoglossus muscle and the posterior pillar is formed by the palatopharyngeus muscle.70 the palatine tonsils which are lodged in the tonsillar fossa.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . It opens anteriorly into the larynx and inferiorly it is continues with esophagus. Capsule Covered with capsule. What is the waldeyer's ring? - Palatine tonsils - Pharyngeal tonsil (adenoid) - Lingual tonsil - Tubal tonsils - Subepithelial lymphoid tissue what is the difference between the adenoids and the palatine tonsils? Palatine tonsils Adenoid Name Palatine tonsils Pharyngeal tonsil Position Oropharynx Nasopharynx Number 2 1 Persistence Remain for life long. The epithelial lining consists of nonkeratinized stratified squamous epithelium. Panorama of jaws: for dental cyst. occlusion. ulcers. The condition of hard and soft palate. the upper surface and inferior surface. Dysphagia. Disorders of speech. ENT. ulcers or tumor. Lateral soft tissue view of the neck and upper thoracic region: for hypopharynx. crypts. Disorder of salivary secretion. Oral fetor. The shape and mobility of the tongue.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . submental. stenosis and swallowing disorders. Globus symptoms. Carotid angiography: for the highly vascular tumors and in cases of bleeding for possible embolization of external carotid branches. Examine the parotid duct in the cheek opposite the upper second molar tooth and the opening of submandibular gland in the floor of the mouth on either side of frenulum. dryness. cheeks are examined for sensation. Respiratory obstruction. temporomandibular joint mobility. floor of mouth and of the lymph nodes at the angle of jaw and below the mandible. Examine the palatine tonsils:. flexible rigid endoscopy Look for: The color. dental arches. Contrast medium: to show pharyngeal pouch. symmetrical mobility of the lips. Examination: Palpation: of lips. mirror. smooth mucosa.size. CT-SCAN: for skull base larynx. TMJs Inspection: by using tongue depressor. skin of the lips. floor of the mouth for swellings .submandibular area. Catarrh. Swellings of the neck. Investigations: Radiography: Lateral view of the skull: for nasopharynx. Burning of the tongue. cysts. The arrangement of the teeth. mobility of soft palate. Blood in the sputum. ulceration. tumors. Adel Adwan . chewing or swallowing. dental caries. mucosa of lips and mouth vestibule.72 Clinical aspects of diseases of the oral cavity and pharynx: Pain on eating. Mucosa of mouth. adenoids and cervical esophagus to show foreign bodies. swellings. Disorders of taste. Dr. Crohns disease 1) Orofacial Granulomatosis (cheilitis granulomatous ) ENT. Gastroenterological diseases 1. Dr. Biopsy: From any swelling which is not acutely inflamed or suspected highly Vascular.73 Microbiology: Culture for bacteriologic. Diseases of the oral cavity and pharynx: Oral manifestations of systemic disease: i.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Mycological and virology examination. Adel Adwan . Celiac disease 1) Aphthous ulcer like lesion 2) Enamel defects 2. Dr. Herpitiform . Major: > 1cm 3. Minor : < 1 cm 2. Adel Adwan . Ulcerative colitis: 1) pyostomatitis vegetans .the most common Aphthous ulcers are divided into: 2) major or minor aphthae 3) pyoderma gangrenosum on tongue ENT.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen 1.74 2) cobblestone appearance of the buccal mucosa 3) Irregular superficial ulcers on ventral surface of tongue 4) Aphthous Stomatitis 3. - Diagnosis: Best diagnostic test is pH metry. Adel Adwan . Chronic liver disease 1) Petechia 2) Jaundice ** GERD: 5. hyperemia of the upper surface of the vocal cords.1 confirms the diagnosis. Flexible pharyngolaryngoscopy: shows hyperemia & congestion of the upper surface of the larynx. Polyposis disease Gardner syndrome: 1) Osteoma in the maxilla - Clinical manifestations: Laryngeopharengeal reflux Continuous throat clearance Night cough Morning hoarsness of voice Postprandial heart burn Globus sensation Chronic laryngitis = reinke's edema Leukoplakia. in which a pH meter is introduced 5 cm above the LES. ventricles & laryngeal surface of the epiglottis. vestibules.75 4. Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . which have 20-25% risk of malignancy transformation. a pH < 4. GERD 1) Erosion of the enamel 6. - 2) Supernumerary teeth 3) Multiple odontomas 4) Impacted teeth ENT. hyperemia & edema of the erytenoid. Treatment: Anti-reflux therapy: PPI for 3 months "at least". taste loss) Pernicious anemia 1) Red and smooth dorsum of the tongue with areas of ulcerations ENT. Anemia Iron deficiency anemia 1) Angular cheilitis ** D.D of angular cheilitis Anemias Fungal infection (candida) Vitamin B2 (Riboflavin)deficiency 2) Atrophic glossitis: smooth and red tongue (may result in burning sensation. Adel Adwan . Dr.76 Petuz-jeghers-syndrome: 1) Perioral pigmented lesions ii.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Hematological diseases 1. 77 Sickle cell anemia 1) Mandibular salmonella osteomyelitis 2) Pulpal necrosis (center of tooth) 3) Dentofacial deformities radiographically usually asymptomatic 2. Leukemia 1) Ulcerations 2) Gingival enlargement and spontaneous gingival hemorrhage 3) Tooth loosening 4) Delayed wound healing 5) Candidiasis and herpetic infections are relatively common oral complications of leukemia. ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen 78 3. Lymphoma 1) Nodular non-Hodgkin's lymphoma in a patient with AIDS 4. Langerhans cell histiocytosis 1) Radiologic findings demonstrate characteristic "floating teeth". 2) Letterer –siwe form : large ulcerations , Ecchymosis ,gingivitis , Periodontitis , And subsequent tooth loss. 3) Hand-schuller christian form: irregular ulcerations of the the hard palate , which may be the primary manifestation of the disease , gingival hyperplasia , difficulty in chewing , and foul-smelling breath may also occur. iii. Endocrine diseases 1. DM 1) Periodontal disease (occurs more frequently and progress rapidly than in normal patients). 2) diabetic sialadenosis (diffuse bilateral enlargement). 3) oral candidiasis 4) migratory glossitis 5) xerostomia 2. Hypothyroidism 1) Thickenning of the lips (accumulation of glyosaminoglycans. 2) Macroglossia (accumulation of glyosaminoglycans. 3) Failing of teeth eruption (childhood). 3. Addison's disease 1) Diffuse or patchy brown macular pigmentation of the oral mucosa caused by excess melanin ( oral melanosis ). ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen 79 4. Acromegaly 1) Enlargement of facial soft tissues (coarse facial appearence) 2) Mandibular prognathism as a result of the increased growth of the mandible (spacing of the teeth) 3) Macroglossia iv. Metabolic diseases 1. Amyloidosis 1) Macroglossia (12 -40 % of patients and may appear as diffuse or nodular enlargement of the tongue). 2) Amyloid nodules of the oral mucosa or of the lips (sometimes associated with ulceration and submucosal hemorrhage). ** Biopsy of gingival tissue or labial salivary gland is alternative specimen sources for diagnosis of amyloidosis. v. Connective tissue & rheumatologic diseases 1. Rheumatoid arthritis 1) TMJ arthritis 2) Cricothyroid & cricoarytenoid subluxation 2. Behcets disease 1) Recurrent oral ulcers 3. Sjogren syndrome 1) Pached appearance of the mouth and oral mucosa due to profound dryness. ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen painless ulcerations of the gingiva . 3) Parotid enlargement 4. reddened.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .81 2) Dryness of the mouth and inadequate saliva formation result in a tendency to dental caries. Pulmonary Wegener's granulomatosis 1) Strawberry gingivitis: gingivae take on a characteristic swollen. Dr. ENT. Sarcoidosis 1) Multipe. ** Biposy reveal noncaseating granuloma surrounded by multinucleate giant cells along with lymphocytic infiltrate. 3) Diffuse injection of oral and pharyngeal mucosa 5. nodular . buccal mucosa . Adel Adwan . labial mucosa.pathognomonic for kawasaki disease. and granular appearance. Kawasaki disease 1) Erythema or fissuring of the lips 2) Strawberry tongue. and palate . 2) Herpes simplex: more aggressive.80 2) Rarely sarcoidosis may involve the tongue with swelling . Mucocutaneous diseases 1. ** HIV infection should be considered with repeated oral candidiasis in absence of other risk factors. ENT. 2) Hypertrophic: resembles leukoplakia 3) Atrophic or erosive: painful 2. 2) Fissured tongue. and diffuse ** Any oral ulcers should be evaluated for HSV in HIV patient. vii. Adel Adwan .and enlargement. first presenting). vi. Psoriasis 1) Geographic tongue. Dr. prolonged. Lichen planus 1) Reticular: fine. lacy appearance on buccal mucosa (Wickam’s striae).Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . HIV 1) Candidiasis (90% of pts. Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . red patches or papules on the hard palate. Purple.82 3) Hairy leukoplakia (white plaques commonly on the lateral portions of the tongue. and gingiva. mucosa. Adel Adwan . 4) Kaposi sarcoma (KS): most common malignancy in HIV patients. 5) aphthous like ulceration …etc ENT. Dr. 4.83 Apnea Definition RDI(Respiratory Disturbance Index): is used in reporting polysomnography (sleed study)findings. - If <10 episodes: mild apnea - 10-30 episodes: moderate apnea - >30 episodes: severe apnea - So. while in adults is obesity. Causes of obstruction according to site: Nose: 1. definition of severe apnea: more than 30 episodes of apnea each more than 10 seconds in a period of 7 hour sleep. Tumors 2. Foreign body 3. Tonsilllar hypertrophy 2. Foreign body 3. Foreign body (rhinolith) 3. such as angiofibroma: characteristically found in males and never in females. according to the number of apnea episodes( cessation of breathing >10 seconds for each) in a period of 7 hours sleep. Adel Adwan . Nasal polyposis 4. Any type of rhinitis 2. Enlarged tongue. if you found this tumor in a female do karyotyping! Oropharynx: 1. Causes of apnea ** The most common cause in children is adenotonsillar hypertrophy. in syndromes such as down syndrome. Tumors Hypopharynx: 1. Tumors Nasopharynx: 1. Adenoid hypertrophy 2. Webs ENT. Dr. Types of apnea 1) Central 2) Peripheral or obstructive: any obstruction above the vocal cords.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Treacher-Collins syndrome. Tumors. retrognathia or micrognathia. Adel Adwan . Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .84 Adenoid face: Due to adenoid hypertrophy Characteristics - Mouth breather Snoring Obstructive sleep apnea High arch palate (V-shaped palate) Protruded mandible (Prognathia) Recurrent chest infections ENT. Clinical features Symptoms: 1. Group A streptococcal bacteria resulting in strep throat. fever and chills. Spread is by droplet infection. Sometimes . and other materials that enter the body through the mouth and sinuses. pus).tonsillitis is caused by a superinfection of spirochaeta and treponema. Severe sore throat (which may be experienced as referred pain to the ears) 2. Acute tonsillitis (< 1 month) can either be bacterial or viral in origin 2. is mostly caused by bacterial infection. It is commonest in winter and spring. Adel Adwan . They also produce antibodies to help fight off infections.e. 2. They act like filters to trap bacteria. Chronic tonsillitis (> 3 months). Q: which muscle is present in the bed of the tonsils? A: Superior constrictor muscle. 3. 2.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . In infants under 3 years of age with acute tonsillitis. 15% of cases were found to be streptococcal. viruses. Enlarged and tender neck cervical lymph nodes. in this case called Vincent's angina or Plaut-Vincent angina. In older children. Signs: 1. located on both sides of the throat that are part of the body immune system. up to 50% of cases are due to streptococcus pyogenes. Red. Viral tonsillitis such as the Epstein-Barr virus (the cause of infectious mononucleosis )or the Adenovirus. 2. Painful/difficult swallowing 3. ENT. Headache. which can last for long periods if not treated.85 Tonsillitis Definition - Tonsillitis is an infection and swelling of the tonsils. Subacute tonsillitis (1-3 months) is caused by the bacterium Actinomyces 3. The tonsils are lymph nodes. Dr. the remainder were probably viral. Etiology 1. Tonsil function Prevent infections in two ways: 1. Types 1. swollen tonsils which may have a purulent exudative coating of white patches )i. Prevalence - - Acute tonsillitis can occur at any age but is most frequent in children under 9 years. by which time treatment should already be initiated. Investigations - Inflammatory parameters: The CBC shows leukocytosis. which can identify the causative organism as a group A streptococcus in just 10 minutes. Adel Adwan . - Grade 4+: Tonsils occupy 75 percent or more of the lateral dimension of the oropharynx (kissing tonsils). - Grade 3+: Tonsils occupy less than 75 percent of the lateral dimension of the oropharynx. Scarlet fever Diphtheria Agranulocytosis HIV ENT. and (ESR) and (CRP) are elevated. - Grade 1+: Tonsils occupy less than 25 percent of the lateral dimension of the oropharynx as measured between the anterior tonsillar pillars. Presents with splenomegaly. It is better to perform a rapid immunoassay.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . called glandular fever.86 Grading of tonsil hypertrophy: - Grade 0: Tonsils are entirely within the tonsillar fossa. severe membranous tonsillitis. Bacteriologic testing: A bacterial culture is rarely taken from throat smears because it usually takes 2–3 days to obtain a definitive result. Dr. - Grade 2+: Tonsils occupy less than 50 percent of the lateral dimension of the oropharynx. Differential Diagnosis - Infectious mononucleosis: Caused by EBV. Congested anterior pillar (dilated vessels) - Complicated tonsillitis: Rheumatic fever. mouth breathing. Encourage the patient to drink Antibiotics in severe cases. Jugulodigastric LAP 6. Penicillin by injection followed by oral treatment remains the treatment of choice. ENT. Soluble aspirin or paracetamol held in the mouth and then swallowed eases the discomfort. Peritonsillar abscess (quinsy). However. when they become more wide and more deep. Intratonsillar pussy cyst 5.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Macrolides or oral cephalosporins can be used in patients allergic to penicillin.87 Treatment - Rest—the patient will usually prefer to be in bed. Adel Adwan . etc. Acute rheumatism. - Chronic tonsillitis: 1. Hypertrophy of the tonsils can result in snoring.glomerulonephritis. - Mild and moderate obstructive sleep apnea. Pulmonary infections (pneumonia.). symptomatic tonsils regardless of being symmetric or asymmetric are also considered an indication for tonsillectomy. Asymmetric tonsils. Tonsillolith 4. 2. the tonsils are called cryptic) 3. Indications for tonsillectomy Absolute indications: - Severe apnea - Suspected malignancy – for biopsy Relative indications: - Recurrent tonsillitis : > 6 times yearly. disturbed sleep. Complications of tonsillitis - Acute otitis media (the most common complication). - 2nd attack of febrile convulsions due to acute otitis media. Cryptic tonsils( each tonsil contains 11-17 crypti. - 2nd attack of peritonsillar abscess (Quinsy). Remember that aspirin should not be given to children under the age of 12 years because of the risk of Reye’s syndrome. 5 times in 2 consecutive years or 3 times in 3 consecutive years. Acute nephritis IgA nephropathy. and obstructive sleep apnea . It is recommended that treatment be continued for 10 days to reduce the risk of reactivation. Dr. the dorsal lingual artery is ligated by one clip and the descending palatine artery is ligated by a third clip. a branch of the external carotid artery. – The descending palatine artery. a branch of the third portion of the maxillary artery which is one of the terminal branches of the external carotid artery.88 - As part of some surgery. Primary: within 24 hours after surgery. a branch of the external carotid artery. this will result in nasal tone speech: ◦ Rhinolalia aperta ◦ Rhinolalia calusa ENT. - CO2 laser tonsillectomy - Coblation: US+ co2 laser - Galotine method(by a snare) Complications of tonsillectomy - Bleeding: 1. – The tonsillar and the ascending palatine arteries. such as UPPP(uvulopalatopharyngoplasty) - Recurrent otitis media Contraindications for tonsillectomy(all are relative) - Patient's medical condition - Acute tonsillitis - Coagulopathy - Obesity Methods of tonsillectomy - Dissecting - Ligation Blood supply to the pharynx(the vessels that are ligated): – The dorsal branches of the lingual artery. which are branches of the facial artery. Reactionary: within 1-5 days 3. ** The facial and the ascending pharyngeal arteries are ligated together. - Velo pharyngeal insufficiency: Because of injury to the posterior pillar(palatopharyngeus muscle). a branch of the external carotid artery. Dr. – The ascending pharyngeal artery. Secondary: after the 5th day till day 14.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 2. either bad surgeon or bad patient. Adel Adwan . usually because of infection. It is also known as ptyalism in pregnancy. the parasympathetic nervous system. Functions of the saliva 1. primarily. it reflects inefficient. ** The most salivary glands to secrete salive in response to stimulus is parotid glands. serous.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . . 2. Submandibular gland: 70% of daily salivary flow.Minor salivary glands: 1% of daily salivary flow. Minor salivary glands 1%. Sublingual gland: 5% of daily flow. mixed serous and mucinous. 4. Moistening of food bolus Prevention of dental caries Protection of mucosa from desiccation Medium for lysozyme. Salivary glands They are divided into: . 4. uncoordinated swallowing and poorly synchronized lip closure. parotid glands: 25% of daily salivary flow. which are supplied by glossopharengeal nerve. Dr. 2.89 Drooling Definition Drooling is the salivary incontinence or the spillage of saliva over the lower lip. mucinous. 5. 3. ENT. ** The most salivary glands to secrete saliva (saliva flow) is submandibular glands.Major salivary glands: 1. ** Salivary glands are controlled by the autonomic nervous system. 3. Adel Adwan . Parotid gland Innervated by parasympathetic fibers originating in the inferior salivary nucleus in medulla CN IX (Glossopharyngeal nerve) Petrosal ganglion Lesser superficial petrosal nerve Otic ganglion Auricotemporal nerve Submandibular & sublingual glands Innervated by Preganglionic PS fibers originating in the superior salivary nucleus in medulla Nervus intermedius CN VII (Facial nerve) Chorda tympani Lingual nerve Submandibular ganglion. salivary peroxidase Digestion by emulgation of food and enzymatic cleavage of starch by α-amylase. Silaorrhea: an increase in salivary flow which can lead to drooling. secretory IgA. Every day . Nasal obstruction secondary to adenoid hypertrophy.Grade 3 – Moderate: humid lips and chin . o Indirect: nasal obstruction. rhinitis.91 Etiology of drooling - Acute: o Epiglottitis causef by H.Grade 2 – Mild: humid lips only .Occasional drooling . clothing changes.Profuse: clothes. nasal deformities Extent of underlying neurologic disease Hearing loss – may be tumor in the middle ear affecting chorda tympani Physical examination - Head posture.Severe . The severity of drooling can be classified with the following scale: .Not every day .Lips and chin wet .Dry . modified barium swallow "using video esophagoscopy".Only lips wet . Dental problems.Grade 1 – Dry. hands. use of bibs. Consider: audiogram.Never drools . Adel Adwan . anti convulsants. perkinoson’s disease. anti cholynesterase. malocclusion. History - Estimated quantity of saliva.Mild . o Peritonsillar abscess. hands & objects wet ENT.Grade 4 – Severe: clothing begins to be affected .Profuse . Dr. Swallowing control. - Chronic: o Neurological: CP. barium swallow.Never drools . no drooling . o Neoplasm. adenoid hypertrophy. strokes. Tongue control.Frequent drooling .Clothing soiled .Grade 5: . sinusitis. o Medication effect: tranquilizers.Constant drooling Measurement of Drooling Thomas-Stonell & Greenberg . large tongue.Moderate .Clothing.emotional state.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . and tray moist and wet The frequency of drooling can be quantitated based on the following scale: . Sores on lips or chin.ifnleunzae. .Regression is common. Addition of sublingual gland excision yielded good results with no ranula formation. complicated by ranula and lateral neck cysts.Glycopyrrolate: 70-90% response rates.Submandibular duct ligation is not advised as saliva constituents (viscous. increase tongue mobility and strength. - Ligation of salivary gland ducts . . Speech therapy: .Parotid duct ligation is technically easy with few complications. . urinary retention. 4. 2. however. there was 35% complication rate. 5.Can be fairly successful in patients with adequate intelligence.Has been used to control drooling in patients with amyotrophic lateral sclerosis with success.Parotid Duct Relocation: parotid duct relocation to tonsillare fossa produced unsatisfactory results. irritability). . Submandibular gland excision was added with success. fistulas. however.90 Treatment options 1.Severely retarded patients and those who drool profusely get little benefit. parotid duct stenosis. Adel Adwan . . This is the best treatment. Botulinum Toxin: . however associated with 50% re-fistulization rate. Surgery: . Behavioral therapy: . . . alkaline. decrease nasal regurgitation. positive and negative reinforcement. wound dehiscince. constipation. . parotid swelling.Goals: improve jaw stability and closure. may be useful in dystonic CP due to tone reduction. 