Orl Mbchb4

ACUTE OTITIS MEDIA (AOM)

1. Definition
a. Acute suppurative inflammation of the middle ear cleft
2. What affects the Eustachian tube?
a. Age
b. Acute inflammatory dis of URT
c. Chr inflammatory dis of URT
d. Environmental – passive smoking, breast feeding, day care
e. Congential creaniofacial anomalies
f. Immune deficiency
3. Pathogeneis
a. AOM follows a cold
b. After a few days of stuffy nose → ear becomes involved → severe pain
c. Pain usu settles over 1-2 days but can last over a week
d. Ear drum may rupture → discharge pus from ear (usu ruptured drum will heal rapidly)
e. Typical progression of AOM occurs when surrounding tissues of ET swell due to URTI, allergies or ET dysfunction
f. ET remains blocked → air present in middle ear slowly reabsorbed into surrounding tissues
g. Strong negative pres creates a vacuum in the middle ear
h. ?Aspiration of bacteria
4. Importance
a. AOM is frequent –
i. 2/3 of children by 1 yr of age
ii. 1/3 of children have multiple infections
b. Complications can be serous – due to close r/ship betw middle ear and cranial cavity
5. ETD (eustachian tube dysfunction) in AOM
a. ETD → negative middle ear pres → aspiration of infections → AOM → [ersostemt f;iod
b. All 3 functions of the ET fail → ventilation, protection, drainage
6. Clinical Hx
a. Exudation 1-2 days
i. Non-specific sxs/signs
ii. Inflamed TM
iii. May not be bulging
iv. Always examine the ears
b. Demarcation 2-7 days
i. Pain, fever, deafness, discharging ear
ii. Purulent effusion middle ear
iii. Rupture of eardrum w otorrhea
iv. May be bloody
c. Healing Phase – up to 4 wks
i. 10% → OME (otitis media with effusion)
ii. Failure to resolve →
1. 1/1000
2. Persistent otorrhea
3. Acute mastoiditis
d. The younger the child, the more severe the generalised sxs are and the more discrete (not connected) the local signs are
e. On occasion, GI signs are the most impressive
7. Microbiology
a. 90% monomicromial
i. S.pneumoniae 30%
ii. H.influenze 25%
iii. M.catarrhalis 10%
b. S.pneumoniae – most likely to be assoc w complications eg mastoiditis
c. Virus – 10% (less common) – respiratory syncytial virus, rhinovirus, parainfluenza virus, influenza virus
8. Management
a. Antibiotics?
i. S.pneumoniae - ↑ resistance to amoxicillin
ii. Augmentin does not overcome this resistance
iii. Overprescribing → resistance
iv. Delayed prescription?
v. No obvious oral replacement
vi. Possible reasons - to avoid serious complications, relieve sxs and shorten dis, several children treated and one will benefit
b. Nasal decongestant
c. Analgesia – paracetamol
d. Detecting those that become OME → review 4-6 wks
9. Recurrent AOM
a. ~1/3 of children
b. Tx each episode separately
c. Prevention → grommets, adenoidectomy, vaccination against S.pneumoniae
10. Complications
a. Rupture TM (usu heals by itself)
b. Mastoiditis
c. Labyrinthitis
11. Referral?
a. Acute – failure to resolve, severe toxicity, evidence of complications
b. Recurrent Acute – when parents have had enough
c. Hearing loss
d. Co-morbidities

CHRONIC SUPPURATIVE OTITIS MEDIA (CSOM)

