ENT Flashcards

1
Q

What is stridor?

A

High pitched noise resulting from turbulent airflow through a partially obstructed upper airway

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2
Q

What is an inspiratory stridor indicative of?

A

Obstruction is glottic (at level of vocal cords) or supraglottic

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3
Q

What type of obstruction is an expiratory stridor indicative of?

A

Tracheal obstruction

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4
Q

What type of obstruction is a biphasic stridor suggestive off?

A

Subglottic obstruction

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5
Q

How might an airway emergency present?

A

Stridor
Respiratory arrest
Hoarse voice (tumour or the larynx)
Pain and discomfort
Drooling (epiglotisits)

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6
Q

What might cause paediatric stridor?

A

CONGENITAL:
Laryngomalacia
Vocal cord paralysis
Subglottic stenosis
AQUIRED:
Laryngotracheobronchitis / tracheobronchitis (croup)
Epiglottitis
Retropharyngeal abcess
Foreign bodies
Iatrogenic

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7
Q

What is laryngomalacia

A

Congenital softening of the tissues in the supraglottic portion of the larynx. The epiglottis is malformed and floppy causing the tissues to fall over the open airway and partially block it.

Cause of stridor (inspiritory)

Slow feeding, failure to gain weight, noisy breathing

Tracheal tug
Subcostal recession

Flexible office laryngoscopy can be offered to diagnose

Management

Watchful waiting: resolution by 18-24 months
Anti reflux meds (H2 blockers, PPIs)

Microlaryngobronchoscopy, supraglottoplasty

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8
Q

What is Subglottic stenosis

A

May be congenital of acquired from repeated intubation
Cricoid cartilage (only COMPLETE ring in the airway) is damaged, causing stenosis and scarring which can result in a stridor

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9
Q

What is laryngotracheobronchitis known as commonly

A

Croup

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10
Q

What organism causes epiglotititis

A

Haemophilus influenzae

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11
Q

Epiglottitis is a life threatening emergency, which group of patients are typically effected?

A

2 to 6 year olds

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12
Q

What triad of symptoms does epiglotitis typically present with?

A

Drooling
Dysphasia
Respiratory distress
(Stridor
Pyrexia)

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13
Q

How might a child with epiglotitis hold themselves

A

Neck extended, sniffing to reduce air hunger

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14
Q

How might you differentiate epiglotitis from croup?

A

Child cannot breathe unless sitting up
Worsening “croup”
Child cannot swallow saliva and drools

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15
Q

An X ray should never be taken in suspected Epiglotitis as the child should not be upset and, but what would be seen if one was taken?

A

Significant swelling of the epiglotitis

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16
Q

How might a retropharnageal abcess present?

A

Typically a young child
Odynophagia (painful swallow)/ dysphagia
Neck held ridgid and upright, pt reluctant to move (toriciollis)
Pyrexia and systemic unwell
Drooling
Widening of the retropharyngeal space of lateral X ray

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17
Q

How is retropharyngeal abcess managed?

A

Secure airway (intubation)
Drain abcess surgically (I+D)
IV Abx

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18
Q

What level on CT would the hyoid bone be seen?

A

C3

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19
Q

What is torticollis?

A

Twisting of the neck that causes the head to rotate and tile at an odd angle (also known as wryneck)

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20
Q

Adult airway emergencies?

A

Infection: Paraphyrangeal, peritonsillar (quinsy) abcess, Ludwig’s angina (submental abcess, dental aetiology) epiglotitits/supraglottic
Tumours
Foreign bodies
Allergic reactions, angioodema
Trauma (iatrogenic)
Vocal cord paralysis

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21
Q

How might a peritonsillar abscess appear?

A

Complete or partial oropharynx obstruction
Uvula may not be visible
Buldging around soft pallet

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22
Q

What is Ludwig’s Angina

A

Submandibular space infection
Usually odontogenic (dental problems)

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23
Q

How might you manage laryngeal cancers presenting with an acute airway problem

A

Tracheostomy, possibly under local anesthesia (intubation not possible)

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24
Q

What is an important risk of a tracheostomy in a patient with laryngeal cancer, and how can it be avoided?

