ENT Flashcards
What is a cholesteatoma?
An abnormal benign destructive growth of squamous epithelium in the middle ear and mastoid that may progressively enlarge to surround and destroy the ossicles, resulting in conductive hearing loss. May be congenital or acquired
Predisposing factors of cholesteatoma
Recurrent AOM or chronic OME
Older age at grommet insertion
Higher number of and interval between grommet insertions
Cleft palate
Craniofacial anomalies
Turner and Down Syndrome
Family history of chronic OME or cholesteatoma
Congenital forms are more common in boys
Presentation of cholesteatoma
Chronic ear drainage, new onset hearing loss (especially if after ear surgery)
Otoscopy: intact TM with white mass behind it, deep retraction pocked +/- granulation and skin debris, focal granulation tissue of TM, attic crust
Complications of cholesteatoma
Hearing loss secondary to destruction of intratemporal structures
CN palsies (VII, VI)
Neurological symptoms: e.g. vertigo
Venous thrombosis
Serious infection (brain abscess, meningitis)
Management of cholesteatoma
Complete excision with tympanoplasty +/- ossiculoplasty as indicated
Complications of surgery: hearing loss, CN VII paralysis, CSF leak, TM perforation
Differentials for hearing loss
Outer ear:
Foreign body, wax, AOE, trauma, ear canal pathology (e.g. osteoma, exostoses)
Middle ear:
OME, haemotympanum, ossicle discontinuity, trauma, barotrauma, iatrogenic, perforated DM, cholesteatoma
Inner ear:
Presbycusis, noise-induced, infective, trauma (temporal bone #), ototoxic drugs, AI (SLE, WG, UC) tumours (schwannoma, leukaemia, myeloma), vascular (CVA, sickle cell), perilymphatic fistula, barotrauma, neuro (MS, migraine), other (DM, sarcoid)
Vestibular Schwannoma: What is it, how common is it, presentation, diagnosis, management
A rare slow-growing, non-malignant tumour on CN VIII
Cause of 0.1% of unilateral hearing loss and tinnitus
Presentation: unilateral hearing loss and tinnitus (usually high-pitched, of similar frequency to hearing loss) and vertigo (initially minimal or transient)
Diagnosis with MRI or CT
Management: watchful waiting if contraindications to surgery, or surgical removal (up to 20% will have worsening tinnitus, 20-60% will remain unchanged, 30-50% improved or eliminated tinnitus)
Ototoxic drugs
Aminoglycosides (e.g. gentamicin) Aspirin Cisplatin Quinine Frusemide
Perilymphatic fistula
What is it, what causes it, presentation, diagnosis, management
An abnormal connection between the inner and middle ear allowing leak of perilymph fluid into the middle ear compartment
Caused by a tear in the oval and/or round window (physical trauma, barotrauma, raised ICP, congenital anomaly of temporal bone)
Presentation: vertigo, fluctuating hearing loss, aural fullness, tinnitus, exacerbation of symptoms with changes in altitude, weather or exertion. Can sometimes see fluid behind membrane on otoscopy
Management with strict bed rest to allow fistula to close
Causes of vertigo
BPPV: vertigo for few seconds-minutes on movement of head (e.g. rolling over in bed)
Labyrinthitis: sudden, spontaneous onset + n&v + gait instability
Brainstem infarct: sudden onset, n&v
Cerebellar: sudden onset, prominent gait impairment, headache, dysphagia, uncoordination
Meniere disease: episodes lasting 20m-24h + hearing loss + tinnitus
Perilymphatic fistula, vestibular schwannoma
Labyrinthitis
Presentation, natural history, management
sudden spontaneous onset of vertigo + n&v + gait instability towards affected side (single episode)
spontaneous nystagmus away from affected side
+ve head thrust test (thrusting head to side of lesion, will not be able to remain fixed on visual target)