1. Otitis Media
a. AOM
i. W/o appropriate tx → AOM can progress to cause TM perforation, mastoiditisis or meningitis
b. OME (fluid collection)
i. Collection of fluid within middle ear space due to negative pressure produced by ET tube dysfunction
ii. Can occur purely from a viral URTI w no pain or bacterial infection or it can precede/follow acute bacterial otitis media
iii. Fluid in the middle ear can cause conductive hearing loss but only if it interferes w the normal vibration of the eardrum by sound waves
iv. Over several weeks, middle ear fluid become very thick and glue like which ↑ the risk of conductive hearing loss
v. Effusion that cause significant hearing loss and do not resolve can be treated by making a small incision in the eardrum (myringotomy) and inserting a plastic/metal tube (grommet)
c. CSOM
i. Perforation in TM and active bacterial inf within middle ear space for several weeks or more
ii. Drainage of pus may be sufficient to cause otorrhea
iii. Hearing impairment common
iv. Infection and eardrum perforation normally expected to resolve, in CSOM it does not and becomes chronic
v. With active middle ear inf, the eardrum does not heal
2. Introduction
a. Chronic otitis media covers both suppurative and non-suppurative disease
b. Non-suppurative – OME
c. Suppurative - CSOM
3. Tubo-tympanic disease
a. Relating to the pharyngotympanic (auditory tube / ET) and the tympanic cavity of the ear (air chamber in temporal bone containing the ossicles; continuous with ET anteriorly and mastoid air cells posteriorly)
b. Most common cause of perforation in pars tensa of ear drum post grommet perforation (previously after recurrent AOMs with a failure of natural healing of the hole); other causes include trauma and otitis externa
i. Pres → discharge of mucus component from the ear (separates from otitis externa where there is only scant fluid)
ii. D/c is usu painless
iii. Organisms are often typical upper respiratory tract ones – Strep, haemophilus, moraxella, but over times the superimposition of other strains such as staph and pseudomonas often occurs
iv. The disease process itself is not intrinsically risky, but complications can be serious – inner hearing loss, facial paralysis, chronic mastoiditis, intracranial dis
c. 3x components to CSOM
i. TM perforation (see picture)
ii. Otorrhea
iii. Conductive hearing loss
d. Dx
i. Take a swab always
ii. Dry mopping or suction of detritus
iii. Do not synringe
iv. Topical antimicrobial drops → sofradex
v. Oral A/Bs if it fails to settle (Ø 1st line)
e. Tx can be conservative or surgical
i. Conservative – do nothing, keep ear dry (if d/c has stopped)
ii. Surgical indications – recurrent episodes of d/c, hearing loss (usu conductive), 90% success rate
4. Attico-antral disease
a. Drum abnormality in either the attic (pars flaccida) or by the annular area (post-sup location)
i. Cholesteatoma (see picture)
1. end result o chronic inf
2. it is an enlarging skin cyst developing within the confined space of the middle ear
3. it causes problems due to expansile growth and en enlarging pocket of desquamated keratin which may become infected by esp pseudomonas (it then produces malodorous d/c and significant pain)
4. can lead to destruction of ear drum and middle ear
b. Distinguishing cholesteatoma from calcification can be difficult
5. Treatment of CSOM
a. Cortical mastoidectomy – most impt operation involving exetneration of the mastoid air space – leaving a hole
b. Canalplasty
c. Combined approach tymphanoplasty – utilises concepts from first two procedures to remove and tx dis of the middle ear through both the mastoid sys and via the external canal
d. Modified radical mastoidectomy – converts the ear into an open cavity
e. Myringoplasty – grafting of eardrum to close a perforation
f. Subtotal petrosectomy – for the most progressive of dis when hearing basically lost – closure procedure performed
6. Hints in clinical practice
a. Always take a swab of a discharging ear – otherwise effective tx can be delayed
b. If an ear makes you wonder if it is safe to syringe – don’t do it
i. If you do syringe – most complications are preceded by pain (as long as the procedure remains painless, you are generally safe)
c. Dx requires familiarity and experience – if you are not confident, refer

DYSPHAGIA

1. Defintion
a. Dysphagia to solids
i. Dysfunction in act of swallowing a solid bolus
ii. Usu manifested by food sticking at some point
b. Dysphagia to liquids
i. Dysfunction in act of swallowing a liquid bolus
ii. Usu manifest by fluid ‘going down the wrong way’, causing a cough
iii. Alternatively may involve fluid being directed into the nose
c. a
2. Phases of swallowing
a. Oral prep – mastication (voluntary control)
b. Oral – bolus to back of tongue (voluntary control) → initiates automatic sequence
c. Pharyngeal – soft palate elev, larynx elev, epiglottic closure, cricopharyngeus (UES) relaxn and retorpulsion of tongue base
i. Duration <1 sec, CN9+10
d. Esophageal – co-ordinated wave of relaxn/contraction
i. Duration related to type of food, esophageal activity influenced by age
3. Etiology
a. Dysphagia to solids
i. Recess in pharynx or esophagus – tonsil, vallectula, diverticulum
ii. Structural narrowing of pharynx or esophagus
1. tumor
2. stenosis – cricopharyngeus fibrosis, caustic burn, GE reflex, Auto-imm (scleroderma)
iii. Incordinate muscle activity – usu esophageal dysmotility, CVAs, head injury
iv. Extrinsic lesion/pressure – eg thyroid
b. Dysphagia to liquids
i. Incompetent soft palate – velopharyngeal insufficiency
1. Lower CN palsy
2. Surgery – for tumor or surgery
ii. Incompetent laryngeal closure
1. Recurrent laryngeal n palsy – tumor (eg thyroid, larynx) or trauma (eg surgery)
2. Laryngeal injury – eg arytenoids dislocation
4. Clinical S/S
a. Dysphagia to solids
i. Pharyngeal recess → lateralised discomfort, pt feels they can almost reach the area with their finger
ii. Hypo-pharyngeal / esophageal diverticulum (pouch) → regurg, cough, weight loss, gurgling, chest inf
iii. Stricture/Tumor → only soft or liq diet, weight loss++, malignancy may affect the voice
iv. Dysmotility → Hx of GERD
v. Extrinsic mass → breathing difficulty, voice changes
b. Dysphagia to liquids
i. Palatal – fluids spilling out of nose, esp fizzy drinks, hyper-nasal speech
ii. Laryngeal – weak and breathy voice, bovine cough, chest inf, dyspnea, hx of surgery or sxs of cancer
c. a
5. Evaulation
a. Dysphagia to solids
i. Full H/N exmn (refer to ORL surgeon)
ii. Flexible endoscope exmn
iii. Modified barium swallow
iv. Rigid endoscopy
b. Dysphagia to liquids
i. Full neuro exmn
ii. Full H/N exmn
iii. Flex Endoscopic exmn
iv. Functioanl Endoscopic exmn of swallowing (FEES)
v. CT/MRI to scan the course of paralysed n
6. Take home messges
a. Swallowing is a complex process
b. Neuromuscular dysfunction is common
c. Dysphagia to solids may signal a ca
d. Dysphagia requires a complete H/N exmn
e. A MBS is a v useful exmn