A

Potential seeding
Ideally intubate patient and debulk tumour

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25
What is the most common type of larngeal tumour?
SCC
26
What might be seen on x ray of a pt with a forgiven body airway obstruction?
The forgiven body Surgical emphysema (air seen in soft tissue)
27
A ruptured AAA cause a posterior pharyngeal wall haematoma leading to airway obstruction, what will be seen on X ray?
Prevertabral space increased in size
28
How large is the prevertabral space usually?
5-8mm
29
Diagnosis and initial management of airway obstruction?
ABC Secure airway first Rapid history and careful examination Give O2/Heliox Pharmacological management: adrenaline steroid antihistamine abx Nasopharyngeal/orophrangeal airway Intubation Cricothyroidotomy (needle/surgical) Surgical tracheostomy
30
What is heliox and why is it used?
Helium and oxygen mixture Helium decreases viscosity of oxygen so it can get to the lungs easier
31
What pharmacological management might be implemented in an airway emergency?
Oxygen or heliox Adrenaline Steroids Antihistamines Antibiotic is
32
What is a crycothyroidotomy
Space between crycoid cartilage and thyroid cartilage incised or needle inserted during airway emergency
33
What are the potential indications for a tracheostomy?
Airway obstruction To protect tracheobronchial tree (e.g. patients who can’t protect their own airway following a stroke) Ventilatory insufficiency (e.g. advanced lung disease) Airway risk during oropharyngeal and laryngeal surgery
34
Where are the thyroid gland and cartilage in relation to the trachea?
Thyroid gland anterior to trachea Thyroid cartilage superior to the cricoid cartilage
35
Where is a tracheostomy inserted?
Window created between the 2nd and 4th tracheal rings, which is where the tracheostomy is inserted
36
How is the airway protected when swallowing?
Larynx moves up Epiglottis comes down and closes off airway Vocal cords close to protect the airway
37
Where does the larynx start and end?
Epiglottis to the cricoid cartilage
38
What is the nervous inner action of the larynx?
Vagus nerve Recurrent, internal and external laryngeal nerves RLN: Motor with exception of the cricothyroid muscle ILN: Sensory ELN: Motor to cricothyroid muscle
39
What is the difference between acute otitis media and glue ear?
Acute otitis media: Bacterial infection of the MIDDLE EAR Glue ear is otitis media with effusion - not infective but can become infected leading to acute otitis media - commmon cause of childhood deafness
40
What is a bacterial infection of the middle ear called?
Acute otitis media
41
How might acute otitis media present?
preceding URTI, unwell Fever Otalgia (or signs of - tugging at ear) Hearing loss Later otorrhoea (if TM ruptures) - pain will settled once this happens due to resolution of increased pressure in the tympanic cavity
42
What causes otalgia in acute otitis media?
Increased pressure in the tympanic cavity Accumulation of pus within the middle ear cavity (cleft) but eardrum remains intact (pain improves if perforated)
43
What might be seen on otoscopy in acute otitis media?
Erythamatous and buldging tympanic membrane If the fluid pressure has perforated the TM a small tear with purulent discharge in the auditory canal may be visible
44
What type of hearing loss does otitis media with effusion cause?
Conductive
45
Complications of acute otitis media?
Acute mastoiditis (osteomyelitis) Intracranial infections: cerebellar abcess, extradural abcess, meningitis, temporal lobe abcess Thrombosis of the sigmoid sinuses (vein travels in close proximity to the mastoid air cells) Bacterial Labyrinthitis Facial nerve palsy - facial paralysis Petroys apicitis Gradanigo's sybdrome Citelli abscess Temp. hearing loss OME
46
How does acute mastoiditis present and how is it managed
Children present unwell Protrusion of the pinna Loss of posterior sulcus Mastoiditis may cause posturicular swelling (abcess formation) Surgical management and IV abx
47
How is acute otitis media managed?
Paracetomol to control fever - this is the only treatment required usually Sometimes abx required to prevent complications or if complications have occured - (Amoxicillin for 5-7 days first-line, Clarithromycin (in pencillin allergy), Erythromycin (in pregnant women allergic to penicillin)) In severe or recurrent cases myringotomy to insert grommet to release pus
48
How to examine a child with forgiven body’s inserted in the nose?
EXAMINE BOTH SIDES Use auriscope
49
What is the most common inhaled foreign body and why can it cause inflammation?
Peanuts, peanut oil invokes inflammation
50
Where are inhaled forigen bodies typically found and why?
Right main bronchus Wider and has more direct extension of trachea
51
When might nasal trauma be an emergency?
Septal haematoma Haematoma becoming in an abcess is not drained/vascular necrosis of cartilage to leading to saddle nose deformity/ infection pain and fever
52
How do you treat a septal haematoma?
Surgical drainage +/- abx
53
What is periobital cellulitis?
URTI leads to infection from anterior ethmoidal space, spreading into the orbit. Lateral deviation of medial recuts Can cause proptosis, loss of colour vision
54
How is periorbital cellulitis managed?