severe symptoms for few days, gradual diminution +/- residual symptoms for months -usually will only suffer once
Prednisolone (full dose 5 days then taper) + IM prochlorperazine or oral diazepam for symptomatic relief
MRI brain to exclude CVA
Meniere disease
Presentation, diagnosis, natural history, management
20-40y/o
Recurrent episodes (20m-24h) vertigo, sensorineural hearing loss, tinnitus
Diagnosis of exclusion
10% have intractable, progressive, unremitting symptoms
Symptomatic mx: hydrochlorothiazide, betahistine OR destructive tx: intratympanic gentamicin, labyrinthectomy Non-dest: intratympanic glucocorticoids
BPPV
Presentation and examination
Positional vertigo provoked by head movement
Recurrent episodes
Differentials for chronic otorrhoea
chronic suppurative otitis media cholesteatoma ear foreign body granuloma immunodeficiency neoplasm
Complications of CSOM
hearing impairment - speech, language delay, poor school performance, psychosodial complications cholesteatoma meningitis, brain abscess mastoiditis facial n palsy sigmoid sinus thrombosis
Diagnosis of CSOM
painless otorrhoea for >6weeks with evidence of perforated TM on otoscopy
BPPV natural history and management
Untreated episodes resolve spontaneously over days-weeks
Recurrences are common
Epley manoeuvres (particle repositioning manoeuvres) +/- stemetil as premedication to tolerate manoeuvres
Systematic assessment of tympanic membrane
COMPLETE: Colour Other conditions (fluid level, bubbles, perforation, otorrhoea, bullae, tympanosclerosis) Mobility Position (retracted v bulging) Lighting Entire surface (examine all 4 quadrants) Translucency External auditory canal and auricle (e.g. deformed, displaced, inflamed, foreign body)
Definition of malignant or necrotising otitis externa
The spread of otitis externa to skull base causing perostitis and osteomyelitis
Risk factors for otitis externa
Bacterial:
- kids (5-10), summer (water activities)
- hearing aids, earphones, diving caps (any occlusion of ear canal)
- dermatological conditions e.g. psoriasis
Malignant:
- DM or ISS
- very rare in children
Fungal:
- 2-10% of OE
- after treatment of bacterial infection
- Candida more common in patients with hearing aids
Most common pathogen in malignant otitis externa
Pseudomonas aeruginosa
Clinical features in bacterial otitis externa
Severe otalgia
Reduced hearing
pruritus
minimal ear discharge
Oedematous, narrow, inflamed ear canal +/- pinna
Erythematous auricle and tragus
tender
Clinical features of malignant or necrotising otitis externa
Severe otalgia out of proportion to severity of ear canal swelling
- tends to be nocturnal and extend to TMJ (esp on chewing)
- Otorrhoea
Only mild swelling of EAC
Facial palsy +/- other cranial n palsies (once there is osteomyelitis)
granulation tissue on floor of EAC
Clinical features of fungal otitis externa
Severe otalgia, pruritus, minimal discharge
Aspergillus: fine, dark coating of EAC
Candida: white, sebaceous-like material
Complications of otitis externa
Malignant otitis externa
Fungal OE may lead to perforation
Invesitgations in malignant otitis externa
CT petrosal temporal bone
Ear swab
ESR, CRP
BGL/identify the underlying immunodeficiency
Management of otitis externa
Ear toilet - tissue spears
Otowick insertion with antibiotic/steroid drops for 7-10 days
suffudex = dexamethasone, framycetin, gramicidin (No anti-fungal activity)
Systemic antibiotics only if cellulitis of pinna/facial skin or fever
Simple analgesia
Water precaution for 2 weeks
If fungal:, must be cleaned thoroughly use antifungal/steroid (clioquinol/flumethasone) ear drops instead, fungal OE must be reviewed!