EPISTAXIS

1. Defintion – bleeding from the nose
2. Etiology
a. Local factors - Nasal
b. Systemic factors - Coagulation defect
3. Nasal Causes
a. Venous
i. Little’s area
ii. More common in children
b. Arterial
i. Spheno-palatine (maxillary)
ii. Assoc w arteriosclerosis, HTN
iii. More common in adults/elderly
iv. Mostly after external trauma
c. Other
i. Infection – eg vestibulitis
ii. FB
iii. Cold dry weather
iv. Tumor – haemangioma, angiofibroma, carcinoma
4. Vascular of Coagulation factor
a. Vascular – HTT (hereditary hemorrhagic telangiectasia)
b. Platelet defect
c. Coagulation factor defect
d. Drugs – warfarin, aspirin
5. Tx
a. First aid (actively bleeding pt)
i. Position → bend head forwards (otherwise they will swallow blood)
ii. Pressure → on little’s area (if blood continues down back of throat, likely source further posterior to venous plexus)
iii. Pack → nasal pack/tampon, balloon
iv. Resuscitate
v.
b. Definitive
i. Venous
1. Cauterise (little’s area)
a. chemical (AgNO3 – silver nitrate)
b. heat (hot wire, diathermy)
ii. Arterial
1. Ligate – maxillary or anterior ethmoid
2. Embolise - maillary

HOARSE VOICE AND VOICE DISORDERS

1. Refer hoarseness >2wks for ORL evaluation (laryngoscopy)
2. Laryngoscopy
a. Indirect (mirror)
b. Endoscopy – flexible transnasal or rigid transoral
3. Tx
a. Voice therapy – voice rest, SLT, exercises
b. Medical tx – PPIs, Antibiotics or antifungals if infection, botulinum toxin for laryngeal dystonia
c. Surgery – eg microlaryngoscopy
4. Summary
a. Voice change is an impt sx
b. Remember swallowing/airway
c. Etiological factors varied, often multiple
d. Underlying pathology may be significant – malignancy (laryngeal or non-laryngeal), neurological dis

Voice Disorders
1. Laryngitis
a. Infective – viral
b. Chronic
i. Irritants – reflux, smoking
ii. Infections – candiadiasis, bacterial
2. Non-neoplastic vocal fold lesions
a. Nodules
b. Polyps
c. Cysts
3. Neoplasms
a. Pre-malignant (dysplasia ieleukoplakia)
b. Malignant (SCC)
4. Laryngopharyngeal reflux
a. Chr inflammation – erythema, edema
b. Rough voice quality
c. Throat clearing
d. Chr cough
e. Globus sensation
f.
5. Vocal process granuloma
a. Reparative granuloma
b. Injury – eg intubation
6. Unilateral VF immobility
a. Rough, weak, breathy voice
b. Aspiration
c. Dyspnea with phonation
d. Paralysis – peripheral nerve disease (eg thyroid surgery), malignancy
e. Fixation - neoplasm
7. Neurological
a. Parkinsons
b. CVA
c. ALS

NASAL OBSTRUCTION

1. Acute obstruction
a. Viral rhinitis → clear mucous
b. Acute sinusitis → green mucous → Antibiotics, saline lavage, +/- prednisone
2. Septal deviation
a. Common
b. Chronic sxs or asx
c. Tx - septoplasty
3. Allergic rhinitis
a. Presentation
i. Nasal obstruction
ii. Clear ?watery rhinorrhea
iii. Sneezing
b. Etiology
i. Strong assoc w asthma
ii. May be seasonal or perennial (grass pollen, dust mite)
c. Tx of rhinitis in asthmatics → improvement of allergic rhinitis AND the asthma
i. Allergic avoidance
ii. Anti-histamines (for intermittent sxs)
iii. Intranasal steroids (for constant sxs) – slow onset of action ~1 week
iv. Immunotherapy – when anti-histamines and steroids ineffective
v. Surgery – submucosal resection (good LT results)
4. Chronic rhinosinusitis
a. Note - Acute rhinitis remits spontaneously or with A/B tx
b. Definition
i. Inflammation of nose and paranasal sinuses
ii. Presentation – green snot, Ø pain
iii. Sxs >3 months
iv. 2 types – w and w/o polpys
c. Pathogenesis
i. Unclear - ?fungal hypersensitivity, ?staphylococcal superantigen and CD4 cell stimulation, ?bacterial biofilms
ii. Up to 10% of popn
d. Ixs → CT
e. Tx
i. Medical
1. Prednisone + A/Bs ~3 weeks
2. Intranasal steroids and nasal lavage → maintenance of improvement
ii. Surgical
1. Nasal polyp removal - majority can be performed endoscopically
5. Tumours
a. Unilateral
b. Acute onset
c. Bleeding!