3.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . improve lip closure. 30-35% will discontinue medication due to side effects (excessive dry mouth. ENT.Decrease drooling with few side effects in this terminally ill population.Usually disappointing results unless started in infancy. high Ca+2. including: cysts. Dr. suppurative parotitis. decreased sweating.Several recent small series report success with intraglandular injection of botulinum toxin. phosphate) are more prone to form stones especially as the route of the duct is uphill. Radiation therapy: . - Submandibular Duct Relocation: Submandibular duct relocation was performed with good results.Trihexyphenidyl: efficacy and side effects similar to glycopyrrolate.Scopolamine patch can also be used and has the advantage of only needing to be changed every three days. overcorrection.Incorporates cuing.Duct rerouting procedures: . 6. Medications: . xerostomia. increase dental & gingival infection. - Excision of salivary glands. Adel Adwan . - Laser photocoagulation of parotid gland ducts . locate and divide chorda tympani which supplies the submandibular & sublingual salivary glands. Surgery is a final option for those patients with severe drooling problems not adequately addressed by noninvasive means or medication.Few complications. . Dr. A trial of medication is warranted if noninvasive methods fail.Showed improvement in drooling. .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . - Transtympanic Neurectomy .Few complications. ENT. .80% success rate. Conclusion - Noninvasive modalities should be attempted first.Lift tympanomeatal flap.92 - Combinations of all the above. ENT. 7. Bilateral incomplete cleft lip. 3.93 Congenital diseases Cleft lip and palate - Cleft lip and palate is the most common congenital malformation involving the head and neck. Left incomplete cleft lip. Cleft classification: Clefts of the lip alone Either right or left-unilateral or bilateral. - Lip and palate embryologic development occurs in two phases. Left complete cleft lip. nose.000 births. Adel Adwan . complete (with extension into the nasal floor) or incomplete (anything from a slight muscle diastasis with intact epidermis to a small bridge of tissue connecting the medial and lateral lip elements or Simonart’s band). There are both syndromic and nonsyndromic clefts. Example: 1. cleft palate alone occurs in 1 in 2.000 births. and loss of the posterior nasal spine or notching).in the case of soft palate due to a merging process to carry the union backwards from the site of initial fusion. 2. premaxilla) and the second at 8 to 9 weeks (secondary palate). Unilateral (the palatal process of one side is fused with the septum. Cleft palate: Due to failure of fusion of the two palatine processes or . Dr. 2. midline diastasis of the levator muscles. Clefts of the palate Palatal clefts also may be: 1. 8. 5. 4. Cleft lip: Due to abnormal development of the medial nasal and maxillary processes at the time that they bulge downwards in front of and below the nasal pit and when their surfaces should touch. - Cleft lip and palate occurs in 1 in 1. the first beginning at 4 to 5 weeks (lip. Right complete cleft lip. and it presents long-term multidisciplinary management problems. Primary (anterior to incisive canal) and secondary (posterior to incisive canal including also bifid uvula. resulting in communication of the oral and nasal cavities on one side only) or bilateral (no connection between either palatal process and the septum). Right complete & left incomplete cleft lip. Right incomplete cleft lip. Bilateral complete cleft lip. the epithelium over them fuse and then break down.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 6. Left complete & right incomplete cleft lip. Common syndromes with facial clefts: - Apert’s syndrome. further therapeutic intervention will be required that may include surgical correction of secondary lip and nasal deformities. about 25%. Prevalence of cleft types in the cleft population: - Clefts of the lip. ENT. or lip and alveolus.94 3. upper airway obstruction. cleft palate. and palate. Clefts of the secondary palate. glossoptosis (posterior displacement of the tongue). Stickler’s syndrome. Clefts of the lip only. Dr. Disturbance of facial growth. speech therapy (and possible correction of velopharyngeal incompetence). Cleft lip & palate are associated with: - Nasal deformity. Van der Woude’s syndrome. Complete cleft palate refers to a cleft of both the primary and secondary palates and is nearly always associated with a cleft lip. Otitis media occurs due to Eustachian tube dysfunction (previously mentioned!). Orofacial-digital II syndrome. otologic and audiologic care. Pieree Robin sequence: Retrognathia/ micognathia. and orthognathic surgery. Cleft palate repair: Cleft palate repair often is performed at 10 to 12 months of age when a lip repair has been performed earlier. In many cases. Treacher Collins syndrome. alveolus. Cleft palate occurs in females > males. Ectodermal dysplasia syndrome. and has a hemoglobin of 10 g. weighs 10 pounds.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Otitis media with hearing loss. Waardenburg’s syndrome. about 30%. Cleft lip repair: The rule of tens of lip repair is performed when the infant is at least 10 weeks old. about 45%. Cleft lip occurs in males > females. Adel Adwan . Incomplete cleft palate is synonymous with a cleft of the secondary palate or may be used to describe a palatal cleft with an area of intact mucosa associated with a cleft lip. Orofacial-digital I syndrome. dental and orthodontic care. 4. the fascia. but as a point of attachment for muscles and ligaments it is essential for laryngeal functions. it extends from C1-C4. The thyroid gland is attached to and covers the side of the larynx from the cricoid cartilage to the level of the oblique line of the thyroid cartilage. and that explains why they are obligate nasal breathers as the epiglottis is high in location and makes a sort of obstruction to the air entering from the mouth. It is situated from the level of C3-C6 or C7. Anteriorly it is covered by the skin. and the infrahyoid muscles.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Hyoid bone: - - Not strictly considered part of the larynx. Dr. The lower 2/3's of the flattened laminas are fused anteriorly in the midline forming an ENT. It is an organ of phonation and breathing. Thyroid cartilage: - - This is the largest cartilage of the larynx composed of two flat wings. It is intimately attached to the larynx by the thyrohyoid and the thyroepiglottic ligaments and the extrinsic muscles of the larynx. the laminas (alas) & two posterior processes. In pediatric age group.95 The larynx Larynx anatomy The skeleton - - - - The larynx extends from the root of the tongue to the trachea. Adel Adwan . horns or cornu (two greater cornu & two lesser cornu). Cricoid cartilage: - This cartilage is shaped like a signet ring. The upper 1/3's of the laminas are not fused and form the thyroid notch. Adel Adwan . most of which are hyaline) and thus it is very flexible. ** All cartilages of the larynx are hyaline cartilage except the epiglottis which is elastic cartilage. the narrow part of ring faces anteriorly (the cricoid arch) while the broad signet part faces posteriorly (cricoid lamina).96 - angle of 90 degrees in the male (forming the Adam's apple) and 120 degrees in the female.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Corniculate: ENT. Artenoid. Epiglottis: - This leaf shaped cartilage is composed mainly of elastic cartilage (unlike the remaining laryngeal cartilages. Cuneiform. ** Laryngomalacia –which is the most common cause of stridor in children – occurs most commonly in the epiglottis because of its hyaline cartilage. It is the only complete cartilagenous ring in the upper airway. Dr. paired. rodlike structures embedded in the margin of the aryepiglottic folds.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Dr. They are found superio-anteriorly to the corniculate cartilages. paired. nodular structures found in the posterior part of the aryepiglottic folds. Cuneiform cartilage: Small.97 - - Artenoid cartilage: Two pyramidal-shaped structures which sit on the lateral part of the superior border of the lamina of the cricoid cartilage(the cricoarytenoid joints). They articulate with the summit of the arytenoid cartilages. Adel Adwan . Corniculate cartilage: Small. ** That's how they look all together: ENT. Dr. 2. - Movements : This joint permits 2 types of movements: 1. This explains why RA patients may present with hoarseness of voice. Cricoarytenoid joint: - Location : It is the articulation point between the inferior surface of the arytenoid cartilages and the posterosuperior surface of the cricoid lamina. - Movement : It permits the thyroid cartilage to rotate anteriorly or posteriorly on the cricoid cartilage.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . whereas lateral sliding causes abduction. ENT.The cricoarytenoid joints are bilateral (work in unison) but operate independent of one another. Cricothyroid Joint: - Location : Located between the facet on the posterolateral sides of the cricoid cartilage and the facet on the medial surface of the inferior cornua of the thyroid cartilage. Rotation of the arytenoid around an axis that runs obliquely from the dorsomediocranial to the ventrolaterocaudal position.Medial sliding causes adduction of the vocal folds. stridor or difficulty breathing). It articulates with the thyroid cartilage via the cricothyroid joints and with the arytenoids via the cricoarytenoid joints. Adel Adwan . Both of these are true synovial joints (so any disease that affect the synovial joints will affect these joints as well. Medial and lateral sliding of the arytenoid . permitting movement of the vocal process medially or laterally. The rotation in which the anterior vocal process deviates medially causes adduction of the vocal folds. When the thyroid cartilage is rotated anteriorly. the anterior arch of the cricoid will come in closer proximity to the lower border of the thyroid cartilage. . whereas a lateral rotation causes abduction.98 The joints ** The cricoid cartilage may be regarded as the base and support for the entire larynx. 