Indications for referring otitis external to ENT
Bacterial OE with no response to appropriate Otowick and antibiotic management
Malignant OE
Fungal OE
Definition of otitis media with effusion
Inflammation of the middle ear cleft accompanied by the accumulation of fluid without the symptoms and signs of acute inflammation
Clinical features of otitis media with effusion
Hearing loss (mild and fluctuating) - may interfere with language development, behaviour, school performance
Otoscopy:
- Air-fluid level behind membrane
- Opacification of TM (cloudy white/grey)
- Retracted TM
- reduced mobility of TM
Complications of otitis media with effusion
- Tympanosclerosis
- Retraction pocket
- Cholesteatoma
- TM perforation
- Ossicular chain erosion
Investigations in otitis media with effusion
Tympanometry
Audometric assessment
Management of otitis media with effusion
Watchful waiting for 3 months (80-90% will spontaneously resolve in this time)
If lasting over 3 months with bilateral hearing loss or in setting of speech delay etc. = surgical therapy for ventilation (grommets, tubes etc.)
SPEECH AND LANGUAGE THERAPY - especially for those with developmental delay
Risk factors for otitis media with effusion
family history of OM Bottle feeding Daycare attendance Adenoidal hypertrophy Cigarette smoke exposure Low socioeconomic status Cleft palate Pacifier use Reflux and allergy Non-immunised status
Main pathogens responsible for mastoiditis
Streptococcus pneumoniae
Streptococcus pyogenes
Staphylococcus aureus
Clinical features of mastoiditis
Ear pain (irritability in young children) Postauricular tenderness, erythema, swelling, fluctuance or mass Displacement of the auricle (usually downa nd out in kids under 2, up and out kids over 2)
Otoscopy may be normal or may be bulging TM + effusion or perforation
Complications of mastoiditis
Rate of complications 10-20%
s pyogenes associated with highest rate of complications at presentation
Subperiosteal abscess Facial nerve palsy Hearing loss Labyrinthitis Osteomyelitis
Management of mastoiditis
MUST CULTURE SPECIFIC BACTERIA
- Drainage of middle ear and/or mastoid cavity
- parenteral antibiotic therapy
If no history of recurrent AOM use vancomycin, if history of recurrent or recent antibiotic use combination therapy to cover P aeruginosa as well (e.g. bactrim or a cephalosporin + vancomycin
Indications for mastoidectomy in mastoiditis
Findings consistent with subperiosteal abscess
CT evidence of coalescent mastoiditis
Other suppurative complications
Acute mastoiditis in a child with chronic OME or cholesteatoma
Progression of symptoms despite IV antibiotics and appropriate drainage
definition of otosclerosis
Bony overgrowth involving the footplate of the stapes leading to fixation of the stapes, gradually reducing conduction through the ossicles and leading to conductive deafness
Cause of otosclerosis
Autosomal dominant inherited condition with variable penetrance (typically age of onset of noticeable hearing loss in 20s)
What is paracusis of Willis
The phenomenon of the apparent hearing improvement in a noisy environment for someone with conductive hearing loss (due to others speaking louder)
Pathognomic sign of otosclerosis
Schwartz sign - red blush over area anterior to oval window on otoscopy
Subjective v objective tinnitus
Subjective: phantom sensation only heard by the sufferer
Objective tinnitus: caused by real sounds generated in the body and transmitted to the ear by conduction through body tissue (e.g. vascular tumours, fistulae, clicking of myoclonus, ear waz, tensory tympani)
Causes of epistaxis
- cold dry environment
- infection
- inflamamtion (rhinosinusitis, Wegener’s granulomatosis, polyposis)
- trauma ( post-nasal surgery, septal perforation, picking, foreign bodies)
- Neoplastic (juvenile nasoangiofibroma, lymphoma, nasopharyngeal carcinoma)
- Systemic (bleeding diathesis, anti-coagulant medications, hereditary haemorrhagic telangiectasia)