NASAL TRAUMA

1. Structure of the nose
a. External nose - Nasal bones and cartilages
2. Fractured nose
a. If injury within the last 1-2 hours → if external nose deviated, push it straight
b. If later or the nose is swollen → re-assess in 7 days
c. External Apperance
i. If the nose has changed shape as a result of the trauma (deviated, depressed or splayed) and the pts is unhappy with the cosmesis → manipulate the nose under anesthesia
d. Internal Function
i. Is the nose blocked as a result of this injury?
ii. Is the septum ….
1. Deviated?
a. If yes to both and the pt is unhappy with function → septoplasty
b. If associated with external deformity → septorhinoplasty
2. Swollen on both sides and tender?
a. Refer immediately for I+D of septal hematoma – otherwise septal abscess may give septal cartilage necrosis w loss of support and saddle nose deformity
3. Summary of fractured nose
a. Immediate (1-2 hrs) → manipulation
b. Intermediate (1-2 wks) → manipulation under anaesthesia +/- septoplasty
c. Late → septo(rhino)plasty

NASAL FOREIGN BODIES

1. Mostly occur in children
2. Presentation → unilateral purulent malodorous discharge
3. Tx → Remove
a. Good light
b. Local anaesthesia
c. Good instruments
d. Good co-operation
e. If unable to follow above → general anaesthesia reqd

MANAGEMENT OF NECK LUMPS

1. Features of a lump
a. Size
b. Site
c. Consistency
d. Edge
e. Colour
f. Attachment
g. Transilluminate
h. Pulsation
i. Tenderness
j. Primary site
2. **Diagnostic features of a neck lump
a. Age
b. Site
c. Moves w swallowing
d. Moves w tongue protrusion
e. Primary site
3. Diagnostic features of a neck lump
a. Age
i. Child → infective/inflammatory or congenital
ii. Young adult → congenital inflammatory
iii. Adult → neoplastic
b. Site
i. Anterior (midline)
1. Suprahyoid
a. Thyroglossal duct cysts (10% occur here)
b. Ectopic thyroid
c. LN
2. Infrahyoid
a. Thryoid
b. Thyroglossal duct cysts (90% occur here)
c. Pretracheal LN (delphian node)
ii. Lateral
1. Carotid/Jugular
2. Posterior supraclavicular
iii. Submandibular
1. Sialadentitis/sialolithiasis
2. Salivary tumor – most common salivary tumour, 80% benign
3. LN
iv. Angle of jaw
1. Parotid tumour
2. Congential cyst – branchial
3. Sialadenititis/sialolithiasis
4. Upper cervical node
v. Post auricular
1. Node
2. Abscess (mastoid)
3. Sebaceous
4. Lipoma
vi. Back of neck
1. Lipoma
2. Sebaceous / Epidermoid cyst
c. Moves w swallowing
d. Moves w tongue protrusion
e. Primary site
4. Thyroid
a. Anterior neck
b. Slightly lateral to midline
c. Rises w swallowing
d. May be retrosternal
e. Pain w thyroiditis or recent bleed
5. Thyroglossal cyst
a. Soft
b. Often L sided
c. Moves w swallowing and tongue protrusion
d. Surgical removal of cyst and tract reqd
6. Lateral Neck swelling
a. Most likely – 2ndry malignant neoplasm above the clavicle
b. Solid
i. Malignant
1. Primary – lymphoma, sarcoma
2. 2ndry – SCC, melanoma
ii. Benign – inflammatory node
c. Cystic
i. Congenital – brachial cleft cyst, hemiangioma
ii. Acquired
7. Management of a Neck lump
a. Hx
i. General
ii. Specific – pain, assoc w eating, dysphagia, dysphonia, oral/pharyngeal pain, skin malignancies, night sweats/fevers, smoking
b. Exmn
i. Site
ii. Upper aerodigestive
iii. Skin – scalp, face, neck
iv. Thyroid
v. Remainder of neck
vi. Axilla, groin
vii. Salivary flow
c. Ix
i. FNA
ii. Imaging
iii. Distant mets
iv. Endoscopy

OTITIS MEDIA WITH EFFUSION (OME)

1. Epidemiology
a. Middle ear effusion – most common cause of acquired conductive hearing loss in children
b. 60% of children will have a middle ear effusion in their first year
c. 90% of all children will develop a middle ear effusion
d. Peak 3-6 years → 30%
e. Only 2% at 11 yrs age
f. Most episodes resolve spontaneously
2. OME Dx → Fluid present behind ear drum for >12 weeks
3. Presentation
a. Often asx
b. Hearing loss
c. Popping ears
d. Otalgia (ear pain)
e. Speech delayed, unclear, loud
f. Additional pathology (adenoid dis)
4. Dx
a. Otoscopy/Otomicroscopy
i. Aerated/fluid
ii. Position – bulging, retracted
iii. Mobility – normal, hypermobile, neg pressure (pneumatic otoscope)
iv. Assoc pathology
b. Impedence → tympanometry
c. Audiogram – document hearing, sooner if high risk
5. Tx
a. Often asx, may resolve with time
b. Conservative
i. A/Bs + Nasal decongestants
ii. Valsalva training
c. Failure to respond
i. Ventilation tubes (grommets)
ii. +/- adenoidectomy
d. Avoid sequelae –
i. Effects of hearing loss (social, educational)
ii. Persistent OME → perforation or cholesteatoma
e. Myringotomy (slice cut in TM)
6. Complications of VTs (ventilation tubes ie grommets)
a. Requires anaesthetic
b. Otorrhea 12%
c. TM perforation
d. Scarring, atrophy, tympanosclerosis of TM
e. Cholesteatoma