Just cellulitis then IV abx sufficient Involve ophthalmology, assess colour vision (pressure on optic nerve), if compromised incision and drainage in theatre
55
Symptoms of tonsillitis?
Sore throat Pyrexia Neck lymphadenopathy
56
Why must tonsillitis be differentiated from glandular fever?
Glandular fever - hepato/splenomegaly, no contact sports for six weeks, and do not give amampacillin can cause rash
57
Common complication of tonsillitis?
Quinsy - peritonsillar abcess: Buldging of the soft pallette Uvula deviation
58
How is a peritonsillar abcess managed?
Drainage under local anaesthetic
59
Management of epiglottitis
Keep child calm as the airway may close if they cry (laryngospasam) Give wafting oxygen Intubation in theatre to protect airway Emergency tracheotomy in rare cases IVabx broad spectrum
60
Neck abscess is very common in children, how might it present?
Typically follows URTI, Cervical lymphadenitis Usually bacterial - painful, spinning temp, neutrophils raised Atypical mycobacteria - purple discolouration - painless, bloods may be normal or lymphocytic picture Rarely, TB is cause
61
How is neck abscess managed?
Incision and drainage Pus to microbiology
62
How does an abscess appear on CT
Ring enhancement
63
Which types of neck abscess are considered surgical emergencies?
Paraphyrangeal abscess Retropharyngeal abscess
64
Causes of neck swelling?
Abscess: Retropharyngeal, parapharyngeal Cystic hygroma (lymphangioma) problems Cervical teratoma
65
What is a cystic hygroma and how is it managed
Also known as lymphangioma Benign congenital neck swelling Respiratory and feeding problems Soft, compressible Managed by excision once airway secured
66
What is a cervical teratoma and how is it managed?
Benign congenital neck swelling Firm consistency Extreme cases require tracheostomy
67
Blood supply to lateral nasal wall
Branches of the internal carotid artery : Anterior and posterior ethmoidal arteries (branches of the opthalmic artery Branches of the external carotid artery: Sphenopalatine Descending palatine Greater and lesser palatine
68
Blood supply to nasal septum
Branches of the internal carotid artery: Anterior and posterior ethmoidal Branches of the external carotid artery: Septal branches of Sphenopalatine artery Septal branch of the superior labial artery Branch of greater palatine
69
From which area of the nose do most bleeds arise from?
Little’s area / Kiesselbach’s plexus - in the septum Area of nasal mucosa at the front of nasal cavity This is where all the branches of ICA and ECA supplying the septum meet When mucosa is disrupted and blood vessels are exposed they become prone to bleeding
70
Local aetiology of nose bleeds.
Idiopathic Traumatic (fracture foreign body picking) Inflammatory (rhinitis) Neoplastic Environmental Iatrogenic (surgery, steroid nasal spray)
71
General causes of nosebleeds?
Anticoagulants Coagulapathies Hereditary haemorrhaged telangiectasia (abnormality of the blood vessel wall) HTN
72
Management of nose bleeds?
Pinch cartilaginous part of nose (soft lower portion) Topical adrenaline +/- cautery with silver nitrate sticks Anterior nasal lacking (merocel tampon, BIPP) Posterior nasal pack (Foley catheter, Brighton balloon) Surgical intervention
73
What can be used for anterior nasal packing
Merocel tampon BIPP
74
What is used for posterior nasal packing?
Brighton balloon
75
How is nasal cautery undertaken?
Anterior bleed visualised with a thudiculum speculum Visualise bleeding point Local anaesthetic spray Control with adrenaline And or Cauterise bleeding point and 5mm radius circle around the bleed
76
How should a nasal pack be inserted?
Horizontally, along floor of nose, to avoid damage to skull base
77
What kind of surgical intervention might be involved in epistaxis management when other methods have failed?
Rigid nasendoscope with electrocautery Sphenopalatine artery ligation Anterior ethmoid artery ligation External carotid artery ligation Embolization of vessels under radiographic control
78
Basic pathophysiology of otitis media?
The Eustation tube (connecting the middle ear to the back of the throat) becomes blocked and causes middle ear secretions to build up in the middle ear space. .Build up of fluid causes loss of hearing in that ear May result in infection (acute otitis media) Otitis media with effusion (glue ear): ET tube dysfunction leading to presence of fluid in the middle ear with intact TM - non infective but can lead to infection Unlike the external ear the epithelium lining the middle ear is respiratory epithelium or pseudostratified collumnar epithelium - regarded as a continutation of the upper respiratory tract and hence susceptible to similar pathogens - streptococcus pneumoniae, haemophillus influenzae, moraxella species (AOM)
79
Investigations and management of glue ear/otitis media with effusion?
Referral to audiometry to establish extent of the hearing loss - pure tone audiogram, tympanogram Conservative management unless persists past 3 months or child has comorbidities (Down's syndrome, clef palate) Surgical: Grommet insertion (ventillation tubes) +/- adenoidectomy Hearing aids
80
What is a grommet?
Device inserted by ENT surgeon. This allows fluid from the middle ear to drain through the tympanic membrane to the ear canal. Usually grommets are inserted under general anaesthetic as a day case procedure.