99 Ligaments and Membranes: ** The laryngeal membranes and ligaments can be divided into two subgroups: The extrinsic ligaments (containing the thyrohyoid membrane. Hyoepiglottic Ligament: - Attaches the anterior upper part of the epiglottis to the hyoid bone. and cricotracheal ligament) The intrinsic ligaments (containing the quadrangular membrane. which is pierced on each side by the superior laryngeal artery and vein and the internal branch of the superior laryngeal nerve. The tips of the superior horns of the thyroid cartilage are connected to the greater cornua of the hyoid bone by the lateral thyrohyoid ligaments. thyroepiglottic ligament. It is pierced laterally on each side by the external branch of the superior laryngeal nerve and recurrent laryngeal nerve. Thyroepiglottic Ligament: - Attaches the anterior lower part of the epiglottis to the thyroid cartilage. Adel Adwan . hyoepiglottic ligament. vestibular ligament.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . which are also thickenings of the thyrohyoid membrane. cricothyroid ligament. It is the site where emergency cricotomy or thyrotomy done. conus elasticus. and vocal ligament). ENT. thyrohyoid ligaments. The extrinsic ligaments: Thyrohyoid Membrane: - - Median thyrohyoid ligament. Dr. Cricothyroid Membrane: - - This broad membrane is attached from the superior border the cricoid to the inferior surface of the thyroid cartilage. The superior edge of the this part of the conus elasticus is free and thickened between its two attachments. extends from the upper border of the cricoid cartilage to the lower border of the thyroid cartilage. * So. ENT. the angle of the thyroid lamina and vocal process of the arytenoid cartilage.Upper edge: Vocal ligament (true vocal cords). The lateral part of this membrane extends from the superior inner border of the cricoid cartilage to the inner surface of the thyroid angle and posteriorly to the tip of the vocal process of the arytenoid cartilage. Dr.Lower edge: Vestibular ligament (False vocal cord) Conus Elasticus (Cricothyroid or the Cricovocal Membrane): - - This membrane arises from the inner surface of the cricoid arch and it consists of two distinct parts: The anterior or superficial part. and forms the vocal ligament (true vocal cord). The intrinsic ligaments: Quadrangular Membrane: - It extends from the lateral margins of the epiglottis within the aryepiglottic fold and attaches to the arytenoid and corniculate cartilages. * So. its: . The superior edge is also free and it is covered with aryepiglottic fold of mucosa.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .Upper edge: Aryepiglottic fold . Adel Adwan . The inferior free edge is thickened to form the vestibular ligament (false vocal cord).011 Cricotracheal Ligament: - The inferior border of the cricoid cartilage is joined to the first ring of the trachea by this ligament. its: . also called the medial cricothyroid ligament. Adel Adwan . ligaments and skeletal structures of the larynx have been shown to delineate several potential spaces and compartments. Inferior border: vocal cords. Inferior border: lower border of cricoids cartilage. The internal cavity of the larynx is divided into: Supraglottic space (vestibule): Superior border: free margin of the epiglottis and aryepiglottic folds Inferior border: lower margin of the ventricular (false vocal folds). ENT.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . ** Between the vestibular ligament (false vocal cord)superiorly & the vocal ligament (true vocal cord) inferiorly is the ventricle. Subglottic space: Superior border: vocal cords. Spaces: The various membranes.010 - Lower edge: Inner surface of cricoid. ** Between the tongue superiorly and the epiglottis inferiorly is the volecule. Dr. Glottic space: Superior border: ventricular folds (false vocal cords). The superior drainage joins the superior and middle thyroid veins and then the internal jugular. 2. the sympathetic fibers arising from the superior cervical ganglion also innervate the larynx. and constrictor muscle. Dr. ** Recurrent laryngeal nerve: supplies sensation below vocal cords & intrinsic muscles of the larynx except the cricothyroid muscle. as well as by the recurrent laryngeal nerve. The vagus reaches the larynx via the internal and external branches of the superior laryngeal nerve. however. The vagus (cranial nerve X) is the main nerve innervating the larynx and it arises from the nucleus ambiguus (branchiomeric nucleus) and the dorsal motor nucleus of vagus (autonomic. The inferior drainage joins the middle thyroid vein and the inferior thyroid vein. ENT. which essentially follow the arteries in their course (see arterial blood supply). Adel Adwan . ** Superior thyroid artery is a branch of the external carotid artery. It is important to note that the innervation of the larynx is mainly from the parasympathetic nervous system. which cause tension of the vocal cords. External branch: supplies cricothyroid muscle. Most of the arteries anastomose freely with each other. ** Superior laryngeal nerve: it is divided into 2 branches: 1. ** Inferior thyroid artery is a branch of the thyrocervical trunk which is a branch of the subclavian artery. parasympathetic nucleus). Blood supply: The arterial blood supply of the larynx is derived from the laryngeal branches of superior and inferior thyroid arteries and to a small extent from the cricothyroid.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .012 Nerve supply: ** The nerve supply to the larynx is derived from the motor nuclei in the medulla oblongata in the brainstem. which empties into the superior vena cava. Internal branch: supplies sensation above the vocal cords. Venous drainage: The venous drainage is supplied by the superior and inferior laryngeal veins. The intrinsic muscles B. It is also called posticus muscle. Inferior group: The area of the larynx below the vocal cords is drained into the middle (level III) and inferior jugular nodes (level IV) as well as to the paratracheal lymph nodes. with the exception of the free margins of the vocal folds themselves. The lymphatics of the larynx are divided into a superior and an inferior group.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .Cricothyroid muscle which causes tension of vocal cords. ** The most important intrinsic muscles are: . ENT.Psterior cricoarytenoid muscle which causes abduction of vocal cords. Posterior cricoarytenoid muscle Interarytenoid muscles a. Superior group: The area of the larynx above the vocal cords is drained into the superior (level II)and middle jugular nodes (level III). . . Transverse arytenoid muscle b. Adel Adwan .Lateral cricoarytenoid muscle which causes adduction of vocal cords. Muscles: ** The laryngeal musculature can be divided into two groups: A. Lateral cricoarytenoid muscle b. It may be considered the most important muscle in the human body to its function. The extrinsic muscles The intrinsic muscles: - - - cricoarytenoid muscles a. Oblique arytenoids muscle Thyroarytenoid muscle thyroepiglottic muscle Cricothyroid muscle ** All the intrinsic muscles of the larynx are supplied by the recurrent laryngeal nerve except the cricothyroid muscle which is supplied by the external branch of the superior laryngeal nerve.013 Lymphatic drainage: The larynx is very well supplied with lymphatics. Dr. Vocalis muscle. e.Deep layer – denser still. .Stylopharyngeus muscle. 2. also called the strap muscles. Vocal Fold Microstructure ** There are 5 histologically discrete layers. respiration and phonation.Superficial layer – composed of loose fibrous matrix.Intermediate layer – composed of elastic fibers and has slightly more mass. ** Stylopharyngeus muscle is the only muscle innervated by the glossopharyngeal nerve.Styhyoid muscle. Infrahyoid muscles: . it provides stability and mass. ** They are divided into 2 groups: 1. . in GERD.Mylohyoid muscle. .014 The extrinsic muscles: ** The extrinsic muscles. . ** Tissues of 3rd & 4th layers together are known as the vocal ligament. Adel Adwan . and here occurs reinke's edema in chronic laryngitis. composed of collagenous fibers. .g.Omohyoid muscle.Main body of the vocal fold.Thyrohyoid muscle. . The vocal ligament develops throughout childhood until the larynx reaches full maturity (puberty). ENT. Dr.Sternohyoid muscle. These layers vary in composition and mechanical properties.Thyrohyoid muscle. . Lamina propria (3 layers): . are capable of moving the larynx up or down during deglutition. composition described as soft gelatin. Suprahyoid muscles: .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .Digastric muscle (anterior & posterior belly). . . . ** 5 histologic layers from most superficial to most deep are: • • • Epithelium – squamous epithelium.Sternothyroid muscle. It is known as reinke's space.Geniohyoid muscle. Fixation of the thorax aided by glottic closure. Acquired: Allergy to specific drugs (e. edema and swelling of the lips. 2. 2. ** Angioedema: two types: 1. False vocal cords (vestibular folds).Closure of the glottis.Cough reflex. Functions of the larynx: 1. epiglottis & arytenoids. 3. Epiglottis.015 ** Quink edema: It is type I hypersensitivity reaction. Dr. insect bites or even emotional stress. Adel Adwan . 3. Protective mechanisms of the larynx: 1.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .g. So. ACEI). 4. intubation or even tracheostomy.Closure of the aditus. . uvula. The edema occurs mainly in the superficial layer of lamina propria. Function of Macula Flava: Hypothesized to protect the membranous portion of the vocal folds during vibration from mechanical damage. oropharynx. 5. any patient presenting with angioedema should be investigated for C1 esterase inhibitor level. 2. tongue. Phonation.Reflex respiratory arrest. It is an emergency which requires management with adrenalin. . Vocal cords The strongest ENT. occurs in anaphylactic shock & angioedema. soft palate. Respiration. Congenital: C1 esterase inhibitor deficiency. . certain foods. Protection of the lower airway: . Patient presents with difficulty breathing. vestibular folds. vocal cords. - Palpation .Rigid . .