OTOLOGY AND NEURO-OTOLOGY

AUDIOMETRY

1. Pure tone audiometry
a. Aims to identify thresholds of hearing at selected frequencies
b. Air conduction testing – using conventional headphones to assess overall hearing performance
c. Bone conduction testing – using a bone vibrator applied to mastoid bone to bypass ear canal and middle ear, assesses inner ear function
d. Air-bone gap indicates mechanical problem w sound conduction due to middle ear or external ear (conductive hearing loss)
e. If no air-bone gap, then problem occurs with cochlea or auditory neural pways (sensori-neural hearing loss)
2. Speech audiometery
a. Test subject repeats words from standardised word lists
b. Gives information about processing of more complex sound info
c. Identifies site of lesion in sensori-nerual hearing loss (cochlear hearing losses assoc w good speech discrimination whereas neural losses tend to show poor discrimination)
3. Acoustic immitance audiometry
a. Gives info about stiffness of middle ear mechanism, middle ear pres (tympanometry) and hence ET function

EXTERNAL EAR

Acute Otitis Externa
1. Furunculosis
a. Staph inf of hair follicle in canal
b. Severe pain, swelling, L/A
c. Tx – local ear toilet, wicks in canal w topical antibacterial/steroid drops, flclox, I+D if not settling
2. Diffuse otitis extrna
a. Bact or fungal
b. Local itching, then pain, swelling + edema, may spread to involve pinna
c. Commonly pseudomonas
d. Mgt
i. Swab for microbiology
ii. Local ear tolet
iii. Topical antibacterial drops (usu containing steroids)
iv. Antifungal agents if fungal material vis or fungal swab growth
v. Systemic A/Bs if resistant
e. Prevention → avoid water in ears, local trauma

OTITIS MEDIA

AOM
a. Epidemiology
i. M>F
ii. Children in daycare, immune deficiency or f.hx etc
b. Etiological factors
i. Poor ET function (esp in children and during URTI)
ii. Lower immunity in children
iii. Nasopharngeal sepsis – eg adenotiditis, acute sinusitis w purulent nasopharyngeal d/c
c. Common organisms
i. Pneumococcus, H.influenzae, moraxella catarrhalis, S.aureus
d. Presentation
i. Sxs – acute ear ache, irritability, pulling at ears, fever, malaise, hearing loss
ii. Signs – bulging red TM → rupture + d/c possible
e. Tx
i. Simple analgesics +/- Oral A/Bs
ii. Review after a period to assess resolution
iii. If recurrent AOM → ventilation tubes (grommets), tx of nasal or nasopharyngeal sepsis (eg adenoidectomy) or low dose prophylactics
f. Complications
i. Incomplete resolution of AOM → a precursor of OME
ii. Recurrent AOM → permanent changes in middle ear (eg tympanosclerosis, permanent perforation etc).
iii. Acute mastoiditis

OME
a. Defintion - Inflammatory process of middle ear cleft w accumulation of fluid behind an intact drum
b. Etiology (multifactorial)
iv. Poor ET function
v. URTI
vi. Recent AOM
vii. Nasopharyngeal pathology – eg adenoid disease in children
viii. Age – incidence ↓ after 6 yrs age
c. Presentation
ix. Sxs – relatively silent, conductive HL, behal change, poor school performance, balance disturbance is possible
x. Signs – dull, hypervascular, immobile drums (sometimes with retraction)
d. Tx
xi. Most resolve spontaneously
xii. If no resolution at 4 wks → consider trial A/Bs (Co-trimox for 4 wks)
xiii. Tx any nasal pathology
xiv. If no resolution at 3 months → refer for consideration of grommets
e. LT sequelae
xv. Lang / educational delay
xvi. Middle ear changes – atelectasis, adhesive otitis media, cholesteatoma

Grommets (Vent tubes, tympanostomy tubes)
g. Common tx for unresolving OME, frequently recurrent AOM and chr ET probs
h. Insertion under GA in children
i. Ventilate middle ear through TM (bypassing ET)
j. Duration 1-2 yrs usu
k. AOM leads to d/c in ear with a grommet
l. Minor swimming restrictions – no diving, deep sweimming, hot pools
m. Low incidence of sig complications – otorrhea, 1-2% have a perforation after tube extrudes, atrophic/sclerotic area in site of old grommet but no LT hearing difference