81
How long do grommets typically last?
Grommets usually fall out within a year, and only 1 in 3 patients require further grommets to be inserted for persistent glue ear.
82
What would be seen on otoscopy and examination in glue ear?
On examination, the tympanic membrane will appear dull (Fig. 2) and the light reflex will be lost, indicating fluid in the middle ear. Air fluid level There may also be a bubble seen behind the TM. The external ear will be normal.
83
Main presenting complaint of glue ear?
Hearing loss - conductive May be sensation of pressure in the ear accompanied by popping or cracking noises Disequilibrium and vertigo (rare)
84
Why are children more likely to suffer from otitis media with effusion?
of chronic inflammatory changes and Eustachian tube dysfunction. The anatomy of the Eustachian tube in younger children is immature, typically short, straight, and wide (only becoming more oblique as the child develops), therefore infection is more likely.
85
Why should any new case of unilateral OME in an adult should be investigated as a ‘red flag’ for a malignant underlying cause?
Adults should have mature anatomy of the ET tube The condition is less common in adults, however will occur if there is any blockage of the Eustachian tube, either from infective causes or from occlusive masses
86
Main risk factors for OME/glue ear?
Bottle fed Paternal smoking Atopy (e.g eczema, asthma) Genetic disorders Mucociliary disorders, such as Cystic Fibrosis or Primary Ciliary Dyskinesia Craniofacial disorders, such as Downs Syndrome
87
How might glue ear be noticed in young children?
In young children this may be noticed as difficulty with attention at school or poor speech and language development
88
How should otitis media with effusion be investigated?
Clinical diagnosis Both pure tone audiometry and tympanometry are nearly always performed in such cases, which will reveal a conductive hearing loss and reduced membrane compliance (a type B tracing) respectively. In adults, a full ENT examination should be performed, including flexible nasoendoscopy (to exclude a post-nasal space mass).
89
Who are recomeded for grommet insertion to manage OME?
> 3 months of bilateral OME and hearing level in better ear < 25-30dBHL
90
Any child with persistent disease and multiple grommet insertion should be considered for what?
Potential adenoidectomy
91
Pathophysiology of acute otitis media?
Bacterial infection of the middle ear results from nasopharyngeal organisms migrating via the eustachian tube. The anatomy of the eustachian tube in younger children is immature, typically being short, straight, wide (only becoming more oblique as the child grows), meaning infection is more likely. Common causative bacteria include S. pneumoniae (most common), H. influenza, M. catarrhalis, and S. pyogenes, all common upper respiratory tract microbiota. Common viral pathogens are respiratory syncytial virus (RSV) and rhinovirus.
92
Why do clefte pallete and Down's Syndrome increase risk of otitis media?
Children with cleft palate, or with genetic conditions such as Down's syndrome, may be more likely to get glue ear as they often have smaller eustachian tubes that don’t function well.
93
RIsk factors of acute otitis media?
Risk factors for AOM include age (peak age 6-15 months), gender (more common in boys), passive (parenteral) smoking, bottle feeding, and craniofacial abnormalities
94
When might recurrent acute otitis media be more common?
Recurrent AOM is seen more commonly with the use of pacifiers, who are typically fed supine, or their first episode of AOM occurred <6months. AOM is most common in the winter season.
95
What should be further examined in a patient with suspected acute otitis media, supported by otoscopy?
It is important to test and document the function of the facial nerve (due to its anatomical course through the middle ear). Examination should also include checking for any intracranial complications, cervical lymphadenopathy, and signs of infection in the throat and oral cavity.
96
When should oral antibiotics be considered to treat acute otitis media?
1. Systemically unwell children not requiring admission 2. Known risk factors for complications, such as congenital heart disease or immunosuppression 3. Unwell for 4 days or more without improvement, with clinical features consistent with acute otitis media 4. Discharge from the ear (ensure swabs are taken prior to commencing antibiotic therapy) 5. Children younger than 2 years with bilateral infections 6. Systemically unwell adult, provided not septic and with no signs of complications
97
When should inpatient admission be considered for otitis media?
All children under 3 months with a temperature >38c, or aged 3-6 months with a temperature >39c, for further assessment. Also, consider admission for those with evidence of an AOM complication or the systemically unwell child. Patients with a cochlear implant will need to be seen by a specialist and may require inpatient treatment.
98
What make mastoiditis concerning in relation to AOM?
The middle ear and mastoid are one cavity, and as such, there will nearly always be a degree of mastoiditis with AOM. However, if the inflammation within the air cells progresses to necrosis and subperiosteal abscess, this is of significant concern.