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . lingual surface of the epiglottis. – The cricothyroid membrane and the cricoid cartilage. This is present in post cricoid carcinoma. Adel Adwan . – The simultaneous movement of the larynx and thyroid gland on swallowing. It moves upward on swallowing. paying attention to the following:– The thyroid cartilage. odema.vertebral soft tissue. . ENT. the thyroid prominence can only be seen in men. and closed in the mid line when patient say's eeeeeeeeeeeee Investigations: - Radiography Plain views in the sagittal or lateral plane for foreign body. But when lost it means there is increase in the thickness of pre. Stroboscopy. etc.inspection by means of mirror or telescopic system 90 degree.Flexable – By all the above methods examine the following areas:– Base of the tongue.The laryngeal skeleton and neighboring structures are palpated during respiration and swallowing. Irritative cough Dysphagia Pain in the neck. Dr. CT scan. Laryngography. – The carotid artery with the carotid bulb which must not be confused with neighboring cervical lymph nodes. edema or abscess. The normal colour of vocal cords is whitish. . Biopsy. which may radiate to the ears Examinations of the larynx Inspection of the larynx Normally.Laryngeal click: Normally it is present and you feel click sensation by moving the larynx side to side. piriform sinus.Direct laryngoscopy:. glossoepiglottic and aryepiglottic folds. epiglottis. surface is smooth. Laryngoscopy . the palpating picks up pulsations. both vallecule.016 Clinical aspects of laryngeal diseases: Symptoms: - Hoarseness Stridor: Inspiratory type. absence of this movement indicates fixation of the larynx by infection or tumor.Indrawing of the suprasternal notch on inspiration combined with inspiratory stridor points to laryngotracheal obstruction by foreign body.Indirect laryngoscopy: . anterior and posterior commissures. tumor. is seen in epiglottitis.g. Vocal cord nodule: hyperkeratinization of mucosa. Vocal cord polyps Polyp: is an edematous or pedunculated or over pouching of mucosa. on lateral view. e. shows tracheal narrowing and suggestive of the diagnosis of croup. on frontal view.017 ** Important radiological signs: 1. Thumb printing sign. ENT. corticosteroids & speech physiotherapy.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Steeple sing ()برج الكنيسة. teachers. Dr. occurs mostly in people who talk loudly. Patients complain of hoarseness of voice. 2. Treated with speech physiotherapy then surgical excision. Most common site: between anterior one third & middle one third. Adel Adwan . singers. Treatment: Medical: Anti histamine. Surgical removal. Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Immediate complications 1. 2. Prophylaxis. 5. 4. bulbar poliomyelitits). To assist weaning from ventilation support in pt in the ICU. centred on the third and fourth rings .018 Tracheostomy Definition It is a surgical procedure to open a direct airway through an incision in the trachea. 3. The neck extended. the head straight (not turned to one side). Indications 1. *In emergency / Pediatric age Vertical incision . To help clear secretions in the upper airway. • The cricoid must be identified by palpation and the tracheal rings counted. infection. *In elective Horizontal incision. Procedure • • • The operation should be carried out under GA + ETT. Adel Adwan . Heamorrhage. • An opening is made into the trachea. • The incision should be centered midway between the cricoid cartilage and sternal notch . trauma. ENT. Impaired respiratory function (head trauma lead to unconsciousness. A transverse incision is preferable to vertical incision. Obstruction of the upper airway like foreign body. laryngeal tumours and facial fractures. • The strap muscles are identified and retracted laterally and the thyroid isthmus is divided. 019 2. Late complication 1. Dr. 4. 3. Subcutaneous emphysema. Cellulitis). for the patient). Good ABGs (relative. Clear lungs. Airway obstruction with aspiration.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 6. ENT. Tracheal stenosis. Adel Adwan . Scarring. Contraindications - No absolute contraindications! A strong relative contraindication to discrete surgical access to the airway is the anticipation that the blockage is a laryngeal carcinoma. 6. Infection (Tracheitis. Subcutaneous emphysema . Tube obstruction or displacement. 4. 5. 6. Trauma to recurrent laryngeal nerve and great vessles. Decannulation - When ventilation or suctioning no longer needed. Apnea. 5. Plugging with mucus . Pneumothorax. 2. and patient can control their own airway and not be at risk for aspiration. 3. Bleeding from tracheostomy site. - Can occur when patient has: Good cough. 1. 5. Atelectasis. Damage to esophagus. Aspiration. Tracheomalacia. Fistula formation (tracheocutaneous or trachea esophagus or trachea-innominate). 3. 2. 4. Bleeding. No pathogens in sputum. 7. Early complications The critical period is the first 48 hrs. Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .001 Head & Neck Headache & facial pain Introduction - Major reason for seeking medical care.symptoms. treatment. alcohol. – Family hx – Social hx • Physical examination Complete head & neck examination – cranial nerves – TMJ & muscles – scalp vessels – trigger points • • Neurological examination Diagnostic tests: EEG CT & or MRI EMG TMJ radiography Cervical spine film labs Clinical features suggesting serious cause – – – – – – Crescendo Early morning Vomiting Fever Seizures & other neurological symptomes Worst headache in my life ENT. tobaco). Adel Adwan . medications: anti hypertensive. quality. 9. precipitating factors). surgeries. time. Dr. 90% is vasculr headache. vasodiators. infections. traction or dilatation of pain sensitive structures: – dura of base of skull – cerebral artries – venous sinuses – cranial nerves 5. C3 Pathophysiology • • Pain Referred pain – Pattern of referred pain Clinical assessment • History – Hx of present illness( 1st occurrence. 10% is mixture of inflammation. 10. – Past medical hx ( head injury. C2 . then NSAIDs. upper lip or lower jaw. Treatment: Analgesics. brief duration (seconds) in the territory of the trigeminal nerve. then carbamazepine. 3) Sluder’s neuralgia and Vidian neuralgia • • • Intractable pain in the nose. cheek and lower jaw. Parietal & occipital. the glossopharyngeal nerve and perivascular carotid sympathetic fibers). Atypical facial pain Pain felt over the cheek. Usually bilaterally symmetrical. Adel Adwan . Females affected more than males. an arterial loop pushing on the sensory root in the posterior fossa. vidian neurectomy 4) Posttraumatic neuralgia 1. Facial pain Typical Neuralgias 1) Trigeminal neuralgia • • • • Characterized by recurring paroxysmal severe pain. Neuroma.000 – – Known malignancy Tenderness 1. Treatment: Start with paracetamol. Could be due to lesion of the sphenopalatine ganglion. eye. spontaneously or initiated by chewing. recur daily • Treated like trigeminal neuralgia. • Pain . touching the affected side of the face. sudden episodes of pain in the tonsil region one side only. 2. then surgical division of the nerve. ** Eagle syndrome is considered a type of glossopharyngeal neuralgia. 3. 90% recovery. Unknown aetiology. or vidian nerve. nose. 2) Glossopharyngeal neuralgia • Unknown cause • Equal both sexes • Severe. talking. Dr. ENT.severe for 1-2 hours.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . with consequent compression or stretching of the vascular and nervous structures contained in the retrostyloid compartment (in particular. Eagle syndrome is characterized by recurrent pain in the oropharynx and face due to an elongated styloid process or calcified stylohyoid ligament. ipsilateral ear. NB: vaccum headache: caused by obstruction of frontal recess which is the opening of frontal sinus as in: frontal sinusitis & deviated septum. No precipitant. sensory loss. Adel Adwan . M. It is more severe in the morning.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . thrombotic lesions. accompanied by reddening of the skin and lacrimation or watering of the nose & that's what differentiates it from the typical facial pain. increased in mid day. Its site depends on the affected sinus. Occurs mostly in females. days or weeks. leaning forwards. Extracranial lesions 1) Nasal : - - Malignant tumours of nose & sinuses. Treatment: Psychological consultation. Dr. burning. NB: contact headache: Caused by contact of septum & middle turbinate. Infection : acute & chronic sinusitis. ENT. Symptomatic neuralgias Intracranial lesions 1) Central lesions • • Tumours of the brain stem.002 Aching. occult nasopharyngeal ca.. Lasts for hours. shooting. Increased by coughing. Characterized by periodic attacks( start in the morning. straining. metastasis. analgesics. 2) Post herpetic neuralgia • • Herpes zoster may affect trigeminal nerve ganglion Vesicular rash covers one division commonly the 1st with severe pain.S. it is due to absorption of air in the sinus). subside by the end of the day. 003 2) Aural: - Infections: otitis externa. Dr.acute exacerbation or rarely malignant transformation. acuostic neuroma.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Tumours: orbital tumour. carcinoma. ASOM. 3) Ocular: - Infections: orbital cellulitis or abscess. Adel Adwan . NB: CSOM (Chronic Suppurative OM) is never painful except in : complication . ENT. complicated OM. Tumours: glomus. by history alone Treatment . 3) Migraine Congenital predisposition Triggered by hunger. stress. meningitis.prevention by avoiding precipitating factors. Etiology: 1) Raised intracranial pressure. sleep .004 - Errors of refraction & glaucoma. certain foods. brain haemorrhage. Headache Headache is one of the commonest symptoms in medical practice. appropriate medication. hormonal variations. NB: dental caries is the most common cause of facial pain.g. subdural haematoma. Dr. 5) Temporomandibular joint pain • • TMJ arthritis Costen's syndrome: – TMJ pain – Deafness – Tinnitus 6) Cervical: Cervical spondyolosis 2. head and face ENT. Trauma: post extraction neuralgia. cerebritis. affects any area of the head. 4) Tension headache More common in adult females Positive family history (40%) Maybe associated with migraine Produced by persistent contraction of the muscles of the neck. abscesses.too much or too little. Pathology-vascular dilatation Females affected more than males ? Proceeded by aura usually visual. Due to tumours. others. aching or throbbing often accompanied by nausea and vomiting Diagnosis . weakness Headache is unilateral or bilateral. paraesthesiae of hands. Adel Adwan . NB: ocular headache is more severe by the end of the day 4) Dental: - Infection: dental caries or peri-apical abscess.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 2) Inflammation of the brain and meninges e. partial or complete loss of vision. Adel Adwan . tenderness over the scalp. anti-histamine. Treatment by physio-therapist or rheumatologist. Due to cervical discs prolapse. Treatment: physio-therapy. ESR Elevated. Dr. no aura Caused by vascular dilatation of branches of external carotid Triggered by histamines.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Psychologic headache - Usually accompanied by depression. throbbing. temporomandibular joint dysfunction. Treatment: Cortisone. Cervical spondylosis - Pain mediates upwards from the neck to the occiput or vertex to the front of the head. steroids 3. anxiety. Temporal arteritis - - Due to acute inflammation of the artery. alcohol Treated by analgesics. swelling and redness of the overlying skin with general malaise. impacted wisdom teeth.x-ray. Pain from upper neck muscles - Can radiate over the head. secondary to other headaches. the cause unknown. Treatment: Refer to interested dental surgeon. Pains from head and neck muscles Pain from temporalis muscles - - Can arise from grinding teeth at night (bruxism). intense.30 Attacks occur in groups.005 Caused by emotional tension. Treatment: Physio-therapy. ENT. referral to rheumatologist. physiotherapy 5) Cluster headache 90% are men Age 20 . affects men and women over the age of 60. Diagnosis . analgesics. anxiety when the patient clenches the jaws too tightly. down to the shoulders. Pain from frontalis muscles - Usually due to bad posture at work or while driving. posture habit Treated by analgesics. Pain over the temples and frontal region. muscle relaxants. No organic lesion. 