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PAEDIATRIC OTOLARYNGOLOGY
NOTES
V AND VI Year MEDICAL STUDENTS
Harvey Coates, AO, MS, FRACS
INTRODUCTION
Paediatric Otolaryngologists provide medical and surgical care to infants and children who have complicated and often rare diseases and disorders that are most effectively and safely managed in institutions that specialise in children’s health care.  Infants are not just “little adults”.  At every age they are different, requiring an understanding of the anatomic, physiologic and psychological changes that occur with their growth and development.  We take care, as Charles Bluestone says, of “special” problems or “special” children, or both, in a “special” institution.
These notes are not meant to be a comprehensive review of the scope of paediatric otolaryngology.  They cover those subjects with which I feel the student with an interest in family practice or paediatrics should be conversant.
OTITIS EXTERNA
Infection of the skin of the ear canal.  It may be bacterial, fungal or viral.  It is usually caused by pH change in the ear canal by water (normal ear canal pH 5.1) and overgrowth of organisms with a breach of canal skin causing invasion.
Organism
• Candida, Aspergillus niger
• Pseudomonas
• Herpes virus
Presentation
• Severe discomfort in the external ear
• Swelling ear canal with discharge
• Tenderness on movement of the tragus and/or pinna
• “Wet cardboard” appearance, fungal OE
Management
• Meticulous cleaning of the ear canal
• Otowick optimal treatment with:
Ciproxin HC ear drops 3 drops three times a day for 5 days
OR Locacorten-Vioform
• Change wick daily prn
• Systemic antibiotics if cellulitis or lymphadenopathy
.If doubt about TM perforation, don’t use potentially ototoxic drops.
Prevention
• Alcohol ear drops/acetic acid 3% (Aqua ear)—not with perforation!
• Ear putty, ear plugs
• Remove wax at the beginning of the swimming season
THE “RED EAR”
60% of red ears are NOT acute OM
• often crying child, febrile, otitis externa, OME
• if diagnosis of OM uncertain, rationale of giving prescription for antibiotics to be taken if paracetamol etc not effective after 24 – 48 hours
ACUTE SUPPURATIVE OTITIS MEDIA
Incidence
• 80% of children will have one attack by the age of four years
• Peaks at 6 – 18 months and 4 – 5 years
Aetiological Factors
• Major Factors
Daycare Centre attendance (“Biologic Zoos”/orphanages)
Cigarette smoke exposure
Prop feeding/reflux
URTI, Acute sinusitis
Bacteriology
• 90% caused by a single organism
Streptococcus pneumoniae 20 – 30%  (becoming less with Pneumococcal immunisation)
Haemophilus influenzae 30 – 40%
Moraxella catarrhalis 8 – 10%
Streptococcus pyogenes 4 – 8%
Recurrent Otitis Media – H. influenzae organism increases to 50 – 60%
Management
• Amoxicillin up to 90 mg/kg/day for 10 days
• If allergic to Penicillin – Rulide D/Septrin/Azithromycin
• Analgesia, local anaesthetic ear drops (only if ear not about to perforate)
• If not improving after 48 hours, i.e. fever/pain persist– suspect resistant organism
Augmentin/Cefaclor
Prevention
• Amoxicillin/Cefaclor 20 mg/kg/day for 4 weeks
Indications for Surgical Intervention (Myringotomy and Ventilation Tubes)
1. Persistent otitis media/impending mastoiditis
2. 6 separate attacks of otitis media in 12 months, OR
4 separate attacks of otitis media in 6 months
Complications
1. Acute mastoiditis
2. Chronic otitis media/perforation
3. Otitis media with effusion
4. Facial nerve palsy
5. Meningitis
6. Cholesteatoma
CHRONIC SUPPURATIVE OTITIS MEDIA
Implies chronic middle ear infection with a tympanic membrane perforation with either active discharge or dry middle ear.—for longer than 6 weeks.
Aetiology
• Sequelae of acute otitis media
• Related to poor hygiene/nutrition
Bacteriology
Multiple organisms
• Pseudomonas sp 60 – 80%
• Staphylococcus aureus 20 – 30%
• Streptococcus pneumoniae 10 – 20%
• Bacteriodes and other anaerobes 25%
Management
• Regular ear toilets (  0.05% Betadine)
• Topical ear drops/powder
• Ciproxin HC or Ciloxan ear drops for recalcitrant ears
• Little place for systemic antibiotics except for bony/soft tissue invasion
• When dry, between age 5 –7 years, consider myringoplasty
OM/CSOM IN ABORIGINAL CHILDREN
• Early colonisation of nasopharynx by Pneumococcus—90% by age 3 months
• Less specific otologic symptoms – “silent” otorrhoea in acute OM
• Higher incidence of chronic otorrhoea (up to 70% of children in some communities)—Ciloxan ear drops now available on authority prescription.
• Relates to overcrowding, poor hygiene and nutrition, passive smoking etc
• As general health improves, so does incidence of OME, retraction pockets and cholesteatoma
OTITIS MEDIA WITH EFFUSION (OME)
Synonyms
• glue ear
• Serous otitis media
• Middle ear effusion
Serous or mucoid middle ear effusion secondary to Eustachian tube dysfunction.  In 50% of cases, low levels of bacterial pathogens are present – usually those seen in acute otitis media.
Aetiologic Factors
• Daycare centre attendance
• Prematurity/low birthweight
• Cleft palate – 80% by age 1 year
• Down syndrome
• Reflux
• Allergic rhinitis/sinusitis
• ?Adenoiditis/adenoid hypertrophy
• Inadequate treatment of otitis media
.    Relationship to bacterial biofilm.
Symptoms
Infants – 3 years
Delayed speech development
Balance disorder – delay in walking
Hearing loss – fail clinical test
Recurrent otitis media
Head banging, nocturnal otalgia
Behavioural problems, FB
3 – 7 years
Partial hearing loss – fluctuating hearing loss
Eustachian symptoms, dull ache
Difficulty at school – “tuning out”
Behavioural problems
Lack of self-esteem
Reading problems (Dunedin study)
Signs of otitis media
• Retracted TM with decreased mobility
• May be opaque, yellow, brown, vascularized or black
• Retraction pockets/adhesive OME
Investigations
• Audiometry
• Tympanometry ‘A’ normal peaked tracing
‘B’ flat tracing
‘C’ negative pressure peak
Management
1. Amoxicillin/Ceclor 20 mg/kg/day 1 dose for 2 – 4 weeks ( becoming more contentious)
2. Steroid nasal spray if atopic—Mometasone 2 months.
3. Modified Valsalva – Otovent
4. Hearing aid (uncommon)
5. Antihistamines/decongestant – not proven
6. Steroids orally – not proven
7. Bisolvon – not proven
8. Surgical
• Myringotomy alone – little help
• Myringotomy and insertion of ventilation tubes (grommets)
• Adenoidectomy with myringotomy and tubes—decreases 2nd op by 50%
9. Look for associated medical conditions
• Oesophageal reflux
• Sinusitis – in infants as young as 12 months
• Allergic rhinitis – association with OME, particularly in >6 year old with persistent OME
• Immunologic deficiency, especially subclass IgG2 and IgG3 deficiency
• Craniofacial abnormality
Tympanogram
Type A
Type B
Type C
MYRINGOTOMY AND TUBES
Indications
Absolute
1. Handicapping hearing loss for 3 months
2. 6 separate attacks of otitis media in 12 months OR 4 separate attacks in 6 months
3. Atelectatic otitis media with effusion
Relative
1. Mild hearing loss for 12 months or greater
2. Marginal child with speech delay
3. Balance problems
4. Recurrent otitis media with facial nerve palsy
5. Mild otitis media with effusion/hearing loss and recurrent otitis media 3 – 4 times
6. Attic retraction pocket
Complications of Ventilation Tubes
1. Otorrhoea with URTI/H2O
2. Polyps/bleeding
3. Early/late extrusion
4. Retraction pockets/cholesteatoma at myringotomy site
5. Persistent perforations 1.6 – 10%
Management of Grommet Infections
1. Local ear toilets with 0. 05% Betadine followed by Ciprofloxacin ear drops 3 drops three times a day for 5 days. Tissue spearing an adjunct—not a cure!