Septal haematoma complications
Can become infected - inflammation - cartilage destruction - saddle deformity
OR infection can spread via blood vessels directly into skull and brain
Diagnostic test for CSF leak
Beta 2 transferrin
Locations of nose bleeds
Anterior bleed: Little’s area/Kisselbach’s plexus (anterior nasal septum)
Posterior bleed: Woodruff’s plexus OR sphenopalatine artery
Management of epistaxis
ABCs and basic first aid
Anterior:
- Cauterisation with silver nitrate (use topical anaesthetic spray because painful)
- Nasal packing (Rapid Rhinos)
Posterior:
- layered packing of all of nose (ensure to place pad under plug on outside of nose or will rapidly produce an ulcer)
Especially dangerous intranasal foreign objects
Button batteries (electrolysis at -ve pole produces OH ions - alkaline tissue necrosis, if -ve pole at septum causes perforation in less than 4 hours)
Paired disc magnets, one in each nostril attached at septum cannot be manually removed - chronic compression causes perforation (over weeks)
Management options for removal of intranasal foreign bodies
Most are removed by GP/mother/ED doctor easily
Positive pressure techniques:
- soft or smooth FB totally occluding anterior nasal cavity
- oral positive pressure by parent while occluding other nostril (if child too young to cooperate with nose blowing)
Instrumentation; for non-occlusive foreign bodies in anterior portion of nose
Acute v chronic rhinosinusitis
Acute = less than 4 weeks duration Chronic = more than 4 weeks duration
Causes of rhinosinusitis
Mostly viral
- rhinovirus
- adenovirus
- influenza
- parainfluenza
Only 0.5-2% have bacterial involvement
- S. pneumoniae
- H. influenzae
- M. catarrhalis
Exquisite facial tenderness early on or no improvement after 10 days likely to be bacterial
Features of rhinosinusitis
Nasal congestion
Post-nasal drip
Facial pain, pressure or fullness
Reduces sense of smell
Management of acute rhinosinusitis
Supportive treatment (as usually viral)
Topical corticosteroids reduce discharge and cough
- Budenoside (rhinocort) if older than 6y
- Mometasone (Nasonex) if older than 3y
TOPICAL OR ORAL DECONGESTANTS AND ANTIHISTAMINES ARE NOT EFFECTIVE
Chronic rhinosinusitis management
Unless severe, no treatment usually necessary
Avoid triggers (allergies, smoke, day care)
Use saline sprays
Teach child to blow nose
If severe symptoms consider testing allergies, immunological assessment, cilial function
Tx: nasal saline and topical steroid sprays
Adenoidectomy if associated nasal obstruction
Most children will improve by 6-8 years mainly due to maturity of the immune system
Prevalence of allergic rhinitis in the community
1/5 adults
1/10 teens
1/15 primary children
Complications of allergic rhinitis
Sleep apnoea
Asthma exacerbations
More frequent sinus and middle ear infections
Impaired concentration, behaviour, slee, learning capacity, exercise tolerance
Clinical features of allergic rhinitis
Itchy nose CLEAR rhinorrhoea Sneezing Nasal congestion Postnasal drip Cough (secondary to postnasal drip) TIMING likely to give clue to allergen: Seasonal: grass/weed/pollen/moulds Perennial: likely indoor allergens (dust mites, pets, moulds)
Classifying severity and duration of allergic rhinitis
Intermittent: less than 4 days per week OR for less than 4 consecutive weeks
Persistnent: More than 4 days per week AND more than 4 consecutive weeks
Severity:
Mild: no criteria meeting mod-sev
Mod-severe: Troublesome symptoms, sleep disturbance, impairment of ADLs, leisure or sport, impairment of school or work performance
Physical findings in allergic rhinitis
Pale and boggy inferior turbinates
Posterior polyps
“allergic shiners” - dark circles under eyes due to lower eyelid venous stasis
“Allergic salute” - transverse nasal crease due to chronic upward wiping of nose
Management of allergic rhinitis
According to symptom duration and severity