006 ENT.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Dr. Adel Adwan . . . .Facial palsy. give corticosteroids. Longitudinal fracture (80%): . just observation. . ENT.Fractures line goes via the middle ear cavity.Conductive hearing loss (CHL).Tinnitus.Lacerations at the external auditory canal.Sensorineural hearing loss (SNHL). - Management: .Audiometry (PTA) is mandatory! If SNHL.Patient comes complaining of: . - Diagnosis: CT scan. .Vertigo.Hemotympanum.Admission to neurosurgery ward for 24 hours for observation & to exclude epidural/ subdural hematoma. tympanic membrane & external auditory canal. Periorbital Ecchymosis (Raccoon’s Eyes). Mastoid Ecchymosis (Battle’s Sign).Admission to neurosurgery ward for 24 hours for observation & to exclude epidural/ subdural hematoma . .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Adel Adwan . .Tinnitus. . - Diagnosis: CT scan.Audiometry (PTA) is mandatory! If CHL. ** Signs of basal skull fracture: 1. Transverse fracture (20%): . - Management: .Farcture line goes through the internal auditory canal & labyrinth.Perforated ear drum.007 Temporal bone fractures: There are 2 types of fractures: 1. Hemotympanum. 3. - Clinical presentation: . 2.Hemotympanum.Facial palsy ! because of the relation of the tympanic segment of facial nerve. .Vertigo. .CSF leak. . Dr. Hemotympanum is basal skull fracture until proven otherwise. 2. . . 2. 1-4% cervical spine injuries. Domestic injuries and falls. and the orbital floor occur. Maxillofacial trauma includes injuries to any of the bony or fleshy structures of the face. The lower midface: where Le Fort I fractures occur. Third part (the lower face): Fractures are isolated to the mandible. Causes of maxillofacial trauma: - Road traffic accident (RTA) in 35-60% of cases. 25% of patients with severe facial trauma will develop Post Traumatic Stress Disorder. Industrial accidents.008 Maxillofacial trauma Definition: - Maxillofacial trauma refers to any injury to the face or jaw caused by physical force. Adel Adwan . o 3.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . The maxillofacial region is divided into 3 parts: 1. Fight and assault (interpersonal violence). foreign objects. or burns.5%) Complications: - 60% of patients with severe facial trauma have multisystem trauma and the potential for airway compromise. Dr. Sport and athletic injuries. ENT. In RTA: Mandible (61%) Maxilla (46%) Zygoma (27%) Nasal (19. Blindness occurs in 0. 20-50% concurrent brain injury. nasoethmoidal or zygomaticomaxillary complex. Second part (the midface): is further divided into: o The upper midface: where maxillary Le Fort II and Le Fort III fractures occur and/or where fractures of the nasal bones. First part (upper face): Fractures involve the frontal bone and sinus.5-3%. Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Adel Adwan .009 Anatomy: ENT. - Suspect if there is trauma to the nose or medial orbit. - Patients complain of pain on eye movement. - Associated with lacrimal disruption and dural tears.Imaging studies: – Plain radiographs are insensitive. Nasal Fractures - Most common of all facial fractures & it is the most common fracture in head & neck region. - Clinical findings: – Flattened nasal bridge or a saddle-shaped deformity of the nose. - 3 types: 4. . Adel Adwan . Dr. Naso-Ethmoidal-Orbital Fracture - Fractures that extend into the nose through the ethmoid bones. Laterally displaced 6. - Associated with: intracranial injuries.Clinical findings: – Nasal deformity – Edema and tenderness – Epistaxis – Crepitus and mobility ENT. – CT of the face with coronal cuts through the medial orbits. – Widening of the nasal bridge (telecanthus) – CSF rhinorrhea or epistaxis. - Caldwell view best evaluates the anterior wall fractures.021 Fractures: Frontal Sinus/ Bone Fractures: - Results from a direct blow to the frontal bone with blunt object. – Intranasal palpation reveals movement of the medial canthus. Nondisplaced . injuries to the orbital roof and dural tears.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Depressed 5. crepitus. – Tenderness. and mobility of the nasal complex. – In cases of noncompliance and late follow up. ecchymosis. Blunt trauma to the globe. swelling. - Management: – In managing nasal trauma. - – Enopthalmus or sunken eyes. then if there is NO edema. Dr. – CT Head to rule out intracranial injuries. – Impaired ocular motility. - Clinical Findings – Periorbital tenderness. do nasal bone reduction. Direct blow to the infraorbital rim. – Step off deformity Imaging studies – Radiographs. if there is edema. Zygomatic arch ENT. – Infraorbital anesthesia. Lateral or Waters view to confirm your diagnosis. Tripod fracture (most serious): consist of fractures through: a. Zygoma Fractures - Two types of fractures can occur: 1. instead. the bone will be already healed and nasal bone reduction would not be done. follow up after 5-14 days till the edema & swelling resolve then do nasal bone reduction. cranioplasty after 6 months will be the appropriate management. Adel Adwan .020 - Diagnosis: History and physical exam. However. 2. first check for septal hematoma (which is an emergency & need to be drained). – CT of orbits. Arch fracture (most common) 2.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Orbital Blowout Fractures - 2 mechanisms of injury: 1. Zygomaticofrontal suture c. – Malocclusion of the teeth. – Motion of the maxilla while the nasal bridge remains stable. LeFort I - Definition: – Horizontal fracture of the maxilla at the level of the nasal fossa. LeFort III ENT.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .022 b. Inferior orbital rim and floor Maxillary Fractures/ LeFort - Classified as LeFort fractures. – Separates the alveolar process and hard palate from the rest of maxilla. – Allows motion of the maxilla while the nasal bridge remains stable. - Clinical findings: – Facial edema. LeFort II - Definition: – Pyramidal fracture Maxilla Nasal bones Medial aspect of the orbits - Clinical findings: – Marked facial edema – Nasal flattening – Traumatic telecanthus – Epistaxis or CSF rhinorrhea – Movement of the upper jaw and the nose. Adel Adwan . Dr. Dr. Mandible Fractures - Mandibular fractures are the third most common facial fracture.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen Clinical findings . nasal bones and zygoma open book facial fracture. - The most common direction for dislocation is anteromedial. – Malocclusion of the teeth ENT.023 - Definition: – Fractures through: Maxilla Zygoma Nasal bones Ethmoid bones Base of the skull - Clinical findings: – Dish faced deformity or donkey face. ** the least common site of mandibular fracture is coronoidal process. ** The most common site of mandibular fracture is condyle process (subchondylar). Adel Adwan . – Epistaxis and CSF rhinorrhea. – Motion of the maxilla. – Mandibular pain. - Assaults and falls on the chin account for most of the injuries. – Severe airway obstruction. craniofacial dissociation. ** All fractures should be treated with antibiotics and tetanus prophylaxis. Adel Adwan . oral surgery referral in 1-2 days – Displaced fractures. Dr.024 - – Separation of teeth with intraoral bleeding – Inability to fully open mouth. – Preauricular pain with biting. – Positive tongue blade test. - Treatment – Nondisplaced fractures: 1. Soft diet 3. ENT.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . open fractures and fractures with associated dental trauma: Urgent oral surgery consultation. Radiographs: Panoramic view is the view of choice for mandible fractures. Analgesics 2. ENT. Motor function: Muscles of facial expression. 3.General Visceral Efferent (GVE).General Visceral Efferent (GVE).025 Facial palsy Facial nerve The facial nerve is the seventh (VII) of twelve paired cranial nerves. Nuclei: 1.Oropharynx above the palatine tonsil. It emerges from the brainstem between the pons and the medulla.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Secretomotor function (parasympathetic innervation): .Taste sensations from the anterior two-thirds of the tongue. 2. . Superior salivatory nucleus . Sensory function: . Lacrimatory nucleus . Stylohyoid muscle.Special Visceral Efferent (SVE). Facial nerve is a mixed nerve. Dr. Stapedius muscle of the middle ear. Lateral sensory root (nervus intermedius). which contains sensory & parasympathetic fibers.Lacrimal glands. Posterior belly of digastrics muscle. 3. .Nasal glands. 2. having 2 roots: 1. 2. . Adel Adwan . Facial nucleus . Function: - 1. Medial motor root.Submandibular & sublingual salivary glands. Posterior auricular nerve: controls movements of some of the scalp muscles around the ear. the nerve expands from the sensory geniculate ganglion to give: Branches inside the facial canal: 1. as well as special taste sensory fibers to the palate via the nerve of pterygoid canal (Vidian Nerve). Branch to Posterior belly of Digastric and Stylohyoid muscle. then through the stylomastoid foramen & passes through the parotid gland. At the bottom of the meatus. Then it descends in the posterior wall of the middle ear. 2. The two roots emerge from the anterior surface of the brain between the pons and Medulla oblongata. sublingual gland and special sensory taste fibers for the anterior 2/3 of the tongue. They pass laterally & forward in the posterior cranial fossa to opening of the internal acoustic meatus. behind the pyramid. the nerve enters the facial canal & runs laterally above the vestibule of the labyrinith until it reaches the medial wall of the tympanic cavity. Nerve to stapedius : provides motor innervation for stapedius muscle in middle ear. Branches distal to stylomastoid foramen: 1. ENT. Adel Adwan . Chorda tympani : provides parasympathetic innervation to submandibular gland. Here.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Greater petrosal nerve : provides parasympathetic innervation to lacrimal gland. Dr.026 Course: The motor part arises from the facial nerve nucleus in the pons while the sensory part arises from the nervus intermedius. 3. it doesn’t innervate it. 2. Though it passes through the parotid gland . Temporal branch 2. Zygomatic branch. Mandibular branch. such as: — Wrinkling the brow — Showing teeth — Frowning — Closing the eyes tightly — Pursing the lips — Puffing out the cheeks ENT. Adel Adwan . Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . 3. 4. it divides into its 5 terminal branches: 1. Testing the facial nerve: Voluntary facial movements. 5. Buccal branch. ** Mastoid surgery (mastoidectomy) to remove cholesteatoma carries a risk of facial paralysis.027 As the facial nerve runs forward within the substance of the parotid gland. Cervical branch. ENT. peripheral. Mouth: slight asymmetry . autoimmune. UMN lesion: In an UMN lesion.028 There should be no noticeable asymmetry. .Gross: slight weakness on close inspection. Studies have shown the benefit of high-dose corticosteroids for acute Bell palsy. . If excessively sensitive to sound in one ear:. Loss of taste:-lesion proximal to the point where it gives of the chorda tympani. If 8th/ 7th N not functioning:-lesion in internal acoustic meatus. lower-motor-neuron facial-nerve paralysis that gradually resolves over time in 8090% of cases.Gross: obvious but not disfiguring difference between two sides. LMN lesion: LMN lesions can result in Bell's palsy. unilateral. Bell's palsy - - - The most common cause of unilateral facial paralysis.Motion: Forehead: moderate to good Eye: complete closure with minimal effort. may have minimal synkinesis. The cause of Bell palsy remains unknown. Facial paralysis: Pathology: - IF 6TH / & 7TH N not functioning:-lesion within the pons. noticeable but not severe synkinesis.lesion involving n. evidence is now available indicating that it may not be useful. called central seven. Increasing evidence implicates herpes simplex type I and herpes zoster virus reactivation from cranial-nerve ganglia. Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . due to the bilateral control to the upper facial muscles. manifested as both upper and lower facial weakness on the same side of the lesion. inflammatory. House brackmann facial nerve grading system: Grade Description Characteristics I Normal (100%) Normal facial function in all areas II Mild dysfunction (75-99%) III Moderate dysfunction (50-75%) . only the lower part of the face on the opposite side will be affected.At rest: normal symmetry & tone. to stapedius. contracture. Adel Adwan . Treatment of Bell palsy should be conservative and guided by the severity and probable prognosis in each particular case. Although antiviral treatment has been used in recent years. and ischemic etiologies. Bell palsy is an acute. though it appears to be a polyneuritis with possible viral. Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen No movement . VI Total paralysis (0%) ENT.At rest: normal symmetry and tone. .Motion: Forehead: none. V Severe dysfunction (0-25%) . Eye: complete closure with effort. Eye: incomplete closure. Eye: incomplete closure. Mouth: slight movement.Motion: Forehead: slight to moderate. Adel Adwan .Gross: obvious weakness and/or disfiguring asymmetry. . . .At rest: asymmetry. Dr.Motion: Forehead: none.Gross: barely perceptible motion.029 and/or hemifacial spasm. Mouth: asymmetry with maximum effort. . Mouth: slightly weak with maximum effort. . IV Moderately severe dysfunction (25-50%) .At rest: normal symmetry and tone. Adel Adwan .031 Neck The upper border of the neck runs along the inferior border of the mandible through the apex of the mastoid process to the external occipital protuberance. Level 2: Upper jugular group (from base of skull to hyoid bone anatomacilly or from base of skull to bifurcation of common carotid artery surgically). Level 7: Mediastinal group. Muscular triangle. Zone III: Angle of mandible to base of skull. Level 6: Anterior compartment group. Inferiorly. Level 5: Posterior triangle group. Level 4: Lower jugular group (from omohyoid muscle to clavicle). the clavicles. Carotid triangle. Deep neck lymph nodes: Level 1: Submental & submandibular lymph nodes. Posterior triangle It is subdivided into: . Anterior triangle It is subdivided into: Submandibular triangle. Zone II: Cricoid cartilage to angle of mandible.Suprasternal triangle. Dr.Occipital triangle. Neck zones: Zone I: Suprasternal notch to cricoid cartilage. and the spinous process of the seventh cervical vertebra. Submental triangle. . Neck triangles: 1. - 2. ENT. Level 3: Middle jugular group (from hyoid bone to omohyoid muscle).Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . the neck ends in a plane formed by the suprasternal notch. Alar layer: Posterior to visceral layer of middle fascia & anterior to prevertebral layer. Viscera: pharynx. Muscles: infrahyoid muscles. Glands: thyroid gland 3. ENT. c. Adel Adwan . Glands: parotid and submandibular salivary glands. Spaces: posterior triangle & suprasternal space. esophagus. Middle layer of deep cervical fascia (pretracheal layer): It covers: a.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Deep layer of deep cervical fascia: Splits into 2 layers: a. Dr. b. Muscles: trapezius & SCM muscles. Prevertebral layer: It encloses vertebral bodies & deep muscles of the neck. 2. superficial veins & superficial lymph nodes 2. b. trachea. larynx. Superficial fascia: forms a thin layer that encloses platysma muscle. Superficial layer of deep cervical fascia (investing layer): It covers: a. Deep cervical fascia: 1. c. b.030 Deep neck infection Cervical fascia: 1. Involved with cellulitis and superficial abscess. Internal jugular vein. Vagus nerve. Dr. Superficial space: . Entire length of neck: a. ENT.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . .Surrounds platysma. . Deep neck spaces (described in relation to hyoid bone): 1. It contains: a. Adel Adwan . c. common & internal carotid arteries.032 Carotid sheath: - It is formed by the 3 layers of deep fascia. b.Treated with incision along langer’s line (tension line) with drainage and ATB. . c.Posterior border is prevertebral layer.Inferior border is posterior tonsil pillar.Posterior border is vertebral body and deep neck muscles. Parapharyngeal space (Pharyngomaxillary space) . .033 b. . Prevertebral space.Superior border is oral mucosa. .Extend from skull base to diaphragm.Inferior border is superficial layer of deep fascia.Can become secondarily involved with any other deep neck space by direct spread. .Carotid sheath = Lincolin’s highway. .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . . . c. e. Submandibular space. Adel Adwan .Anterior border is pharynx and esophagus (buccopharyngeal fascia).Superior border is anterior tonsil pillar. b. Dr. .Extends along the entire length of vertebral column (so complications can reach sacrum). d. . . Peritonsillar space. Danger space. . Visceral vascular space. Suprahyoid a. .Lateral border is superficial layer of deep fascia.Lateral border is superior pharyngeal constrictor. 2. .Anterior border is alar fascia.Posterior border is alar layer of deep fascia.Danger because of risk of mediastinitis. . . ENT.Anterior border is prevertebral fascia. .Medial border is buccopharyngeal fascia. Retropharyngeal space: .Medial border is capsule of palatine tonsil. .Most common cause of DNI in pediatrics is tonsillitis and adenitis. aureus . so below the mouth floor. ENT.Sore throat or pain and trismus. Pott’s disease 5.Klebsiella .Usually mixed aerobic and anaerobes that represent the flora of the oral cavity. and certain parts of the ears and eyes.Swelling of the face and neck.Strept viridians .Infection can also spread to the deep neck space by the path of communication b/w spaces. face or superficial neck to deep neck space via lymphatic system. .Stridor and dyspnea.Asymmetry of the oropharynx with purulent oral discharge.034 d. . erythema. . Unknown (20%) Bacteriology: .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen Trismus means the pterigoids (mostly. . f. . Masticator space (dental abscess) e. Deep neck infection (DNI) . Trauma 8. Anterior visceral space.Lymphadenopathy. . Instrumentation 10.Late findings may include dysphonia and hoarseness. Upper respiratory tract infection 7.S. Parotid space. . Dental infection 2.Often a rapid onset and may progress to fatal complications. Tonsillar and peritonsillar infection 3.The most common is: . upper respiratory tract. Infrahyoid: a. . . . . . 3. Sialadenitis 6. Retropharyngeal lymphadenitis 4.Spread of infection can be from the oral cavity.Dysphagia and odynophagia.Direct infection may occur by penetrating trauma. Spread from superficial infection 11.Anaerobes Clinical features: . Etiology 1. the medial pterigoid) are involved and airways will become inceasingly hard to access which is a red flag. Dr. Temporal space.Most common cause of DNI in adults is odontogenic origin by the 2nd and 3rd molar because their roots extend below mylohyoid muscle. Adel Adwan . Foreign body 9. Clinical manifestation: . Secure the airway. . sore throat. Dr. stridor.In adults: pain.. snoring and nasal obstruction.MRI.CT.C7 > 14 mm in children. Retropharyngeal space abscess forms abscess lateral to midline while prevertebral space abscess forms abscess in midline. tonsillitis. LAP. .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . . On exam: . 2.US. 4. metronidazole or clindamycin). 2. Adel Adwan . Investigation 1. ABC. instrumentation.lateral posterior oropharyngeal wall bulge.Extension b/w spaces could occur. extension from other spaces. Treatment 1. Lateral neck film .035 Diagnosis . fever.Usually unilateral due to fascia between 2 spaces which differentiate it from the danger space which is usually bilateral bulging. ATB: Maximum doses of IV systemic antimicrobials regimens according to the site of infection (Ampicillin or Augmentin. dysphagia. > 22 mm in adult. . torticollis due to edema or compression on SCM muscle. 3. tachycardia.X-ray (lateral cervical soft tissue view): we find air in unusual places. . which is firmly attached to the prevertebral fascia . .The abscess is limited to one side of the midline by the median raphe of buccopharyngeal fascia. . drooling. Mediastinitis signs & symptoms: Dyspnea.In children: fever. chest pain. . ENT.In adults: trauma. Causes: .In pediatrics: suppurative process in LN of nose (retropharyngeal lymphadenitis). adenoiditis and sinusitits.C2 > 7 mm in both children and adults. 90% before 6 years of age. Clinical features 1. irritability. Surgical drainage. Retropharyngeal abscess: 50% usually in children (6-12 months of age). Bilateral bulging .Presentation and exam like above.Dysphagia or dyspnia.Causes: Pott’s abscess.Incision of the abscess should be carried out without delay. Second & third molars: infection enter submaxillary space. widened mediastinum).036 2. . Dr. Submandibular space infection Most common cause: Dental caries Anterior teeth & first molar: infection enters sublingual space. Clinical features (True Ludwig’s angina) .Antibiotics should be given in full doses.Extension from retrophryngeal. . Retropharyngeal abscess Treatment . Adel Adwan . shoulder and neck pain.Starts unilaterally and progresses bilaterally ENT.Back. prevertebral and parapharyngeal spaces. Danger space infection: .