2. Consider otowick/drops/Ciproxin HC
3. Rarely IV antibiotics/removal of tube
4. If organism is cultured and pseudomonas etc – drops only
5. If H. influenzae or Strep. Pneumoniae – consider oral antibiotics also
Reintubation
• 20% of patients
• Particularly cleft palate/Down syndrome/allergic rhinitis
Protection of ear with tubes in place
1. Sea water none or ear plugs
2. Pools silicone ear putty, Bluetac
Earplugs, moulded ear plugs
Avoid prophylactic eardrops
Complications of otitis media with effusion
1. Cholesteatoma
2. Ossicular complications
3. Language problems/ reading difficulties
4. Central auditory processing disorder
5. Hearing loss in background noise as adults?
CHOLESTEATOMA
• More aggressive in children
• Cystic structure associated with invagination of tympanic membrane, with accumulation of skin, debris, bacteria eroding middle ear structure
.    Aboriginal children with CSOM over age 10 years—10% chance of cholesteatoma.
Complications
Intratemporal bone
• Hearing loss
• Ossicular damage
• Perforation TM/otorrhoea
• VII nerve palsy
• Mastoiditis
• Labyrinthitis
• Perilymph fistula
Extratemporal bone
• Meningitis
• Sigmoid sinus thrombosis
• Intracranial abscess
Surgery for cholesteatoma
Individualised
Varies with:
• Location/extent of cholesteatoma
• Status of hearing and infections
• Socioeconomic issues regarding followup
• Likelihood of compliance with plan
SENSORINEURAL HEARING LOSS
Incidence
• Severe sensorineural hearing loss in 1 in 1000 infants
Aetiology
• 50% congenital sensorineural hearing loss is genetic
• Non-genetic TORCH syndrome (perinatal infection)
Toxoplasmosis
Rubella
Cytomegalovirus
Herpes simplex
Syphilis
• Maternal ototoxic medications
Thalidomide
Quinine
Aminoglycosides
Ethyl alcohol?
• Metabolic Diseases
• Asphyxia/birth trauma
• Hyperbilirubinaemia
• ICU admission
• Neonatal meningitis
• Ototoxic medications
• Prematurity/low birthweight
• Noise trauma
In essence, all children who are graduates of the neonatal intensive care unit should be identified as “at risk” for sensorineural hearing impairment.  The prevalence of moderate to profound sensorineural hearing loss in the “at risk” group is higher that the rate in the well baby population.
Over 100,000 West Australian babies have had neonatal hearing screening using various technologies. ANY BABY CAN HAVE A HEARING SCREENING FROM DAY 1-
Using objective screening methods.—Otoacoustic emission testing/aABR testing.
Babies with normal hearing at birth can develop progressive or acquired SNHL (eg meningitis/ head injury) –doubling the incidence by 5 years and tripling it by 10 years.
COMMONLY OCCURING TYPES OF GENETIC HEARING IMPAIRMENT
Syndromic
Autosomal Dominant
• Treacher Collins syndrome
• Goldenhar syndrome
• Waardenburg syndrome
• Branchio-oto-renal syndrome
Autosomal Recessive
• Usher syndrome
• Pendred syndrome
• Jervell and Lange-Nielson syndrome
• Alport syndrome
Non-syndromic
• Autosomal dominant delayed onset progressive sensorineural hearing loss
• X linked recessive mixed-stapes fixation with mixed hearing loss and perilymph gusher
Meningitis
• Sensorineural hearing loss is most common permanent sequelae of bacterial meningitis (10% of infants).  31% with S. pneumoniae
• If sensorineural hearing loss persists for 2 –3 weeks – permanent
• Progressive sensorineural hearing loss may occur and will require serial audiograms till age 3 years or 2 years after the meningitis.
• Consideration of cochlear implantation within 12 months for meningitis patients
Perilymph Fistula
• Accounts for 8% of congenital sensorineural hearing loss
• Fluctuating or progressive hearing loss. Balance problems less common in children.
• Oval window leak more often than round window
• High index of suspicion; explore middle ear
HEARING SCREENING IN CHILDREN
1. Otoacoustic emission screener
Initial screening test for infants
If infant fails OAE screening, then automated Auditory Brainstem Screening (ABR) is performed
Diagnostic ABR is gold standard diagnostic tool
2. 6 months – 2 1/2 years – visual reinforcement audiometry
3. 2 1/2 years to 4 years – play audiometry
4. 4 years and older – adult type audiometry with earphones
HEARING ASSESSMENT RESOURCES IN WA
1. Princess Margaret Hospital for Children Audiology Department/ENT Department
2. State Child Development Centre, Rheola Street, West Perth
3. Australian Hearing, City,
4. Lions Hearing Centre, QEII Medical Centre at SCGH, Joondalup
5. Telethon Speech and Hearing Centre, Wembley
6. Private Otolaryngologists and Audiologists
SPEECH DELAY
Normal speech development
• Generally 20 words or short phrases at 18 months
• Generally 50 words/short sentences at 2 years
Causes of speech delay in a 2 year old
• Variation of normal development
• Hearing loss
• Intellectual disability
• Environmental deprivation
• Neurological abnormalities
• Autism
Also Bilingual households
Twins
Premature infants
NASAL PROBLEMS
Neonatal Nasal Obstruction
Respiratory distress can occur anywhere from nasal vestibule to the lungs.
The neonate may be an obligate nasal breather (until 8 – 16 weeks) because of the proximity of the soft palate to the base of the tongue, the epiglottis and the larynx.
Causes
Anterior obstruction
• Deformed lower lateral cartilages
• Septal deformity
• Pyriform aperture stenosis
• Lacrimal duct cysts
• Turbinate hypertrophy
Posterior obstruction
• Encephalocoele
• Dermoid
• Haematoma
• Chordoma, teratoma
• Rhabdomyosarcoma
• Unilateral/bilateral choanal atresia
• Adenoid hypertrophy
Investigations
• Mirror misting test
• Passage of nasal catheter
• Septal strut testing
• Telescope/fibrescope
• CT scan/contrast (atresia)
CHOANAL ATRESIA
• Most common anatomic obstruction in nasal cavity
• Unilateral more frequent – girls more common
• Complete/incomplete persistent bucco-pharyngeal membrane
• Bony/membranous or bony (90%)
Associated Congenital Lesions
C Coloboma
H Heart defects
A Atresia choanae
R Retarded growth
G Genital hypoplasia
E Ear defects/deafness
Also Branchial arch defects, microcephaly, micrognathia, palatal defects, mandibulofacial dystostosis
Management
• Bilateral – life threatening – oral airway
• Surgery
Transnasal
Transpalatal approach
Stenting for 4 – 6 weeks
OLDER CHILDREN – Nasal Obstruction
History
• Duration
• Association with obstructive sleep apnoea
• Family history of atopy, epistaxis history
• Nasality of speech
Examination
• Adenoid facies
• Open Mouth
• Short upper lip, flat middle 1/3 face
• Dull facial appearance, dental malocclusions
Allergic facies
• As above, plus:
‘Allergic shiners’, Denny’s line
Broad nasal tip, transverse crease
Examine
• Ears (secondary to NPX obstruction)
• Septum, nasal cavity (otoscope)
• OPX – tonsil size
• Palate shape and length
• Nasopharynx if possible
• Voice – hyper/hyponasality
Investigations
• Sinus X-rays
Lateral – to assess adenoids
Waters – to assess antra
• CT Scan
Coronal mini-series CT Scan
For sinus disease, ostial disease
• Polysomnography
If OSA noted
• Allergy Tests
Skin tests, RAST testing
Management
Remember to consider nose, adenoid region and tonsil area as a whole – the airway obstruction occurs in series, not in parallel.  Many obstructed children will need adenoidectomy and tonsillectomy to affect a cure. In fact the upper and lower respiratory tract are ‘ONE AIRWAY’.
ADENOIDECTOMY
• Snores loudly, obstructive sleep disorder
• Avoid with short or cleft palate
• Rule out submucous cleft palate, i.e.