CSOM (2 main variants)* 1 exam Q
n. Mucosal CSOM (tubo-tympanic dis) – safe ears
i. Repeated or unresolved infection may lead to chr perforation of TM w hearing loss and recurrent d/c (otorrhea)
ii. Other sequlae – middle ear fibrosis, tympanosclerosis causing HL + ossicular defects from erosion or scarring
iii. Exmn
1. central perforation w or w/o purulent d/c
2. visible white plaques of tympanosclerosis in drum
3. Conductive HL
iv. Mgt
1. Tx of active infection – swabs for microbiology, local ear toilet, topical A/Bs/steroid drops
2. +/- Systemic A/Bs
3. +/- Surgery to repair TM or ossicular defects – myringoplasty or ossiculoplasty
v. Generally a relatively benign dis, but can occasionally lead to intracranial complications
o. *Cholestesteatoma (attico-antral dis) – dangerous ears
i. Pathology
1. Pathogenesis unclear, some combination of chr negative middle ear pres, inflammation in middle ear cleft
2. Leads to formation of an expanding, cyst-like lesion in middle ear/attic, mastoid sys
3. It is lined w keratinising stratified squamous epith full of kdratin and often surrounded by granulation tis when infected
ii. Erosion of surrounding structures
1. ossicular chain → conductive HL
2. Labyrinth → sensorineural HL, vertigo
3. Facial n canal → facial n palsy
4. Intracranial c/ment → intracranial sepsis (meningitis, extrodural/brain abscess)
iii. Potential life threatening due to potential intracranial involvement
iv. Clinical features
1. chr, often offensive smelling d/c
2. HL from drum and ossicular defects
3. attic or postero-superior marginal perforations
4. sxs and signs of complications
v. Mgt
1. Local tx as for non-cholesteatomatous CSOM to settle acute inflammation
2. Surgical removal + reconstruction of hearing mechanism where possible (mastoidectomy, tympanoplasty)
3. Tx complications as necessary – eg drainage of an intracranial abscess

Otosclerosis
1. Definition
a. D/o of the otic capsule in which new spongy bone formation causes fixation of the stapes and footplate and a conductive HL
b. Sometimes invades the cochlea, causing a sensorineural loss also
c. Do not confuse w tympanosclerosis which is seen after chr or recurrent inf
2. Etiology
a. Hereditary – 50% have pos family hx
b. Exacerbated by high E2 levels in preg
c. Immature spongy bone formation (active phase) w later replacement by hard mineralised bone
d. Present w HL and assoc tinnitus, often both ears
3. Tx
a. Sodium fluoride, Calcium supplements, VIt D → stabilise active dis
b. Surgery – stapedectomy/stapedotomy) – to correct conductive deafness (small risk of severe sensorineural loss after surgery)
c. Hearing aids – if sugery unacceptable

INNER EAR

Sensorineural deafness
1. Congenital
a. Genetic
b. Environmental – rubella, CMV, perinatal asphyxia, kernicterus)
2. Aim – early detection and mgt
a. Ave detection is at 26 months (higher for non-risk children)
b. Many parents have previously expressed suspicion of a hearing problem but have been falsely reassured → formal testing is reqd of ANY child in whom a parents suspects a hearing problem
c. Early detection depends on constant awareness of the possibility by health professionals, selective screening of at risk babies (eg pos f.hx, abnormal preg, perinatal probs, post meningitis etc)
3. Management
a. Assessment of nature and severity of HL
b. Accurate dx when possible
c. Amplification by hearing aids
d. Counselling of family
e. Speech and language therapy
f. Cochlear implant – preferably <2 yrs age
4. Acquired sensorineural deafness
a. Presbyacusis
i. HL in the elderly - ?normal
ii. Sev path processes seen – loss of ahir cells, neural atrophy in spiral ganglion, reduced elasticity of basilcar membr
iii. Gradually ↑ sensorineural deafness – loss of high freqs first
iv. Assoc tinnitus common
v. Tx – amplification (hearing aids), counselling to maximise hearing (eg improve listening sits, explanation to fam etc)
b. Noise induced HL
i. Prolonged expos to loud noise
ii. Damage depends on intensity, duration, susceptibility
iii. Assoc tinnitus common
iv. Damage and loss of hair cells + subseq degeneration
v. Irreversible lossvi. Once present – hearing aids may be reqd, ?ACC funding possible, prevent further damage w ear protectors etc
c. Ototoxicity
i. Main risk aminoglycosides but other agents implicated (eg cytotoxics), furosemide
d. Sudden sensorineural deafness
i. Many etiologies -
1. Hair cells – ototoxicity, trauma incl noise, viral inf (mumps, measles, rubella), meningitis, labyrinthitis
2. Hydrops – menieres, syphilis
3. Rupture of round window membrane
4. Neural lesions – acoustic neuroma (hemorrhage into tumor), MS, other b/stem tumors, CVA affecting b/stem nuclei
5. Idiopathic – ¼ have no identifiable cause after ixs
ii. Tx – controversial, systemic steroids, vasodilators (due to some of the potential causes above)
e. Acoustic neuroma (vestibular schwannoma)
i. Definition
1. Slow growing benign tumor arising in auditory canal on vestibular division of CN8
2. Derived from neurilemmal (nerve sheath) cells
ii. Epidem
1. Most common intracranial tumour
iii. Presentation
1. Insidious (slow growing)
2. Unilateral sensorineural HL w assoc tinnitus
3. Vertigo unusual – bec slow growth allows adaptation of balance
iv. Ixs
1. Any unilateral or asymmetrical sensorineural HL must be investigated to exclude an acoustic neuroma
2. MRI
v. Complications
1. If left untx → may cause CN7 sxs, sometimes CN5 sxs, ↑ ICP and eventually death
vi. Tx
1. Excision
2. Risk of CN7 damage
3. Most lose hearing – although can be preserved if tumor still small