99
How does mastoiditis present?
It presents clinically as a boggy, erythematous swelling behind the ear, which if left untreated progressing to pushing the pinna forward
100
How is mastoiditis managed?
Any suspected cases should be admitted for IV antibiotics and investigated further via CT head if no improvement is seen after 24 hours of IV antibiotics. There is a higher risk of intracranial spread and meningitis, hence cases are often considered for mastoidectomy as definitive management if there is no improvement with IV antibiotics
101
What is considered the middle ear?
The middle ear is the space that sits between the tympanic membrane (eardrum) and the inner ear.
102
What oral antibioitics does NICE recommend for AOM if required?
Amoxicillin for 5-7 days first-line Clarithromycin (in pencillin allergy) Erythromycin (in pregnant women allergic to penicillin
103
What is conductive hearing loss?
Conductive hearing loss relates to a problem with sound travelling from the ENVIRONMENT TO INNER EAR. The sensory system may be working correctly, but the sound is not reaching it. Putting earplugs in your ears causes conductive hearing loss.
104
What is sensioneural hearing loss?
Problem with the sensory system or vestibulocochlear nerve in the inner ear
105
Basic structures of the ear (outside to in)
Pinna External auditiory canal Tympanic membrane ET Malleus, incus and stapes (small bones in the middle ear that connect the tympanic membrane) Semicircular canals (responsible for sensing head movement (vestibular system) Cochlea (converting vibration into nervous signal) Vestibulocochlear nerve (transmits nerve signals from the semicircular canals and chochlea to the brain)
106
What symptoms might be associated with hearing loss?
Tinnitus (ringing in the ears) Vertigo (the sensation that the room is spinning) Pain (may indicate infection) Discharge (may indicate an outer or middle ear infection) Neurological symptoms Sudden onset (less than 72hrs) requires a thorough assessment to establish the cause
107
Cognitive benefit of hearing aids?
Reduces risk of dementia (hearing loss increases) Improved speech and language development in children
108
What is the vestibulocular reflex and how can it be demonstarted?
Information about the position of the head is used to coordinate balance and the vestibulo-ocular reflex. The vestibulo-ocular reflex (also called the oculocephalic reflex) allows images on the retina to be stabilised when the head is turning by moving the eyes in the opposite direction. It can be demonstrated by holding one finger still at a comfortable distance in front of you and twisting your head from side to side whilst staying focused on the finger. Simple three neuron system: vestibular nerve to vestibular nuclei to ocular muscle nuceli to eye muscles The ability to remain focused upon and object as the head is turned rapidly from or towards the object and maintain balance Lateral semicircular canals engaged when head moved sideways (horizontal acceleration) action potentials increase in nerve on side the head turns, decreased input on the contra lateral side Eyes move to contra lateral side Gain: ratio of the lapse between one command in another The gain in this reflex is nearly 1
109
Most common non ENT causes of balance problems in the elderly?
Postural hypotension - drop of more than 20mm in systolic BP, loss of blood pressure control with age and polypharmacy OA
110
In which direction does nystagmus beat in a peripheral vestibular lesion?
In the opposite direction to the defect Eyes move wrong way as no input from the vestibular nerve when head is turned in direction of defect (loss is vestibulocular reflex)
111
Labyrinthitis vs vestibular neuritis
112
What is a vestibular migraine?
113
CT orientations?
Coronal Axial Saggital
114
CT windows?
Soft tissue windows - expansion of the greys pertaining soft tissue Bone windows - detail of the bone including density
115
How to differentiate between cause of nasal septum defect on CT?
Trauma - same size inferior terminal on both sides of CT Developmental - hypoplastic terminal and enlarged terminal on CT
116
What causes a nasal pseudohump?
Loss of cartilage (secondary to repeated trauma for example) Repaired with costal cartilage
117
What type of obstruction causes stertor?
Above the larynx e.g. large adenoids and tonsils, oropharngeal mass, etc Snoring - obstruction is above the larynx e.g. nose, tongue, younger base, back of nose
118
Why is a biphasic stridor more concerning than monophasic?
Obstruction is at level of the vocal cords or below Subglottic stenosis
119
What is rhinosinusitis?
Inflammation of the nose and paranasal sinuses characterised by two or more symptoms, one of which should be nasal blockage/discharge/congestion or nasal discharge - anterior or posterior +/-Facial pain or pressure +/-reduction/loss of smell
120
Classiification of rhinosinusitus?
Acute: resolution within 12 weeks VS chronic with and without nasal polyposis Allergic vs non allergic
121
History in rhinosinusitis
Nasal blockage/congestion and discharge Loss/reduction of smell Itchy runny eyes Permenant/intermittent Time of day Jobs/hobbies Pets- Cats - wash them with grooming glove and damp water!
122
Aetiology and pathogenesis of allergic rhinitis?