Bifid uvula
Thin median raphe
Bony notch in hard palate
• Can be done and home in 6 hours (same day care unit)
• Rhinolalia (hypernasality)
ALLERGIC RHINITIS
• 40-80% have parental atopy
• Seasonal (hayfever) or perennial (PAR)
• PAR – dry, stuffy, blocked nose – sniffer
• Inhalant or food allergy as cause
• RAST testing – for inhalant antigen
• Avoidance – provocation tests for foods
Management and Prevention
• Avoidance of allergen e.g. HDM
• Desensitization – ID/Sublingual
• Nasal steroid sprays eg Mometasone
Medical Treatment
• Antihistamines – sedating/non-sedating
• Nasal steroid sprays
NOTE: Cortisone absorption effect on growth in children
Beclomethasone 40% absorbed
Rhinocort 8% absorbed
Nasonex 0.1% absorbed
Surgical Treatment – NOT A CURE!
• Cautery of turbinates/cryosurgery
• Trimming of turbinates
Note: Cautery of turbinates may be combined with tonsillectomy and adenoidectomy.  Remember allergy may manifest as eczema, asthma and hayfever and also tonsillar and adenoid hypertrophy, otitis media with effusion and sinusitis.
OBSTRUCTIVE SLEEP DISORDER
A spectrum of symptoms ranging from mild snoring through to apnoea with cardiac failure.  In general, if a child has apnoea lasting more than 10 seconds or seven apnoeic episodes per hour then they have significant obstructive sleep disorder (Especially if they desaturate to less than 90%)
Features
Snoring 100%
Chronic mouth breathing  50%
OSA – apnoea  25%
Hypersomnolence  20%
Nocturnal sweating  20%
Restless sleep  20%+
Nightmares, waking  10%
Sleepwalking  10%
Enuresis    5%
Growth problems    5%
Meat dysphagia    5%+
Neuro-cognitive, behavioural symptoms.
Diagnosis
1. History
2. Examinations – nose/adenoids/tonsils
3. Investigations
Sinus views
Modified sleep study
Polysomnography
Management
1. Medical
Nasal steroid sprays
CPAP (Down syndrome/Craniofacial abnormality)
2. Surgical
Ts + As + CIT
Tracheostomy
It is essential for post-operative tonsillectomy and adenoidectomy patients with obstructive sleep disorder to have overnight pulse oximetry to avoid apnoea/hypoxic drive stimulus.  Great care to avoid oversedation with narcotics.
In Australia 0.7% of children have Ts/Ads  (0.5% for OSD) yet 10% of children snore and 3% have OSD/OSA—indicating significant under-diagnosis.
PAEDIATRIC SINUSITIS
Factors
• Air pollution, allergic rhinitis, URTI, day care attendance, reflux (new concept)
Definitions
• Acute Sinusitis
Persistent no longer than 6 – 8 weeks
Resolves with medical therapy with no significant mucosal damage
• Chronic Sinusitis
Persistent disease not alleviated by medical therapy alone.  12 weeks of persistent symptoms or six episodes per year of acute sinusitis
Pathogens
Streptococcus pneumoniae 40%
Haemophilus influenzae 35%
Anaerobes   7%
Streptococcus species   7%
Diagnosis
1. Acute viral URTI – commonly the precipitating event (“the cold that lasts a month, Doctor”)
2. The most common cause is bacterial infection secondary to obstruction
3. Plain sinus x-rays may be misleading
4. With persistent symptoms – CT scan (especially modified coronal CT) and endoscopy.  The key to sinusitis is blocked ostiomeatal complex.
5. In WA, allergic rhinitis is often implicated
Symptoms
• Nasal obstruction and congestion
• Pressure with pain
• Thick nasal discharge
• Toothache
• Fever
• Cough or irritability
Maxillary Cheek pain, frontal headache, tooth ache
Ethmoid Inner canthal pain/pressure, periorbital headache
Frontal Frontal headache, tenderness over frontal sinus
Sphenoid Deep seated headache, PUO
Treatment of Acute Sinusitis
1. Most patients respond to appropriate decongestant and antibiotics in adequate dosage for sufficient duration
2. Antibiotic resistance – suggest Cefaclor, ‘Augmentin’ or Septrin for 10 – 14 days
3. Antihistamines not helpful, inhalations often helpful
4. Rule out reflux as cause
5. Topical decongestants/saline nasal spray
Systemic or Predisposing Factors for Sinusitis
• Cystic fibrosis
• Ciliary dyskinesia
• Young’s syndrome
• Serious immune deficiency
• AIDS (30% have sinusitis)
• Anatomic abnormalities
• Environmental and genetic factors
• Hyper-reactive respiratory lining, especially in patients with asthma
Management Goals for Sinusitis
• Control infection
• Reduce tissue oedema
• Facilitate drainage
• Maintain patency of sinus ostia
• Break pathological cycle leading to chronic sinusitis
Surgical Management
• Aim to establish ventilation for sinuses especially at keystone area of ostiomeatal complex
• Antral washout, intranasal antrostomy, functional endoscopic sinus surgery
Epistaxis in Children
• Uncommon under the age of 2 years
• Related to hot dry summers, heating in winter
• Little’s area on septum commonest site of bleeding
• 80% can be prevented by Vaseline or Nozoil b.d. in nares
• Nose picking, rubbing (allergy), trauma as causes
• Foreign bodies may present as epistaxis
• Neoplasms – juvenile Angiofibroma (NPX) – rare tumour in adolescent males
• Cauterisation
Use Cophenylcaine either on cotton wool or directly by spray.  Then use AgNO3 cautery stick.  If 3 cauteries performed – elective surgery with electro-surgery. Packing uncommon.
Foreign bodies in nose
• Suspect if foul smelling unilateral discharge
• Adequate light decongestion/anaesthesia and instrumentation for success
• Cophenylcaine on cotton wool pledget – into nose and then remove both cotton wool and foreign body
• Look for secondary sinusitis if long standing
Fractured nose in children
• Uncommon to fracture nasal bones in infants – usually septal cartilage/soft tissue injuries
• Rule out septal haematoma (like prow of boat)
• Often wait 7 days for swelling to subside, then review
• Radiography not always necessary except for medico-legal reasons
• Reduction of nasal fracture at 7 – 14 days optimally
.Ensure an ENT surgeon sees the child by 10-14 days after injury before the    fracture sets
TONSILLITIS AND TONSILLECTOMY INDICATIONS
Tonsillitis
• Acute, viral or bacterial
• Streptococcus (Group A beta haemolytic)
• Penicillin treatment of choice 7 – 10 days
• If Lactamase producing bacteria (non-responsive to Penicillin) consider Augmentin/Cefaclor
• If  6 attacks of bacterial tonsillitis in 12 months in child over 4 years with 2 weeks off preschool/school – consider tonsillectomy
• “Chronic tonsillitis” – other older children with cryptic debris coughed up, frequent sore throat and halitosis
Peritonsillar Abscess (Quinsy)
• Abscess may point or be ‘subacute’
• Trismus drooling, pain, fever
• Two management options
1. IV antibiotics, subsequent tonsillectomy
2. Quinsy or immediate tonsillectomy
• The latter is favoured as one hospitalisation and decreased pain and morbidity
• Recurrence rate if not operated – 20%
Indications for Tonsillectomy in the 2010’s
• Obstructive Sleep Disorder
Upper airway obstruction secondary to tonsillar or tonsillar and adenoid hypertrophy
Commonest indication for tonsillectomy in paediatric hospitals worldwide
• Severe recurrent bacterial tonsillitis
• Quinsy – 1 – 2 episodes
• Biopsy purposes – to rule out e.g. lymphoma
Tonsillectomy Procedure
• General intubation anaesthesia and protection of airway
• Often combined with adenoidectomy
• Sharp/blunt dissection to remove tonsils.Coblation/electro-surgery may cause higher incidence of 2ndry haemorrhage/
• Meticulous attention to haemostasis
• Post-operative overnight pulse oximetry mandatory for children with OSD
• Post-operative antibiotics for 7 days reduce pain, incidence of secondary haemorrhage
• Avoid ASA, NSAIDS
.