- Education, identification and avoidance of allergens
- Saline irrigation
- Oral antihistamines
- Intranasal antihistamines
- Intranasal corticosteroids
- Intranasal sodium cromoglycate
- Montelukast (children)
- Intranasal ipratropium
Review after 2-4 weeks, if no improvement increase steroid dose
depo steroid IM (celestone or depo medrol)
Last resort: immunotherapy (desensitisation 80-90% effective, response may be up to 5 years)
Types of oral antihistamines (brand name and generic)
Cetirizine (Zyretc) - least likely to cause sedation
Loratadine (Claratyne)
Desloratadine (Clarinex)
Fexofenadine (Telfast)
Intranasal antihistamines (generic and brand name)
Azelastine (Azep)
Levocabastine (livostin)
Tips for using nasal spray effectively
- Clear nasal passage first (?nasal saline spray may work)
- Shake bottle and follow package re: priming
- bend neck forward and look down
- Use one hand over the opposite nostril
- Put nozzle just inside the nose, aiming towards the outer wall
- Avoid sniffing too hard (will just go to back of throat)
Definitions of acute, subacute, chronic, recurrent acute sinusitis
Acute: less than 4 weeks with complete resolution of symptoms
Subacute: 4-12 weeks with complete resolution of symptoms
Chronic: inflammation more than 12 weeks with persistent URT symptoms
Recurrent acute: one episode of acute sinusitis every 12 months
Factors predisposing to acute sinusitis
Tumours Polyps Foreign bodies Congenital choanal atresia Allergies Asthma
Pathogens most commonly implicated in acute bacterial sinusitis
S. pneumoniae
H. influenzae
M. catarrhalis
Anaerobic infections seen more commonly in chronic sinusitis and in cases associated with dental infection
Clinical features of sinusitis
Cough Purulent nasal secretion Facial pain or pressure Headache Maxillary toothache Ear fullness Postnasal drip Poor sense of smell Poor response to decongestants (irritability and vomiting in children)
PAIN IS HALLMARK OF ACUTE SINUSITIS
Investigations in sinusitis
None indicated for uncomplicated acute sinusitis
If chronic - distinguish from allergic rhinitis with CT
Management of acute sinusitis
Amoxycillin + clavulanic acid for 5-7 days
Definition of tonsillitis
An acute infection causing inflammation of the palatine tonsil +/- pharyngeal tonsils or adenoids
Most common pathogen causing pharyngitis in children
Group A streptococcus (s. pyogenes)
20-30% of cases
Only responsible for 5-15% of pharyngitis in adults
Groups at high risk for complications secondary to tonsillitis
2-25y/o in area with high incidence of ARF (e.g. indigenous communities)
Patients with existing rheumatic heart disease
Patients with scarlet fever
GIVE ANTIBIOTICS
Complications of streptococcal tonsillitis
Nonsuppurative: - Scarlet fever - Acute rheumatic fever - Post-streptococcal glomerulonephritis Suppurative: - peritonsillar abscess (quinsy) - Parapharyngeal space abscess - retropharyngeal anscess - Acute otitis media - Acute sinusitis
Management of tonsillitis
Supportive symptomatic relief
Antibiotic therapy: phenoxymethylpenicillin BD for 10 days
(if poor compliance suspected: benzathine penicillin IM single dose)
Definition of quinsy
AKA peritonsillar abscess
An infection of the Weber’s glands which causes an abscess in the back of the throat, displacing the tonsils
Pathogens in quinsy
Often polymicrobial
- S. pyogenes
- S. aureus
- respiratory anaerobes
- occassionally H. influenzae
Clinical features of quinsy
Unilateral throat pain Trismus Hot potato voice Dysphagia, odynophagia Neck pain Referred ear pain Fever Inferior and medial displacement of ipsilateral tonsil Downward displacement of swollen uvula Tender cervical lymphadenopathy Palatal oedema
Management of quinsy
Drainage (incision or needle aspiration)
+/- quinsy tonsillectomy
IV cephazolin + metronidazole
Elective tonsillectomy if recurrent quinsy (10% risk) or history of recurrent tonsillitis
Acute epiglottitis definition