Type 1 hypersensitivity reaction to allergens Increased permeability of capillaries Mucosal infiltration of oesinophils and oedema
123
CRS management
Conservative - allergy avoidance Medical - nasal sprays, long course of macrolides (calithromycin, up to 12 weeks) Surgical management of sinus: septoplasty, turbinate surgery (SMD reduction of inferior turbinates) Nasal polypectomy Functional endoscopic sinus surgery (FESS)
124
Nasal cautery dos and don’ts
Use local anesthetic lignocaine with adrenaline on cotton wool Don’t simply spray Don’t allow silver nitrate to drop out the nose Don’t use silver nitrate for more than 20 seconds each side
125
Inner ear symptoms?
Hearing loss (sensioneural) Vertigo Tinnitus
126
Outer ear symptoms
Pain Discharge - scant serous Late hearing loss (conductive hearing loss)
127
Otology examination
Wash hands, intro Tenderness Which ear is better Inspect pinna, mastoid area, Otoscopy: external auditory canal, tympanic membrane Hearing test Cranial nerve VII, co-ordination and Romberg
128
Otological investigations?
Pure tone audiogram Tympanogram CT MRI
129
Rinne Test
Air conduction should be better than bone conduction and persiist) - POSITIVE TEST Begin by striking a 512 Hz tuning fork against your knee or elbow. Place the base against the patient’s mastoid process (for those who like to watch it on a video, check one out here) Allow it to stay there for 2-3 seconds to allow them to appreciate the intensity of the sound then promptly raise the fork off the mastoid process and place the vibrating tips about 1cm from their external auditory meatus Leave it there for a few seconds before taking the tuning fork away from their ear Ask the child whether the sound was louder at the beginning (when it was held against their mastoid) or whether it became louder (when it was held in front of their ear). If bone conduction is better than air conduction (negative test) indicates conductive hearing loss
130
Webers test
Should not localise Localises to affected ear in conductive hearing loss Localises to the unaffected ear in sensioneural hearing loss As in Rinne’s test, begin by striking the 512 Hz tuning fork against your knee or elbow Then, place the base of the fork in the midline, high on the patient’s forehead Ask whether they hear the sound in the midline or if the sound lateralises to either the affected or good ear.
131
What is Haematoma/Seroma of the Pinna and how is it managed?
Collection of blood between skin and cartillage, can lead to avascular necrosis and change in shape of the ear (cauliflour ear) Aspirate x2 in sterile conditions and apply compression bandage (review in 24 hours)
132
What is otitis externa?
Otitis externa is inflammation of the skin in the external ear canal, also known as swimmers ear.
133
What predisposes to otitis externa?
Water exposure (swimming) Removal of earwax (as it is protective) Ear canal trauma (ear plugs, cotton buds) Immunosupression
134
What causes inflammation in otitis externa?
Bacterial infection Fungal infection (e.g., aspergillus or candida) Eczema Seborrhoeic dermatitis Contact dermatitis
135
Main causative organisms of otitis externa?
Pseudomonas aeruginosa (gram-negative aerobic rod-shaped bacteria. It likes to grow in moist, oxygenated environments, also causes resp problems in CF pts) Staphylococcus aureus
136
Typical symptoms of otitis externa?
Ear pain (severe due to stretching of nerve fibres with inflammation) Discharge (serous) Itchiness Conductive hearing loss (if the ear becomes blocked) *Tympanic membrane is intact - if not points to OM
137
Signs seen in otitis externa?
Erythema and swelling in the ear canal Tenderness of the ear canal Pus or discharge in the ear canal Narrowing or ear canal TM may be red but often obstructed by debris (earwax, discharge) Lymphadenopathy (swollen lymph nodes) in the neck or around the ear
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What is seen on otoscopy in otitis externa?
The tympanic membrane may be obstructed by wax or discharge It may be red if the otitis externa extends to the tympanic membrane. If it is ruptured, the discharge in the ear canal might be from otitis media rather than otitis externa.
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Most common treatment for otitis externa?
Otomize spray (Neomycin/Dexamethasone/Acetic Acid)
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How is mild otitis externa managed?
Mild otitis externa may be treated with acetic acid 2% (available over the counter as EarCalm). Acetic acid has an antifungal and antibacterial effect. This can also be used prophylactically before and after swimming in patients that are prone to otitis externa. Topical toilet
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How to differientate between UMN and LMN facial palsy?
Forehead sparing - upper motor neuron
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How is moderate otitis externa managed?
Moderate otitis externa is usually treated with a topical antibiotic and steroid, for example: Neomycin, dexamethasone and acetic acid (e.g., Otomize spray) Neomycin and betamethasone Gentamicin and hydrocortisone Ciprofloxacin and dexamethasone
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When do aminoglycosides need to be used with caution to treat otits externa and what should be ruled out)