Tonsillectomy Complications
• Bleeding
primary or reactive
secondary – to 14 days post-operative
• Seen in 1 in 50 procedures
• Secondary bleeding if tonsil bed infection or early separation of slough
• Secondary healing often controlled by admission, IV drip, antibiotics, removal of clot/AgNO3
• Late complication of scarring or velopharyngeal incompetence (VPI) causing rhinolalia or hypernasality (cleft palate type speech)
Tonsillar Hypertrophy Revisited (See OSD)
• All large tonsils are not always associated with OSD
• Relatively small tonsils (Grade II) may be floppy or in patients with lax tissues e.g. Down syndrome may be obstructive
Tonsil Size
Grade 1 Grade 2 Grade 3 Grade 4
Increasing Severity of Obstruction Symptoms
• Chronic mouth breathing and snoring
• Increased URTI, oral-dental ill health
• Orthodontic abnormalities, altered taste, smell
• Restless sleepers, 2 – 3 pillow, head arched
• Waking for drinks, sleep walking, enuresis
• Thin, poor eaters, meat dysphagia
• Chronic nocturnal cough (micro aspiration)
• Decreased stamina for day time activities
• Nocturnal sweating, morning headaches (CO2 retention)
• Hypoxia, apnoea, pulmonary hypertension
• Right heart failure, cardio-respiratory arrest
PAEDIATRIC LARYNGOLOGY
Stridor
Symptom not a diagnosis
Inspiratory superior part of upper airway obstruction
Expiratory obstruction distal to vocal cords
Biphasic subglottic (or glottic) obstruction
Age relationship
• At birth – choanal atresia/congenital subglottic stenosis
• Several weeks after birth – laryngomalacia
Subglottic haemangioma
(Inflammatory disorders rare in neonates)
• 1 – 6 years – inflammatory
• croup, epiglottitis
• 8 – 12 years – bacterial tracheitis
Acute stridor
• Inflammation, trauma, FB
Chronic Stridor
• Fixed lesion, e.g. VC palsy/subglottic stenosis
Increasing Severity
• Papilloma, subglottic haemangioma
Examination
• Auscultation of neck
• Position e.g. leaning forward in epiglottitis
• Colour
• Respiratory rate, cardiac rate
• Retractions
Care with examination of mouth, pharynx (especially epiglottis)
Flexible fibre-optic scope is useful
Radiology
• AP/Lateral neck and chest
• (inspiratory and expiratory if suspect a foreign body)
• Fluoroscopy, barium swallow
• CT, MRI
Endoscopy
Team approach – with anaesthetists
Differentiating Features of Three Paediatric Inflammatory Diseases
DISEASE
FEATURE CROUP BACTERIAL TRACHEITIS EPIGLOTTITIS
AGE <2 years Any age 3-4 years
ORGANISM RSV Parainfluenza Staph. aureus H. influenzae
SITE OF INVOLVEMENT Subglottis Trachea Supraglottis
STRIDOR Biphasic Expiratory Inspiratory
VOICE Barking cough Hoarseness Unaffected
(Hot potato)
POSITION Not characteristic Not characteristic Erect, chin jutting forward
SWALLOWING Unaffected Unaffected Drooling
TREATMENT Humidity
Adrenalin
?Steroids Bronchoscopy
Suctioning
IV antibiotics
ICU Intubation
IV antibiotics
Humidity
ICU
Note: With the increasing use of Hib vaccination, epiglottitis is becoming less common
CONGENITAL ABNORMALITES OF THE LARYNX
Laryngomalacia
• Common laryngeal anomaly
• Intermittent low-pitched crowing inspiratory stridor
• Abnormal flaccidity or tightness of supraglottic structures
• Often worse when supine
• May cause respiratory distress, feeding difficulties and FTT, associated with neurological condition
• Tubular epiglottis, prominent arytenoids, short ary-epiglottic fold
• Subside usually after 1 – 2 years
• Occasionally laser surgery to AE fold in severe cases
Vocal Cord Paralysis
Symptoms
• Stridor 65%
• Dyspnoea, dysphonia
• Inhalation, respiratory distress 17%
• Cyanosis 12%
Bilateral
• CNS disease, birth trauma, Arnold-Chiari malformation
• Most present by 6 weeks of life
• Respiratory distress, normal cry
• 50% will need intubation or tracheostomy
Unilateral
• Idiopathic 35%, obstetric 24%
• Cardiac surgery, neurologic, vascular
• Left 72%, Right 28%
• Weak cry, stridor on exertion
Diagnosis
• Endoscopy of larynx
• CT if CNS problem suspected
Management
• Observation
Unilateral, treat cause (e.g. hydrocephalus)
Bilateral – ETT/tracheostomy (50%)
• Late
Arytenoidectomy for bilateral VC palsy
Subglottic Stenosis
• Congenital or acquired
• Stridor, respiratory distress, recurrent LTB
• Circumferential narrowing at cricoid level
• Post extubation (cause) and failure extubate
• Bronchoscopy, radiology
• Occasionally need cricoid split operation, OR
Laryngotracheal reconstruction
Subglottic Haemangioma
• Smooth compressible mass in subglottis
• 50% associated cutaneous lesions
• Present as increasing stridor, or a persistent laryngotracheobronchitis
• Diagnosis X-ray, Bronchoscopy (no biopsy)
• Usually involute in 1 – 4 years
• Observe/tracheostomy, CO2 Laser and Interferon
OTHER LARYNGEAL CONDITIONS
Recurrent Respiratory Papillomatosis (RRP)
• Low incidence, on the increase HPV 6, HPV 11
• Condyloma-like papilloma on vocal cords, larynx
• Increasing hoarseness, stridor (avoid tracheostomy)
• Frequent endoscopies, CO2 laser, interferon
• Rarely seed to tracheo-bronchial tree
Vocal Cord Nodes
• Vocal abuse, cough
• Often resolve in teenage years
• Occasionally surgical removal if over the age of 10 – 12 years and failed speech therapy for 6 months
CHRONIC COUGH IN CHILDREN
Holinger “Symptom not a diagnosis”
Jackson “Cough is the watchdog of the airway”
“Don’t drug the watchdog!”
Diagnostic Protocol
1. Histology
• Immunization, allergies, asthma, sinusitis, URTI
• Passive smoking history
a) Dry Barking (Brassy) Cough – Infections
• Subglottic stenosis
• Aberrant innominate
• Tracheomalacia
b) Wet Productive Cough
• Specific infection LRT or chronic bronchitis
c) Cough with associated throat clearing
• PND, reflux
2. Physical Examination
3. Radiology
• Chest x-ray, sinus views (?mini CT)
• Barium swallow
4. Blood Tests
• CBC. Diff, Pertussis Ab titres
• IgGs,  1 – Antitrypsin
5. Skin Testing
• Allergy, PPD, Sweat Chloride
Endoscopy
• If cough greater than 6 – 8 weeks
• History of foreign body/obstructive lesion
• Most valuable diagnostic tool (followed by sinus x-rays)
Results
Birth to 18 months
• Cough variant asthma
• Aberrant innominate artery
• Reflux
(most effective studies – endoscopy/Ba Ex/Rx asthma)
1 1/2 years to 6 years
• Sinusitis
• Asthma
• Subglottic stenosis
(most effective studies – sinus x-rays, endoscopy, Rx asthma)
6 to 16 years
• Cough variant asthma
• Psychogenic
(most effective studies – PFT, endoscopy, Rx asthma)
Overall
1. Cough variant asthma 32%
2. Sinusitis 23%
3. Reflux 15%
4. Aberrant innominate artery 12%
FOREIGN BODIES
Sixth most common cause of accidental death
Chest
• Peanuts 50%, carrot and apple
• 20% of children with a foreign body not seen by GP for 1 month
High index of suspicion
• Choking episode, wheeze
• Recurrent or migrating pneumonia
• Unexplained persistent respiratory symptoms
Investigations
• Insp/Exp chest films
• Fluoroscopy
Air trapping
Mediastinal shift
Obstructive emphysema
Oesophagus
• May cause fatal airway obstruction by impinging on airway
• Commonly – coins, plastic toys
• C6 level, stricture, aortic arch
• Careful removal
CORROSIVE INJURY OF THE OESOPHAGUS
Scenarios
1. Accidental ingestion by toddlers
2. Older children – mislabelled containers
3. Adolescents – suicide
4. Child abuse
Agents
Corrosive, e.g. caustic soda, dishwashing liquid (pH 11)
Acids, e.g. HCl, H2SO4
Non-phosphate detergent powders – airway problems > oesophageal problems
Management
1. Emergency
• H2O/milk
• No acid to neutralise
• No vomiting
2. Oesophagoscopy – first 48 hours
• Oesophageal burns in absence of oral burns
• To level first circumferential burns
• Nasogastric tube
• Antibiotics, steroids
• Re-oesophagoscope at 10 – 14 days
3. Sequelae
• May need dilatations
• Occasionally oesophageal replacement
• Increased risk of oesophageal malignancy 40 years later

PAEDIATRIC OTOLARYNGOLOGY
NOTES

V AND VI Year MEDICAL STUDENTS

Harvey Coates, AO, MS, FRACS

INTRODUCTION

Paediatric Otolaryngologists provide medical and surgical care to infants and children who have complicated and often rare diseases and disorders that are most effectively and safely managed in institutions that specialise in children’s health care.  Infants are not just “little adults”.  At every age they are different, requiring an understanding of the anatomic, physiologic and psychological changes that occur with their growth and development.  We take care, as Charles Bluestone says, of “special” problems or “special” children, or both, in a “special” institution.