BALANCE

Overview of balance mechanisms
1. Maintenance of equilibrium with respect to the evt depends central integration of multiple inputs
a. Inner ears (vestibular end organs)
b. Eyes
c. Proprioceptors in limbs and elsewhere
d. Modulation by cerebellum
e. Output via vestibule-spinal tracts to postural muscles and eye muscles to maintain optic fixation
2. D/o of input may lead to –
a. Vertigo – false sens of mvment
b. Nystagmus – effort by the oculomotor pways to fixate on the apparently moving evt
c. Ataxia and staggering – inappropriate mvment by the postural muscles in an attempt to maintain stability in the apparently moving evt
d. Involvement of other b/stem centers – eg vomiting etc
3. Rules of thumb
a. Vertigo = hallucination of mvment
i. Worsened by mvment
ii. Inability of pt to keep going
b. Vertigo + unilateral auditory sxs = peripheral
c. Vertigo + CNS sxs = central
d. Vertigo recover = peripheral
4. a
5. a
6. a

Labyrinthine d/os of balance
1. Meniere’s dis (idiopathic endolymphatic hydrops)
a. Uncommon
b. Presentation
i. Episodes of severe vertigo
ii. Sensorineural HL (transient) – Ø HL = Ø Menieres
iii. Tinnitus (transient)
iv. Ear fullness (transient)
v. Nystagmus – easily suppressed by visual fixation
c. Etiology
i. Idiopathic
ii. Assoc w a distension (hydrops) of the endolymphatic c/ment of the inner ear
iii. Triggering factors incl stress, local sepsis, nicotine, hypothyroidism, DM
d. Tx of acute attacks
i. Vestibular suppressants
ii. Bed rest
e. Tx of underlying dis
i. Correction of triggering factors
ii. Medications – diuretics, vasodilators
iii. Surgery – resistant cases w incapacitating dizziness (decompression of endolymphatic sac, vestibular n section, labyrinthectomy)
2. Vestibular neuritis
a. Etiology
i. Probably viral with damage to vestibular n fibers
b. Presentation
i. Sudden severe onset vertigo with n/v
ii. Ø HL
iii. Acute sxs last for several days with progressive dimishing of severity - bal disturbance settles slowly over weeks or months as central adaptation occurs
1. Rules of 2s → disabled 2 days, unwell 2 weeks, recover 2 months
iv. Nystagmus – easily suppressed by visual fixation
c. Tx
i. Symptomatic w vestibular suppressants and sedation during the acute phase
ii. Failure to improve rapidly → refer for scan
3. Acute supurative labyrinthitis
a. Etiology – complication of middle ear sepsis (sometimes meningitis)
b. Feats – rapid, permanent damage to cochlea and vestibular apparatus, often w later fibrosis and ossification
c. Pres - Severe vertigo resembling neuronitis, but w acute HL in affected ear
d. Tx – Parenteral A/Bs to try and limit damage and prevent intracranial spread through patent cochlea aqueduct
4. Benign paroxysmal positional nystagmus
a. Most common cause of balance disturbance
b. Etiology – thought to be due to otoliths (otoconia) breaking free of gelatinous utricular macule in inner ear and sinking back int o posterior semicircular canal on lying in certain positions (canalithiasis) with subsequent stimulation of PSCC cupula on certain head mvments causing a sensation of sudden vertigo of brief duration
c. Pres – always assoc w a particular mvment (eg turning to L while lying in bed)
i. 3 cardinal sxs – rollover in bed giddiness, kitchen cupboard giddiness, top shelf/washing line giddiness
d. Dx –
i. Hx
ii. Dx-hallpike position test - produces brisk geotropic torsional nystagmus on position the affected ear down (usu fatiguable on repeated positions)
e. Tx
i. Self limiting condition – over time, loose crystals thought to scar into place or dissolve where upon the sxs settle
ii. Particle reposition manoeuvre (epiley) – propels the otoconial debris out of affected ear canal towards the utricle (abolishes sxs immediately in ~80%) – manoeuvre may need repeating

Non-labyrinthine causes of dizziness
1. Frequently associated neurological signs
a. CN defects – esp VF defects
b. Cerebellar signs
c. Peripheral n deficits
d. Nystagmus – not suppressed by visual fixation
2. Vascular problems
a. Postural hypotension
b. Vaso-vagal attacks
c. TIA/CVA
d. Vertebro-basilar ischemia (other NC s/s)
3. Neurologic dizziness
a. Atypical migraine (dizziness can occur in absence of headache)
b. MS
c. B/stem and cerebellar tumors etc
4. Mediations
5. Hyperventilation syndrome
a. Atypical sxs – typically dizzy all the time for prolonged periods (months or more)
b. Sxs often reproduced by hyperventilation
c. Refer for respiratory PT once other causes excluded