A cellulitis of the epiglottis and adjacent supraglottic structure (aryepiglottic folds etc.) that can progress to life-threatening airway obstruction if left untreated
Clinical features of acute epiglottitis in a child
Abrupt onset and rapid progression (hospitalised within 12h) 3 Ds: Dysphagia, Drooling, Distress High fever Severe sore throat, odynophagia Chokin sensation Hot potato voice Tripod position Stridor Tenderness of anterior neck Cough TEND NOT TO HAVE HOARSENSS
Clinical features of epiglottitis in an adult
Slower progression than child (most present within 2 days)
- sore throat or odynophagia
- fever
- muffled voice
- drooling
- stridor or respiratory compromise (far less common than in children)
- hoarseness
Management of acute epiglottitis
MEDICAL EMERGENCY IN CHILDREN
Secure airway ASAP (early ETT, have tracheostomy set at hand)
Adults: defer intubation, closely follow if no signs of current obstruction
Empiric antibiotics - Ceftriaxone or cefotaxime IV 5d
+/- dexamethasone single dose every 24h as required to reduce airway inflammation
Risk factors for sialolithiasis
Dehydration Diuretics Anti-cholinergic medications Trauma Gout Smoking
What are sialoliths most commonly formed from
Calcium phosphate and hydroxyapatite
+ smaller amounts of Mg, K and ammonium
Most common gland from which salivary stones arise
80& from submandibular glands
- largest, most often in the duct
(duct is long and flow of saliva is slow and against gravity + saliva more alkaline and higher Ca content)
20% Parotids - tend to be smaller, often multiple, often within the gland itself
Salivary ducts names from each gland
Submandibular gland - Wharton’s duct
Parotid gland - Stensen’s duct
Imaging in sialolithiasis
80-95% submandibular are radioopaque
only 60% parotid stones radiopaque
USS detects over 90% of stones
CT will pick up most stones PROVIDED FINE CUTS ARE REQUESTED so that small stones aren’t missed
Sialography - better at detecting other diagnoses (e.g. stricture, degeneration of duct etc.)
MRI will not visualise stones
Complications of sialolithiasis
Sialadenitis
Salivary gland abscess
Airway compromise
Chronic sialadenitis
Management of sialolithiasis
Stones under 2mm can generally be cleared non surgically
- good hydration
- moist heat to area
- massage gland “milk” duct
- avoid anticholinergic medications
- Pain relief NSAIDs
Minimally invasive approaches:
- extracorporeal or laser lithotripsy
- sialendoscopy
- wire basket retrieval
Surgical intervention
What is a ranula
A retention cyst on the floor of the mouth secondary to damage of salivary duct and sublingual glands
Differentials for lateral congenital neck mass
Branchial cleft cyst
Lymphatic/venous malformation
Cystic hygroma
Differentials for midline congenital neck mass
Thyroglossal duct cyst
Dermoid cyst
Laryngocele
differentials for acquired neck masses
Inflammatory/infective - reactive lymphadenopathy (tonsillitis etc.) - Glandular fever - Kawasaki disease etc. - HIV - salivary gland calculi - sialadenitis - thyroiditis - Granulomatous disease (TB, sarcoid) Neoplastic: - lymphoma - salivary gland or thyroid tumours - metastatic malignancy - Schwannoma - lipoma - benign skin cysts
Symptoms to ask for in neck mass
Pain: ?rapid growth or expansion OR direct neural invasion of certain malignancies
Vocal changes or dysphagia: ?mets from upper aerodigestive tract malignancy
B-symptoms: ?lymphoma
High spiking fevers: acute infection
Risk factors for primary head and neck cancer
Cigarette smoking (10x) Excessive alcohol consumption (5x) HIV status HPV: (oropharynx) EBV (Nasopharynx) HIV Radiotherapy for local cancers IVDU Occupational exposure (dry cleaning, asbestos, pesticides, woodworkers, plastic and rupper products)
Likely tissues involved for preauricular and angle of jaw masses
Salivary or lymphoid tissue in the parotid system
Likely tissues involved for central neck masses
thyroid
Malignant secondary
Dermoid cyst