These notes are not meant to be a comprehensive review of the scope of paediatric otolaryngology.  They cover those subjects with which I feel the student with an interest in family practice or paediatrics should be conversant. OTITIS EXTERNA
Infection of the skin of the ear canal.  It may be bacterial, fungal or viral.  It is usually caused by pH change in the ear canal by water (normal ear canal pH 5.1) and overgrowth of organisms with a breach of canal skin causing invasion.
Organism • Candida, Aspergillus niger• Pseudomonas• Herpes virus
Presentation • Severe discomfort in the external ear• Swelling ear canal with discharge• Tenderness on movement of the tragus and/or pinna• “Wet cardboard” appearance, fungal OE
Management • Meticulous cleaning of the ear canal• Otowick optimal treatment with: Ciproxin HC ear drops 3 drops three times a day for 5 days OR Locacorten-Vioform• Change wick daily prn• Systemic antibiotics if cellulitis or lymphadenopathy      .If doubt about TM perforation, don’t use potentially ototoxic drops.Prevention • Alcohol ear drops/acetic acid 3% (Aqua ear)—not with perforation!• Ear putty, ear plugs• Remove wax at the beginning of the swimming season
THE “RED EAR”
60% of red ears are NOT acute OM• often crying child, febrile, otitis externa, OME• if diagnosis of OM uncertain, rationale of giving prescription for antibiotics to be taken if paracetamol etc not effective after 24 – 48 hours ACUTE SUPPURATIVE OTITIS MEDIA
Incidence • 80% of children will have one attack by the age of four years• Peaks at 6 – 18 months and 4 – 5 years
Aetiological Factors• Major Factors Daycare Centre attendance (“Biologic Zoos”/orphanages) Cigarette smoke exposure Prop feeding/reflux URTI, Acute sinusitis
Bacteriology• 90% caused by a single organism Streptococcus pneumoniae 20 – 30%  (becoming less with Pneumococcal immunisation) Haemophilus influenzae 30 – 40% Moraxella catarrhalis 8 – 10% Streptococcus pyogenes 4 – 8% Recurrent Otitis Media – H. influenzae organism increases to 50 – 60%
Management• Amoxicillin up to 90 mg/kg/day for 10 days• If allergic to Penicillin – Rulide D/Septrin/Azithromycin• Analgesia, local anaesthetic ear drops (only if ear not about to perforate)• If not improving after 48 hours, i.e. fever/pain persist– suspect resistant organism Augmentin/Cefaclor
Prevention• Amoxicillin/Cefaclor 20 mg/kg/day for 4 weeks
Indications for Surgical Intervention (Myringotomy and Ventilation Tubes)1. Persistent otitis media/impending mastoiditis2. 6 separate attacks of otitis media in 12 months, OR 4 separate attacks of otitis media in 6 months
Complications1. Acute mastoiditis2. Chronic otitis media/perforation3. Otitis media with effusion4. Facial nerve palsy5. Meningitis6. Cholesteatoma CHRONIC SUPPURATIVE OTITIS MEDIA
Implies chronic middle ear infection with a tympanic membrane perforation with either active discharge or dry middle ear.—for longer than 6 weeks.
Aetiology• Sequelae of acute otitis media• Related to poor hygiene/nutrition
BacteriologyMultiple organisms• Pseudomonas sp 60 – 80%• Staphylococcus aureus 20 – 30%• Streptococcus pneumoniae 10 – 20%• Bacteriodes and other anaerobes 25%
Management• Regular ear toilets (  0.05% Betadine)• Topical ear drops/powder• Ciproxin HC or Ciloxan ear drops for recalcitrant ears• Little place for systemic antibiotics except for bony/soft tissue invasion• When dry, between age 5 –7 years, consider myringoplasty
OM/CSOM IN ABORIGINAL CHILDREN
• Early colonisation of nasopharynx by Pneumococcus—90% by age 3 months• Less specific otologic symptoms – “silent” otorrhoea in acute OM• Higher incidence of chronic otorrhoea (up to 70% of children in some communities)—Ciloxan ear drops now available on authority prescription.• Relates to overcrowding, poor hygiene and nutrition, passive smoking etc• As general health improves, so does incidence of OME, retraction pockets and cholesteatoma OTITIS MEDIA WITH EFFUSION (OME)
Synonyms • glue ear• Serous otitis media• Middle ear effusion
Serous or mucoid middle ear effusion secondary to Eustachian tube dysfunction.  In 50% of cases, low levels of bacterial pathogens are present – usually those seen in acute otitis media.
Aetiologic Factors• Daycare centre attendance• Prematurity/low birthweight• Cleft palate – 80% by age 1 year• Down syndrome• Reflux• Allergic rhinitis/sinusitis• ?Adenoiditis/adenoid hypertrophy• Inadequate treatment of otitis media      .    Relationship to bacterial biofilm.
Symptoms Infants – 3 years Delayed speech development Balance disorder – delay in walking Hearing loss – fail clinical test Recurrent otitis media Head banging, nocturnal otalgia Behavioural problems, FB
3 – 7 years Partial hearing loss – fluctuating hearing loss Eustachian symptoms, dull ache Difficulty at school – “tuning out” Behavioural problems Lack of self-esteem Reading problems (Dunedin study)
Signs of otitis media• Retracted TM with decreased mobility• May be opaque, yellow, brown, vascularized or black• Retraction pockets/adhesive OME
Investigations• Audiometry• Tympanometry ‘A’ normal peaked tracing ‘B’ flat tracing ‘C’ negative pressure peak
Management1. Amoxicillin/Ceclor 20 mg/kg/day 1 dose for 2 – 4 weeks ( becoming more contentious)2. Steroid nasal spray if atopic—Mometasone 2 months.3. Modified Valsalva – Otovent4. Hearing aid (uncommon)5. Antihistamines/decongestant – not proven6. Steroids orally – not proven7. Bisolvon – not proven8. Surgical• Myringotomy alone – little help• Myringotomy and insertion of ventilation tubes (grommets)• Adenoidectomy with myringotomy and tubes—decreases 2nd op by 50%9. Look for associated medical conditions• Oesophageal reflux• Sinusitis – in infants as young as 12 months• Allergic rhinitis – association with OME, particularly in >6 year old with persistent OME• Immunologic deficiency, especially subclass IgG2 and IgG3 deficiency• Craniofacial abnormality

Tympanogram
Type A
Type B

Type C

MYRINGOTOMY AND TUBES
Indications
Absolute1. Handicapping hearing loss for 3 months2. 6 separate attacks of otitis media in 12 months OR 4 separate attacks in 6 months3. Atelectatic otitis media with effusion
Relative1. Mild hearing loss for 12 months or greater2. Marginal child with speech delay3. Balance problems 4. Recurrent otitis media with facial nerve palsy5. Mild otitis media with effusion/hearing loss and recurrent otitis media 3 – 4 times6. Attic retraction pocket
Complications of Ventilation Tubes1. Otorrhoea with URTI/H2O2. Polyps/bleeding3. Early/late extrusion4. Retraction pockets/cholesteatoma at myringotomy site5. Persistent perforations 1.6 – 10%
Management of Grommet Infections1. Local ear toilets with 0. 05% Betadine followed by Ciprofloxacin ear drops 3 drops three times a day for 5 days. Tissue spearing an adjunct—not a cure!2. Consider otowick/drops/Ciproxin HC3. Rarely IV antibiotics/removal of tube4. If organism is cultured and pseudomonas etc – drops only5. If H. influenzae or Strep. Pneumoniae – consider oral antibiotics also
Reintubation• 20% of patients• Particularly cleft palate/Down syndrome/allergic rhinitis
Protection of ear with tubes in place1. Sea water none or ear plugs2. Pools silicone ear putty, Bluetac Earplugs, moulded ear plugs Avoid prophylactic eardrops
Complications of otitis media with effusion1. Cholesteatoma2. Ossicular complications3. Language problems/ reading difficulties4. Central auditory processing disorder5. Hearing loss in background noise as adults? CHOLESTEATOMA
• More aggressive in children• Cystic structure associated with invagination of tympanic membrane, with accumulation of skin, debris, bacteria eroding middle ear structure      .    Aboriginal children with CSOM over age 10 years—10% chance of cholesteatoma.