PAEDIATRIC AIRWAY

1. Basic facts
a. 80% of neonates are obligate nose breathers
b. Narrowest at level of cricoid cartilage – it is also a complete ring
c. Smaller, larynx placed higher
d. Reduction in a/w size by ½ → airflow reduced by ¼
2. Airway Noises
a. Stridor – inspiratory, expiratory or biphasic musical nose due to a/w obstruction, usu obstr around larynx or in trachea
b. Stretor – harsher inspiratory noise due to upper upper a/w obstruction – from nose, soft palate or tonsilar area
3. Airway obstruction
a. Sxs – noisy breathing, difficulty breathing, choking, apneas, blue spells, unsettled baby, poor feeding pattern, FTT
b. Signs – stridor, stretor, tachpnea, choking, tracheal tug, costal recession, vomiting/spills, aspiration
4. Ixs
a. Initial – CXR, Lat Neck XR, Airway views + overnight oximetry
b. ORL referral – flexible endoscopy, laryngoscopy, bronchooscopy, esophagoscopy (under GA → complete assessment)
5. Common pediatric a/w disorders
a. Congenital – laryngomalacia, hemiangioma
b. Acquired – croup, epiglottitis, subglottic stenosis, foreign bodies
6. Laryngomalacia
a. Epidem
i. Most common cause neonatal stridor
ii. Starts a few days after birth
b. Pathology
i. Immature floppy cartilage and soft tissue
c. Presentation
i. Rhythmic/musical inspiratory stridor
ii. Worse when awake, feeding or crying
iii. 80% have reflux GERD
d. Tx
i. Majority resolve by 18 months
ii. Apneas, FTT, poor feeding, aspiration → concerning signs
iii. Severe cases require surgical intervention
7. Haemangioma (aka birthmark)
a. Epidem
i. Most common benign tumor in children
b. Pathology
i. Vascular tumor
ii. 50% in H/N
iii. Stages – proliferation, rest then involution (disappears)
iv. Can cause a/w obstruction if located around larynx
v.
c. Tx
i. Steroids
ii. Surgery
8. Subglottic stenosis (SGS)
a. Epidem
i. ↓ incidence due to better neonatal care and CPAP → ↓ requirement for intubations
b. Etiology
i. Caused by intubation trauma of the cricoid
ii. Congenitally narrowed cricoid
c. Presentation
i. Stridor, SOB, tachynea, exercise intolerance, FTT
d. Dx
i. Endoscopy – laryngoscopy and bronchoscopy
e. Tx
i. Laryngotracheal reconstruction (surgical) – cricoid stenosis divided then expanded w pts own rib cartilage after removal of scar tis
9. Foreign bodies
a. Common in 2-5 yr age group
b. Presentation
i. Hx impt – witness choking episode
ii. Cough, wheeze, stridor in acute setting
iii. Prolonged hx of atypical asthma or pn unresponsive to Rx
c. Bottom line
i. A child w a chronic cough, persistent stridor, atypical asthma or pneumonia → requires referral for endoscopy
ii. Is you suspect an inhaled FB on hx – regardless of current sxs → ORL referral reqd
d.
10. Tracheostomy
a. Indications
i. Upper a/w obstruction
ii. Prolonged or LT ventilation
iii. A/w protection and or toilet

TONSILS AND ADENOIDS

1. Anatomy
a. Tonsils
i. Aka palatine tonsil
ii. Intraepithelial collection of lymphocytes forming a lymphoepithial ring in the pharynx
b. Adenoids
i. Aka pharyngeal tonsils
ii. Collection of unncapsulated lymphoid tis in nasopharynx
2. Infections
a. Common cold eg rhinovirus – sore throat, dysphagia, fever, pharyngeal erythema, enlarged tonsils
b. Infectious mononucleosis – EBV (see picture)
i. Presentation
1. Sore throat, dysphagia, malaise, high temp
2. Large white tonsils w dense grey exudates
3. Hepatosplenomegaly and generalised L/A
ii. Ixs
1. Lymphocytosis w variant lymphocytes
2. Abnormal LFTs
3. Monospot test may not be pos for 2 wks
iii. Tx
1. Tx symptomatically
2. A/Bs to prevent 2ndry infection
3. Nasopharygneal a/w reqd if a/w comprimise
c. Streptococcal pharyngotonsillitis (see picture)
i. Grp A Strep most common bact cause
ii. Pres
1. Age 5-6 peak
2. Sore throat, otalgia, dysphagia, odynophagia (pain on swallowing)
3. Systemic sxs
4. Erythematous, enlarged tonsils, purulent exudates, L/A
iii. Ixs
1. Throat swab if grp A b-hemolytic strep suspected
2. Anti-streptolysin-O titre differentiates acute inf from carrier
iv. Tx
1. Penicillin 10 days
2. Add b-lactamase inhibitor for failures
v. Complications
1. Acute RF
2. GMN
3. Scarlet fever
4. Peritonsilar cellulitis/abscess (quinsy)
d. Adenotonsillar hypertrophy
i. Chr enlargement of T/A due to incr loads pathogenic bact
ii. Common cause upper a/w obstr in children
iii. Clinical feats – snoring, mouth breathing, apneas, poor sleep, daytime somnolence, poor school performance, FTT, cor-pulmonale
iv. Mgt - adenotonsillectomy
v. Complications – sinusitis, otitis media (adenoids as a reservoir for pathogens, obstruction of choanae)
3. Surgical mgt of adenotonsillar dis
a. Indications tonsillectomy
i. Recurret actute inf – 6x per year or 4x per year in 2 successive years)
ii. Complications of acute inf
iii. Chr inf
iv. A/w obstruction – acute or chr
v. Malignancy
vi. Complications of tonsillectomy – incl pain, infection, hemorrhage in 5%
b. Indications adenoidectomy
i. Adenoid enlargement with obstruction
ii. Reucrrent/persistent otitis media
iii. Recurrent/chronic rhinosinusitis

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