Typmanic membrane perforation or when it cannot be visualised Aminoglycosides (e.g., gentamicin and neomycin) are potentially ototoxic, rarely causing hearing loss if they get past the tympanic membrane. Therefore, it is essential to exclude a perforated tympanic membrane before using topical aminoglycosides in the ear. (This can be difficult if the patient has discharge, swelling or wax blocking the ear canal. Patients with a blocked ear canal may need to be seen by ENT to microsuction the debris from the canal and visualise the tympanic membrane. They will also require a referral if the canal is so blocked or swollen that topical treatments cannot reach the site of infection.)
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How should patients with severe otitis externa be managed (or if they are systemically unwell)?
Patients with severe or systemic symptoms may need oral antibiotics (e.g., flucloxacillin or clarithromycin) or discussion with ENT for admission and IV antibiotics.
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Why are peadatric airways difficult to manage?
Children have narrow airways and respond poorly to small changes in radius
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How do paediatric airways differ to adults?
Children have narrow airways and respond poorly to small changes in radius Obligate nasal breaters Larger toungues Laryncy is more cranial and anterior Subglottiss (cricoid) is the narrowest part of the airway (as opposed to the vocal cords in adults)
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How is fungal otitis externa managed?
clotrimazole ear drops
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Risk factors for mallignant otits externa?
Diabetes Immunosuppressant medications (e.g., chemotherapy) HIV
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What is malignant otitis externa?
Malignant otitis externa is a severe and potentially life-threatening form of otitis externa. The infection spreads to the bones surrounding the ear canal and skull. It progresses to osteomyelitis of the temporal bone of the skull. Malignant otitis externa is usually related to underlying risk factors for severe infection
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Presenation of mallignant otitis externa?
persistent headache, severe pain and fever History of chronic ear discharge despite topical treatment Deep seated ear pain Sometimes cranial nerve palsies (CNVII) - facial nerve
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Key finding that indicated mallignant otitis externa?
Granulation tissue at the junction between the bone and cartilage in the ear canal (about halfway along) is a key finding that indicates malignant otitis externa.
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Management of mallignant otitis externa?
Admission to hospital under the ENT team IV antibiotics Imaging (e.g., CT or MRI head) to assess the extent of the infection
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Potential complications of mallignant otitis externa?
Facial nerve damage and palsy Other cranial nerve involvement (e.g., glossopharyngeal, vagus or accessory nerves) Meningitis Intracranial thrombosis Death
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Management of otitis sleep apnoea in children?
Adenotonsillectomy Sleep study
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Classic presentation of Meneires Disease
recurrent attacks of vertigo, hearing loss, tinnitus, and the sensation of aural fullness.
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Management of chronic otitis externa?
Topical toilet and steroids Eczema
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Which hobby might predispose a patient to exostoses?
Cold water swimmers
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What is an osteoma?
Benign neoplasia of the bone, may be visable on otoscopy of external ear if involved
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What does a retracted typmanic membrane ocassionally progress to?
Cholesteatoma Although often no treatment required
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When might a TM perforation require repair and when might it not?
Dry: may need no treatment Recurrent infection: can be repaired
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What should be considered in the clinic presentation of a child with an airway complaint?
Onset Duration Exaccerbating/relieving factors Fever H/O coughing/choking (FB) Change in voice Swallowing/feeding Weight gain/loss History of prolonged intubation
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Management of severe croup?
Humidified O2 Nebulised adrenaline Systemic steroids Theatres to secure airway - intubation/tracheostomy if not responding
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What is recurrent respiratory papilomatosis and how is it managed?
Recurrent respiratory papillomatosis (RRP) is a disease in which benign (noncancerous) tumors called papillomas grow in the air passages leading from the nose and mouth into the lungs (respiratory tract). Tracheal tug, inspiratory stridor and subcostal recession may be present. Microlaryngobronchoscopy, surgical debridement