Complications Intratemporal bone• Hearing loss• Ossicular damage• Perforation TM/otorrhoea• VII nerve palsy• Mastoiditis• Labyrinthitis• Perilymph fistula
Extratemporal bone• Meningitis• Sigmoid sinus thrombosis• Intracranial abscess
Surgery for cholesteatoma Individualised
Varies with:• Location/extent of cholesteatoma• Status of hearing and infections• Socioeconomic issues regarding followup• Likelihood of compliance with plan SENSORINEURAL HEARING LOSS
Incidence• Severe sensorineural hearing loss in 1 in 1000 infants
Aetiology• 50% congenital sensorineural hearing loss is genetic• Non-genetic TORCH syndrome (perinatal infection) Toxoplasmosis Rubella Cytomegalovirus Herpes simplex Syphilis• Maternal ototoxic medications Thalidomide Quinine Aminoglycosides Ethyl alcohol?• Metabolic Diseases• Asphyxia/birth trauma• Hyperbilirubinaemia• ICU admission• Neonatal meningitis• Ototoxic medications• Prematurity/low birthweight• Noise trauma
In essence, all children who are graduates of the neonatal intensive care unit should be identified as “at risk” for sensorineural hearing impairment.  The prevalence of moderate to profound sensorineural hearing loss in the “at risk” group is higher that the rate in the well baby population.
Over 100,000 West Australian babies have had neonatal hearing screening using various technologies. ANY BABY CAN HAVE A HEARING SCREENING FROM DAY 1-Using objective screening methods.—Otoacoustic emission testing/aABR testing. Babies with normal hearing at birth can develop progressive or acquired SNHL (eg meningitis/ head injury) –doubling the incidence by 5 years and tripling it by 10 years. COMMONLY OCCURING TYPES OF GENETIC HEARING IMPAIRMENT
Syndromic
Autosomal Dominant• Treacher Collins syndrome• Goldenhar syndrome• Waardenburg syndrome• Branchio-oto-renal syndrome
Autosomal Recessive• Usher syndrome• Pendred syndrome• Jervell and Lange-Nielson syndrome• Alport syndrome
Non-syndromic• Autosomal dominant delayed onset progressive sensorineural hearing loss• X linked recessive mixed-stapes fixation with mixed hearing loss and perilymph gusher
Meningitis• Sensorineural hearing loss is most common permanent sequelae of bacterial meningitis (10% of infants).  31% with S. pneumoniae• If sensorineural hearing loss persists for 2 –3 weeks – permanent• Progressive sensorineural hearing loss may occur and will require serial audiograms till age 3 years or 2 years after the meningitis.• Consideration of cochlear implantation within 12 months for meningitis patients
Perilymph Fistula• Accounts for 8% of congenital sensorineural hearing loss• Fluctuating or progressive hearing loss. Balance problems less common in children.• Oval window leak more often than round window• High index of suspicion; explore middle ear HEARING SCREENING IN CHILDREN
1. Otoacoustic emission screener Initial screening test for infantsIf infant fails OAE screening, then automated Auditory Brainstem Screening (ABR) is performed Diagnostic ABR is gold standard diagnostic tool2. 6 months – 2 1/2 years – visual reinforcement audiometry3. 2 1/2 years to 4 years – play audiometry4. 4 years and older – adult type audiometry with earphones
HEARING ASSESSMENT RESOURCES IN WA
1. Princess Margaret Hospital for Children Audiology Department/ENT Department2. State Child Development Centre, Rheola Street, West Perth3. Australian Hearing, City, 4. Lions Hearing Centre, QEII Medical Centre at SCGH, Joondalup5. Telethon Speech and Hearing Centre, Wembley6. Private Otolaryngologists and Audiologists
SPEECH DELAY
Normal speech development• Generally 20 words or short phrases at 18 months• Generally 50 words/short sentences at 2 years
Causes of speech delay in a 2 year old• Variation of normal development• Hearing loss• Intellectual disability• Environmental deprivation• Neurological abnormalities• Autism
Also Bilingual households Twins Premature infants NASAL PROBLEMS
Neonatal Nasal Obstruction
Respiratory distress can occur anywhere from nasal vestibule to the lungs.
The neonate may be an obligate nasal breather (until 8 – 16 weeks) because of the proximity of the soft palate to the base of the tongue, the epiglottis and the larynx.
Causes Anterior obstruction• Deformed lower lateral cartilages• Septal deformity• Pyriform aperture stenosis• Lacrimal duct cysts• Turbinate hypertrophy
Posterior obstruction• Encephalocoele• Dermoid• Haematoma• Chordoma, teratoma• Rhabdomyosarcoma• Unilateral/bilateral choanal atresia• Adenoid hypertrophy
Investigations• Mirror misting test• Passage of nasal catheter• Septal strut testing• Telescope/fibrescope• CT scan/contrast (atresia)
CHOANAL ATRESIA
• Most common anatomic obstruction in nasal cavity• Unilateral more frequent – girls more common• Complete/incomplete persistent bucco-pharyngeal membrane• Bony/membranous or bony (90%)
Associated Congenital Lesions
C Coloboma H Heart defects A Atresia choanae R Retarded growth G Genital hypoplasia E Ear defects/deafness
Also Branchial arch defects, microcephaly, micrognathia, palatal defects, mandibulofacial dystostosis
Management• Bilateral – life threatening – oral airway• Surgery Transnasal Transpalatal approach Stenting for 4 – 6 weeks

OLDER CHILDREN – Nasal Obstruction
History• Duration• Association with obstructive sleep apnoea• Family history of atopy, epistaxis history• Nasality of speech
Examination• Adenoid facies• Open Mouth• Short upper lip, flat middle 1/3 face• Dull facial appearance, dental malocclusions
Allergic facies• As above, plus: ‘Allergic shiners’, Denny’s line Broad nasal tip, transverse crease

Examine• Ears (secondary to NPX obstruction)• Septum, nasal cavity (otoscope)• OPX – tonsil size• Palate shape and length• Nasopharynx if possible• Voice – hyper/hyponasality
Investigations• Sinus X-rays Lateral – to assess adenoids Waters – to assess antra• CT Scan Coronal mini-series CT Scan For sinus disease, ostial disease• Polysomnography If OSA noted• Allergy Tests Skin tests, RAST testing
Management
Remember to consider nose, adenoid region and tonsil area as a whole – the airway obstruction occurs in series, not in parallel.  Many obstructed children will need adenoidectomy and tonsillectomy to affect a cure. In fact the upper and lower respiratory tract are ‘ONE AIRWAY’.