Likely tissues involved for anterior aspect of SCM masses
High jugulo-digastric region
Malignancies common in adults
Congenital: 2nd branchial cleft cyst
Likely tissues involved for posterior triangle neck masses
High suspicion for malignancy
Nasopharyngeal carcinoma
investigations of neck mass
CT head, neck and chest BEFORE biopsy (if biopsy first, may cause a reactive lymphadenopathy)
FNA, core biopsy
Definition of cyst
Persistent sinus with no external opening
Definition of sinus
Blind-ended tract opening to one cavity
Definition of fistula
Persistent communication between two cavities
Definition of branchial cleft cyst
A congenital epithelial cyst that arises on the lateral part of the neck due to failure of obliteration of the 2nd (in 99% of cases) branchial cleft
Location of second branchial cleft cysts
Just inferior to angle of mandible
Anterior to SCM
Superficial to carotid sheath
Dorsal to submandibular gland
Clinical features of branchial cleft cyst
Neck mass anterior to SCM, just inferior to angle of mandible
- smooth
- painless
- slowly enlarging, often after URTI
Complications of branchial cleft cysts
Recurrent infections
Fistula tract to skin may develop
Management of branchial cleft cyst
Surgical excision (ensure no active infection)
epidemiology of branchial clet cysts
make up 20% of paediatric neck masses
Aetiology of thyroglossal duct cysts
First and second pharyngeal pouches for foramen caecum of the tongue - descend in midline as thryoglossal tract to position of normal thyroid - usually atrophies and disappears by GA 10w, but portions associated with thyroid tissue may persist at any point between tongue and thyroid
epidemiology of thyroglossal duct cysts
Most common congenital neck anomaly (70%)
Second most common benign neck mass after lymphademopathy
Usually diagnosed in childhood (up to 40% may present after 20y)
Clinical features of thyroglossal duct cyst
Midline mass in anterior neck
Moves with swallowing and elevates with tongue protrusion
Often asymptomatic until become infected (red warm painful lump)
Can be diagnosed with USS, CT or MRI
Management of thyroglossal duct cyst
Excision of cyst and tract
- undergo careful histologic examination as thyroid carcinoma can be present in 1-2%
Prevalence of thyroid carcinoma in thyroglossal duct cyst
1-2%
What is a haemangioma
The most common type of vascular tumour occurring almost exclusively in children
Natural history of haemangioma
Rapid growth phase (first 1-2y) followed by slow regression
Majority will resolve spontaneously
Management of haemangioma
Watchful waiting If symptomatic: - beta blockers - systemic glucocorticoids OR - surgical laser excision
Management of vascular malformations (HAEMANGIOMA IS A TUMOUR NOT A MALFORMATION)
Complete excision, sclerotherapy or laser treatments
Apnoea hypopnoea index scores: normal-severe categories
Normal: less than 5 events per hour of sleep
Mild: 5-15
Moderate: 15-30
Severe: more than 30 events per hour
Definition of apnoea
Cessation of oraonasal air flow
definition of Obstructive sleep apnoea
More than 10 seconds apnoea with respiratory arousal or desaturation due to collapse of airways despite adequate respiratory drive
Definition of central sleep apnoea
Over 10 seconds of apnoea due to absent respiratory drive from respiratory centre
Definition of hypopnoea
Less than 50% ventilation for over 10 seconds with respiratory arousal or desaturation
Causes of obstructive sleep apnoea in children
Adenotonsillary hypertrophy Obesity Long term allergies or hay fever Medical conditions associated with weak muscles or low muscle tone (e.g. Down syndrome) Children with flat faces of small jaws
Indications for CPAP/BiPAP inc children
Children with syndromes or neuromuscular disorders
Refractive OSA post-surgery
Normal flora of external auditory canal
Staphylococcus epidermis Pseudomonas aeruginosa Staphylococcus aureus Streptococcus saprophyticum Candida albicans