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . . Chest film (detection of mediastinitis. Prevertebral space infection: . . General anaesthesia is advisable but requires great skills. trauma and osteomyelitis. odynophagia. odynophagia. Adel Adwan . torticollis. fever. Parotid space infection Most common cause: Bacterial retrograde from oral cavity.It is an emergency.Fever. sublingual & submaxillary spaces . Horner’s syndrome). trismus. Trismus. Swelling of angel of mandible. drooling.pus at stensen’s duct. No purulence(due to no time to developed). . mark swelling and tenderness of parotid gland. 3. .Dysphagia. malaise.037 - Induration of submandibular region and floor of mouth (severe cellulitis).fluctuation.N 9.It is cellulitis not abscess. Drooling. trismus.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .The most common one. Medial displacement of lateral pharyngeal wall. Dr. Tongue trusted posteriorly and superiorly (causes airway obstruction). . 4. . ENT. neurologic deficit (C. Parapharyngeal abscess Most common cause: Peritonsillar infection Typical findings: 1. Ludwig’s angina .Cause: extension from tonsillitis.10.It is limited to submandibular space & its compartments. limited neck motion. weakness. deviation of uvula. . . .“Hot-potato” voice. Others: fever. Clinical features High fever. bulging of superior tonsil pole and soft palate. Peritonsillar Space infection.12. 2. .Mediastinitis.Suppurative mediastinitis . .038 Descending necrotising mediastinitis (DNM) and lincoln’s highway .Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . .Septic shock . thyroglossal cyst or lymphangioma. .Sepsis.Deep neck infections can spread easily into the mediastinum & pleural cavities commonly through the carotid sheath. Emergencies . .Carotid artery erosion-rupture.Neurological deficits. internal carotid artery and lead to syncope).Carotid blowout . Complications .Internal jugular vein thrombosis ENT. . Adel Adwan . Dr. endotracheal intubation).Pulmonary edema. . . Since vagus nerve is involved. .Mortality rate 40% despite aggressive medical and surgical interventions.Pericarditis. .Airway obstruction (need tracheostomy.Cavernous sinus thrombosis. .Loss of airway . .Carotid space surrounded by the carotid sheath that descends into the chest and continues into the mediastinum to fuse with the pericardium has been considered a possible conduit for infection.In recurrent DNM think of congenital abnormalities as 2nd branchial cleft cyst. . the patient may have referred otalgia of vagal origin.Internal jugular vein thrombosis (Lemierre’s syndrome): can cause pressure on vagus. .Grisel syndrome: atlanto-axial subluxation in association with inflammation of adjacent soft tissues. .Aspiration.Osteomyelitis. ENT. - The remaining neck musculature gains contributions from cervical somites. – Type I is preauricular. mylohyoid. masseter.039 Embryology of the Neck & Neck Masses Neck Masses A mass in the neck is a common clinical finding. mandible. Adel Adwan . - Anamoly in first branchial cleft produces cyst. First Branchial arch - It is also known as mandibular or maxillary arch/ Meckel's arch. tensor tympani and tensor veli palatine. - ** Patient with hypoplasia in mandible is suspected to have anomalies in the malleeus & incus!! Muscles: Muscles of mastication (medial & lateral pterigoid. anterior belly of digastrics. - Nerve: Trigeminal nerve - Artery: Maxillary artery - Skeleton: Malleus. Branchial system 1. temporalis muscles). its internal opening is in the middle ear. at the angle of the mandible. First branchial cleft cysts are divided into type I and type II. and cartilaginous structures (skeleton). - Each arch consists of a nerve.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Embryology and Anatomy - Branchial System: 6 pairs of pharyngeal arches separated by endodermally lined pouches and ectodermally lined clefts. – Type II is post-auricula. - Benign Neoplasm - Malignant Neoplasm - Infectious - Congenital An appreciation for the embryological development of the cervical structures must be made to competently understand and treat the disorders of the neck. artery. incus. sphenomandibular ligament and anterior malleolar ligament. If it is a fistula. If it is a fistula. Dr. its internal opening is in the external auditory canal. sinus or fistula. 4. 3. - Anomaly in third branchial cleft produces cyst. if there is a fistula its external opening is in the neck and its internal opening is in the thymus.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . - Artery: Right Subclavian artery and ortic arch. If it is a fistula. - Artery: Stapedial artey. Dr. its internal opening is in the tonsillar fossa. the ** Ant. because it accounts for 90% of cases. and stapedius. - Anamoly in second branchial cleft produces cyst. - Skeleton: stapes. If it is a fistula. sinus or fistula on anterior margin of SCM muscle between the first one third and second one third. stylohyoid. ENT.041 2. - Muscles: Stylopharyngeus muscle. posterior belly of digastric. ** How to differentiate between second & third branchial cleft cyst ? It is second branchial cleft cyst until proven otherwise. - Fourth branchial pouch: Superior parathyoid glands and parafollicular thyroid cells - Rarely to have cysts or fistula. - Nerve: Facial nerve. - Muscles: cricothyroid muscle. & this applies to the rest of muscles according to which branchial arch they are derived from! styloid process and stylohyoid ligament. the upper half & lesser cornu of the hyoid. - Muscles: platysma. thymus gland Stylopharyngeus muscle is the only muscle that is supplied by the glossopharyngeal nerve. - Artery: Common carotid and proximal portions of the internal and external carotid. Belly of digastrics is supplied by a branch of trigeminal nerve & post. Fistulogram can be done to confirm that. Second branchial arch - It is also known as facial arch/ Reichert’s arch. - Skeleton: Lower body of the hyoid and greater cornu. Belly of digastrics is supplied by a branch of the facial nerve. muscles of facial expression. Adel Adwan . - Nerve: Glossopharyngeal nerve. and thymic duct. - Third branchial pouch: Inferior parathyroids. However. sinus or fistula on anterior margin of SCM muscle. Third branchial arch - It is also known as glossopharyngeal arch. Fourth branchial arch - Nerve: Superior laryngeal nerve. its internal opening is in the piriform fossa. Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Sixth branchial arch - Nerve: Recurrent laryngeal nerve. Adel Adwan . Fifth branchial arch - The fifth arch only exists transiently during embryologic growth and development. ** Fourth and Sixth Branchial arches fuse to form the laryngeal cartilages. ENT. 6. Dr. It disappears before birth.040 5. - Muscles: Intinsic muscles of larynx. - Artery: Pulmonary artery and ductus arteriosus. Growth. Risk Factors: major aetiological factors. Possibility of second primary (recurrence). Squamous Cell Ca of floor of mouth Squamous Cell Ca of tongue ENT. Bleeding. o Tobacco o Alcohol More common in men than women. Induration on palpation. Squamous Cell Carcinoma: - - Most common Head & Neck tumor (90%). Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Ulceration. Adel Adwan .042 Principles of Diagnosis and Treatment Head & Neck Cancer Benign\Malignant Tumor • Benign proliferation of cells without control – Slow growing tumor – Capsule – No metastasis – No mortality • Malignant (cancer): – Invasion of adjacent tissues – Metastasis – Rapid growth – Mortality Histopathology: 1. Tumor of adults (mostly). Pain. Tumor develops from skin or mucosa. Exophitic. 043 Squamous Cell Ca of larynx Squamous Cell Ca of nasopharynx 2. Hair follicles ENT. Sebaceous gland. Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Adenocarcinoma: - Tumors of glands • Salivary glands • Skin – Sweat gland. Adel Adwan . May ulcerates the mucosa and the skin.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Dr. Lymphoma: - - Origin: lymphoid tissues.044 • • Bulging under normal mucosa or skin. Adel Adwan . ENT. Waldeyer ring: – Palatine tonsils – Pharyngeal tonsil (adenoid) – Lingual tonsil – Tubal tonsils – Subepithelial lymphoid tissue Cervical lymph nodes. Adenocarcinoma of major salivary glands Adenocarcinoma of minor salivary glands 3. it Odynophagia is an indication to do karyotyping ! Weight loss Loose dentition Trismus: Most common muscle to be involved is medial pterigoid.Chondrosarcoma . 2. 3.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen .Fibrosarcoma . Otalgia Neck mass Serous otitis media: The first sign of nasopharyngeal carcinoma is unilateral serous/secretory OM. Adel Adwan . occurs Dysphonia characteristically in young males Dysphagia (9-19 years).045 Lymphoma of the tonsil 4. Nasal obstruction Epistaxis ENT. Progressive Signs and symptoms Indicating Head & Neck Cancer: - ** Angiofibroma.Ostesarcoma . Dr. Melanoma 6. Unilateral secretory OM.Liposarcoma…. If found in a female. Soft palate immobility & trismus. 5. Trigeminal neuralgia. Sarcoma . Metastasis Etiology: - Tobacco Alcohol Radiation (thyroid) –Tinea capitis Hardwood dust (adenocarcinoma of sinuses) Viruses (EBV: nasopharyngeal carcinoma) Chemical Trotter's triad of nasopharyngeal carcinoma: 1. T2: Tumor extension to other region. T4: Invasion of surrounding organs such as cartilage or skin. N0: No regional lymph nodes. T3: T2 + impairment of vocal cord mobility. Nx: Regional lymph nodes cannot be assessed. Adel Adwan .046 - Facial pain Cranial Neuropathies Airway obstruction Bulging of mass Oral Fetor Physical Examination: - Laryngoscopy Imaging: - CT MRI Scintigraphy - FNA Endoscopy Biopsy: TNM Classification of larynx CA: T1: Tumor is limited to 1 region without impairment of mobility & without extension to other region. ENT. Dr.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . theraputic ND Types: – Radical ND: Removal of all lymph node groups & functional structures: SCM muscle. ENT. Neck dissection (ND): - Removal of lymph nodes tissue from the neck. – Modified Radical ND: Removal of all lymph node groups & one or two of the functional structures (Preservation of some functional structures). N3: Ipsilateral or bilateral single or multiple lymph nodes > 6 cm.047 N1: Single ipsilateral lymph node 3 cm. accessory nerve & internal jugular vein.Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen . Dr. Adel Adwan . – Selective ND: Selective lymph node removal. N2: Ipsilateral or bilateral single or multiple lymph nodes < 6 cm. Elective vs. – Functional ND: Removal of all lymph nodes only. (Preservation of the functional structures).