ADENOIDECTOMY
• Snores loudly, obstructive sleep disorder• Avoid with short or cleft palate• Rule out submucous cleft palate, i.e. Bifid uvula Thin median raphe Bony notch in hard palate• Can be done and home in 6 hours (same day care unit)• Rhinolalia (hypernasality)
ALLERGIC RHINITIS
• 40-80% have parental atopy• Seasonal (hayfever) or perennial (PAR)• PAR – dry, stuffy, blocked nose – sniffer• Inhalant or food allergy as cause• RAST testing – for inhalant antigen• Avoidance – provocation tests for foods Management and Prevention• Avoidance of allergen e.g. HDM• Desensitization – ID/Sublingual• Nasal steroid sprays eg Mometasone
Medical Treatment• Antihistamines – sedating/non-sedating• Nasal steroid sprays NOTE: Cortisone absorption effect on growth in children Beclomethasone 40% absorbed Rhinocort 8% absorbed Nasonex 0.1% absorbed
Surgical Treatment – NOT A CURE!• Cautery of turbinates/cryosurgery• Trimming of turbinates
Note: Cautery of turbinates may be combined with tonsillectomy and adenoidectomy.  Remember allergy may manifest as eczema, asthma and hayfever and also tonsillar and adenoid hypertrophy, otitis media with effusion and sinusitis. OBSTRUCTIVE SLEEP DISORDER
A spectrum of symptoms ranging from mild snoring through to apnoea with cardiac failure.  In general, if a child has apnoea lasting more than 10 seconds or seven apnoeic episodes per hour then they have significant obstructive sleep disorder (Especially if they desaturate to less than 90%)
Features Snoring 100% Chronic mouth breathing  50% OSA – apnoea  25% Hypersomnolence  20% Nocturnal sweating  20% Restless sleep  20%+ Nightmares, waking  10% Sleepwalking  10% Enuresis    5% Growth problems    5% Meat dysphagia    5%+           Neuro-cognitive, behavioural symptoms.Diagnosis1. History2. Examinations – nose/adenoids/tonsils3. Investigations Sinus views Modified sleep study Polysomnography
Management1. Medical Nasal steroid sprays CPAP (Down syndrome/Craniofacial abnormality)2. Surgical Ts + As + CIT Tracheostomy
It is essential for post-operative tonsillectomy and adenoidectomy patients with obstructive sleep disorder to have overnight pulse oximetry to avoid apnoea/hypoxic drive stimulus.  Great care to avoid oversedation with narcotics.
In Australia 0.7% of children have Ts/Ads  (0.5% for OSD) yet 10% of children snore and 3% have OSD/OSA—indicating significant under-diagnosis. PAEDIATRIC SINUSITIS
Factors• Air pollution, allergic rhinitis, URTI, day care attendance, reflux (new concept)
Definitions• Acute Sinusitis Persistent no longer than 6 – 8 weeks Resolves with medical therapy with no significant mucosal damage• Chronic SinusitisPersistent disease not alleviated by medical therapy alone.  12 weeks of persistent symptoms or six episodes per year of acute sinusitis
Pathogens Streptococcus pneumoniae 40% Haemophilus influenzae 35% Anaerobes   7% Streptococcus species   7%
Diagnosis1. Acute viral URTI – commonly the precipitating event (“the cold that lasts a month, Doctor”)2. The most common cause is bacterial infection secondary to obstruction3. Plain sinus x-rays may be misleading4. With persistent symptoms – CT scan (especially modified coronal CT) and endoscopy.  The key to sinusitis is blocked ostiomeatal complex.5. In WA, allergic rhinitis is often implicated
Symptoms• Nasal obstruction and congestion• Pressure with pain• Thick nasal discharge• Toothache• Fever• Cough or irritability
Maxillary Cheek pain, frontal headache, tooth acheEthmoid Inner canthal pain/pressure, periorbital headacheFrontal Frontal headache, tenderness over frontal sinusSphenoid Deep seated headache, PUO Treatment of Acute Sinusitis1. Most patients respond to appropriate decongestant and antibiotics in adequate dosage for sufficient duration2. Antibiotic resistance – suggest Cefaclor, ‘Augmentin’ or Septrin for 10 – 14 days3. Antihistamines not helpful, inhalations often helpful4. Rule out reflux as cause5. Topical decongestants/saline nasal spray
Systemic or Predisposing Factors for Sinusitis• Cystic fibrosis• Ciliary dyskinesia• Young’s syndrome• Serious immune deficiency• AIDS (30% have sinusitis)• Anatomic abnormalities• Environmental and genetic factors• Hyper-reactive respiratory lining, especially in patients with asthma
Management Goals for Sinusitis• Control infection• Reduce tissue oedema• Facilitate drainage• Maintain patency of sinus ostia• Break pathological cycle leading to chronic sinusitis
Surgical Management• Aim to establish ventilation for sinuses especially at keystone area of ostiomeatal complex• Antral washout, intranasal antrostomy, functional endoscopic sinus surgery Epistaxis in Children• Uncommon under the age of 2 years• Related to hot dry summers, heating in winter• Little’s area on septum commonest site of bleeding• 80% can be prevented by Vaseline or Nozoil b.d. in nares• Nose picking, rubbing (allergy), trauma as causes• Foreign bodies may present as epistaxis• Neoplasms – juvenile Angiofibroma (NPX) – rare tumour in adolescent males
• CauterisationUse Cophenylcaine either on cotton wool or directly by spray.  Then use AgNO3 cautery stick.  If 3 cauteries performed – elective surgery with electro-surgery. Packing uncommon.
Foreign bodies in nose• Suspect if foul smelling unilateral discharge• Adequate light decongestion/anaesthesia and instrumentation for success• Cophenylcaine on cotton wool pledget – into nose and then remove both cotton wool and foreign body• Look for secondary sinusitis if long standing
Fractured nose in children• Uncommon to fracture nasal bones in infants – usually septal cartilage/soft tissue injuries• Rule out septal haematoma (like prow of boat)• Often wait 7 days for swelling to subside, then review• Radiography not always necessary except for medico-legal reasons• Reduction of nasal fracture at 7 – 14 days optimally      .Ensure an ENT surgeon sees the child by 10-14 days after injury before the    fracture sets TONSILLITIS AND TONSILLECTOMY INDICATIONS
Tonsillitis• Acute, viral or bacterial• Streptococcus (Group A beta haemolytic)• Penicillin treatment of choice 7 – 10 days• If Lactamase producing bacteria (non-responsive to Penicillin) consider Augmentin/Cefaclor• If  6 attacks of bacterial tonsillitis in 12 months in child over 4 years with 2 weeks off preschool/school – consider tonsillectomy• “Chronic tonsillitis” – other older children with cryptic debris coughed up, frequent sore throat and halitosis
Peritonsillar Abscess (Quinsy)• Abscess may point or be ‘subacute’• Trismus drooling, pain, fever• Two management options1. IV antibiotics, subsequent tonsillectomy2. Quinsy or immediate tonsillectomy• The latter is favoured as one hospitalisation and decreased pain and morbidity• Recurrence rate if not operated – 20%
Indications for Tonsillectomy in the 2010’s• Obstructive Sleep DisorderUpper airway obstruction secondary to tonsillar or tonsillar and adenoid hypertrophyCommonest indication for tonsillectomy in paediatric hospitals worldwide• Severe recurrent bacterial tonsillitis• Quinsy – 1 – 2 episodes• Biopsy purposes – to rule out e.g. lymphoma
Tonsillectomy Procedure• General intubation anaesthesia and protection of airway• Often combined with adenoidectomy• Sharp/blunt dissection to remove tonsils.Coblation/electro-surgery may cause higher incidence of 2ndry haemorrhage/• Meticulous attention to haemostasis• Post-operative overnight pulse oximetry mandatory for children with OSD• Post-operative antibiotics for 7 days reduce pain, incidence of secondary haemorrhage• Avoid ASA, NSAIDS     .    Tonsillectomy Complications• Bleedingprimary or reactivesecondary – to 14 days post-operative• Seen in 1 in 50 procedures• Secondary bleeding if tonsil bed infection or early separation of slough• Secondary healing often controlled by admission, IV drip, antibiotics, removal of clot/AgNO3• Late complication of scarring or velopharyngeal incompetence (VPI) causing rhinolalia or hypernasality (cleft palate type speech)
Tonsillar Hypertrophy Revisited (See OSD)• All large tonsils are not always associated with OSD• Relatively small tonsils (Grade II) may be floppy or in patients with lax tissues e.g. Down syndrome may be obstructive
Tonsil Size
Grade 1 Grade 2 Grade 3 Grade 4

Increasing Severity of Obstruction Symptoms• Chronic mouth breathing and snoring• Increased URTI, oral-dental ill health• Orthodontic abnormalities, altered taste, smell• Restless sleepers, 2 – 3 pillow, head arched• Waking for drinks, sleep walking, enuresis• Thin, poor eaters, meat dysphagia• Chronic nocturnal cough (micro aspiration)• Decreased stamina for day time activities• Nocturnal sweating, morning headaches (CO2 retention)• Hypoxia, apnoea, pulmonary hypertension• Right heart failure, cardio-respiratory arrest PAEDIATRIC LARYNGOLOGY
Stridor Symptom not a diagnosis Inspiratory superior part of upper airway obstruction Expiratory obstruction distal to vocal cords Biphasic subglottic (or glottic) obstruction
Age relationship• At birth – choanal atresia/congenital subglottic stenosis• Several weeks after birth – laryngomalacia Subglottic haemangioma (Inflammatory disorders rare in neonates)• 1 – 6 years – inflammatory• croup, epiglottitis• 8 – 12 years – bacterial tracheitis
Acute stridor• Inflammation, trauma, FB
Chronic Stridor• Fixed lesion, e.g. VC palsy/subglottic stenosis
Increasing Severity• Papilloma, subglottic haemangioma
Examination• Auscultation of neck• Position e.g. leaning forward in epiglottitis• Colour• Respiratory rate, cardiac rate• Retractions
Care with examination of mouth, pharynx (especially epiglottis)Flexible fibre-optic scope is useful Radiology• AP/Lateral neck and chest• (inspiratory and expiratory if suspect a foreign body)• Fluoroscopy, barium swallow• CT, MRI
Endoscopy Team approach – with anaesthetists

Differentiating Features of Three Paediatric Inflammatory Diseases
DISEASEFEATURE CROUP BACTERIAL TRACHEITIS EPIGLOTTITISAGE <2 years Any age 3-4 yearsORGANISM RSV Parainfluenza Staph. aureus H. influenzaeSITE OF INVOLVEMENT Subglottis Trachea SupraglottisSTRIDOR Biphasic Expiratory InspiratoryVOICE Barking cough Hoarseness Unaffected (Hot potato)POSITION Not characteristic Not characteristic Erect, chin jutting forwardSWALLOWING Unaffected Unaffected DroolingTREATMENT HumidityAdrenalin?Steroids BronchoscopySuctioningIV antibioticsICU IntubationIV antibioticsHumidityICU
Note: With the increasing use of Hib vaccination, epiglottitis is becoming less common CONGENITAL ABNORMALITES OF THE LARYNX
Laryngomalacia• Common laryngeal anomaly• Intermittent low-pitched crowing inspiratory stridor• Abnormal flaccidity or tightness of supraglottic structures• Often worse when supine• May cause respiratory distress, feeding difficulties and FTT, associated with neurological condition• Tubular epiglottis, prominent arytenoids, short ary-epiglottic fold• Subside usually after 1 – 2 years• Occasionally laser surgery to AE fold in severe cases
Vocal Cord Paralysis Symptoms• Stridor 65%• Dyspnoea, dysphonia• Inhalation, respiratory distress 17%• Cyanosis 12%
Bilateral• CNS disease, birth trauma, Arnold-Chiari malformation• Most present by 6 weeks of life• Respiratory distress, normal cry• 50% will need intubation or tracheostomy
Unilateral• Idiopathic 35%, obstetric 24%• Cardiac surgery, neurologic, vascular• Left 72%, Right 28%• Weak cry, stridor on exertion
Diagnosis• Endoscopy of larynx• CT if CNS problem suspected
Management• Observation Unilateral, treat cause (e.g. hydrocephalus) Bilateral – ETT/tracheostomy (50%) • Late Arytenoidectomy for bilateral VC palsy Subglottic Stenosis• Congenital or acquired• Stridor, respiratory distress, recurrent LTB• Circumferential narrowing at cricoid level• Post extubation (cause) and failure extubate• Bronchoscopy, radiology• Occasionally need cricoid split operation, ORLaryngotracheal reconstruction
Subglottic Haemangioma• Smooth compressible mass in subglottis• 50% associated cutaneous lesions• Present as increasing stridor, or a persistent laryngotracheobronchitis• Diagnosis X-ray, Bronchoscopy (no biopsy)• Usually involute in 1 – 4 years• Observe/tracheostomy, CO2 Laser and Interferon
OTHER LARYNGEAL CONDITIONS
Recurrent Respiratory Papillomatosis (RRP)• Low incidence, on the increase HPV 6, HPV 11• Condyloma-like papilloma on vocal cords, larynx• Increasing hoarseness, stridor (avoid tracheostomy)• Frequent endoscopies, CO2 laser, interferon• Rarely seed to tracheo-bronchial tree
Vocal Cord Nodes• Vocal abuse, cough• Often resolve in teenage years• Occasionally surgical removal if over the age of 10 – 12 years and failed speech therapy for 6 months CHRONIC COUGH IN CHILDREN
Holinger “Symptom not a diagnosis” Jackson “Cough is the watchdog of the airway” “Don’t drug the watchdog!”
Diagnostic Protocol1. Histology• Immunization, allergies, asthma, sinusitis, URTI• Passive smoking historya) Dry Barking (Brassy) Cough – Infections• Subglottic stenosis• Aberrant innominate• Tracheomalaciab) Wet Productive Cough• Specific infection LRT or chronic bronchitisc) Cough with associated throat clearing• PND, reflux
2. Physical Examination
3. Radiology• Chest x-ray, sinus views (?mini CT)• Barium swallow
4. Blood Tests• CBC. Diff, Pertussis Ab titres• IgGs,  1 – Antitrypsin
5. Skin Testing• Allergy, PPD, Sweat Chloride
Endoscopy• If cough greater than 6 – 8 weeks• History of foreign body/obstructive lesion• Most valuable diagnostic tool (followed by sinus x-rays) Results Birth to 18 months• Cough variant asthma• Aberrant innominate artery• Reflux (most effective studies – endoscopy/Ba Ex/Rx asthma)
1 1/2 years to 6 years• Sinusitis• Asthma• Subglottic stenosis (most effective studies – sinus x-rays, endoscopy, Rx asthma)
6 to 16 years• Cough variant asthma• Psychogenic(most effective studies – PFT, endoscopy, Rx asthma)
Overall1. Cough variant asthma 32%2. Sinusitis 23%3. Reflux 15%4. Aberrant innominate artery 12% FOREIGN BODIES
Sixth most common cause of accidental death
Chest• Peanuts 50%, carrot and apple• 20% of children with a foreign body not seen by GP for 1 month
High index of suspicion• Choking episode, wheeze• Recurrent or migrating pneumonia• Unexplained persistent respiratory symptoms
Investigations• Insp/Exp chest films• Fluoroscopy Air trapping Mediastinal shift Obstructive emphysema
Oesophagus• May cause fatal airway obstruction by impinging on airway• Commonly – coins, plastic toys• C6 level, stricture, aortic arch• Careful removal CORROSIVE INJURY OF THE OESOPHAGUS
Scenarios1. Accidental ingestion by toddlers2. Older children – mislabelled containers3. Adolescents – suicide4. Child abuse
Agents Corrosive, e.g. caustic soda, dishwashing liquid (pH 11) Acids, e.g. HCl, H2SO4Non-phosphate detergent powders – airway problems > oesophageal problems
Management1. Emergency• H2O/milk• No acid to neutralise• No vomiting
2. Oesophagoscopy – first 48 hours• Oesophageal burns in absence of oral burns• To level first circumferential burns• Nasogastric tube• Antibiotics, steroids• Re-oesophagoscope at 10 – 14 days
3. Sequelae• May need dilatations• Occasionally oesophageal replacement• Increased risk of oesophageal malignancy 40 years later

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