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What is vertigo?
A hallucination of movement of oneself or one's surroundings. The movement is often rotatory (e.g. pt may feel floor is tilting)
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Causes of vertigo?
On held tilt: Benign positional paroxysmal vertigo (BPPV) Hearing loss and tinnitus: Acute labyrinthitis No hearing loss nor tinnitus: Vestibular neuritis Unilateral hearing loss progressing to involve CN 5,6,9,10 and the ipsilateral cerebellum: Acoustic neuroma Sensioneural hearing loss, tinnitus, feeling of aural fullness: Meniere's disease Facial nerve palsy (+/- tinnitus, hearing loss): Ramsay Hunt syndrome Ototoxicity features: aminoglycoside abx, loop diuretics
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What AD disorder can predispose patients to recurrent epistaxis but not other kinds of bleeds?
Heriditary haemorrhagic telangiectasia (Osler Weber Rendu disease - telangiectasia on skin and mucous membranes, malformations within the nasal mucosa prone to bleeding)
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After how long can abx be considered for sinusitis?
After 5 days
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What can be used it otitis externa if the patient's ear canal is very swolen?
An ear wick may be used if the canal is very swollen, and treatment with ear drops or sprays will be difficult. An ear wick is made of sponge or gauze. They contain topical treatment for otitis externa (e.g., antibiotics and steroids). Wicks are inserted into the ear canal and left there for a period of time (e.g., 48 hours). As the swelling and inflammation settle, the ear wick can be removed, and treatment can continue with drops or sprays.
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What common condition is seen here?
Otitis externa - 'swimmers ear'
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Why are patients advised against cleaning their ears with cotton buds?
Possible trauma/perforation of TM Likely to further impact earwax Risk of ear canal trauma - OE
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Management of a TM perforation?
Watch + wait Perform otoscopy and audiogram Water precautions, keep dry, no more cleaning, avoid FB in ear Review pt after 4 weeks If no resolution after 6 months consider surgical intervention - myringoplasty
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What is the surgical management (if indicated) of TM perforation?
Myringoplasty
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TM perforation
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General management of otitis externa?
Topical eardrops empirically (e.g. Gentamycin) Swab any discharge in resistant cases Microsuction of pus/debris - allows eardrops to reach source of infection Wick (severe) Topical antifungals if fungal MOE- aggressive IVAbx therapy
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What is the sensory supply to the pinna?
Upper lateral surface - CNV3 - auriculotemporal nerve Lower lateral surface - C3 - greater auricular nerve Superior medial surface - C/2 C3 - less occiputal nerve Auricular branch of vagus - external auditory meatus
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Potential causes of ear trauma?
Laceration: simple primary closure of the skin with sututres after adequete cleaning is all that is required usually, it is important to ensure that any exposed cartillage is covered with skin - otherwise seek plastics Bites: significant risk of infection from skin commensals or oral commensals - require hx to ascertain likely organisms involved in potential infection - MUST LEAVE WOUND OPEN - treatment includes wound irrigation and topical abx Hematoma: Pinna haeamtoma causes disruption in blood supply to the cartillage which would normally obtain nutrients via diffusion from vessels in the overlying perichondrium (hence disruption can lead to avasucluar necrosis - risk of cauliflower ear) REQUIRES URGENT DRAINAGE AND DRESING TO PREVENT RE-ACCUMULATION Perforation of Tympanic membrane - direct or indirect trauma or otitis media - pain, possible conductive deafness Haemotympanum (blood in middle ear): May be associated with temporal bone fracture. Can be seen through tympanic membrane and is associated with conductive hearing loss. Conservative treament with follow up to ensure no residual hearing loss from damage to ossicles
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When might ear trauma lead to hearing loss - and what kind?
Tympanic membrane perforation and haemotypanum (blood in middle ear) - conductive hearing loss
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Haemotympanum
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Subtypes of otitis media?
Chronic: squamous (inactive/active) or mucosal Acute
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Oral antibiotics used (if indicated) in acute otits media?
Amoxicillin for 5-7 days first-line Clarithromycin (in pencillin allergy) Erythromycin (in pregnant women allergic to penicillin)
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What is meant by active chronic otitis media?
Squamous: Cholesteatoma Mucosal: Chronic discharge from the middle ear through a TM prtforation Associated with chronic ear discharge and often a conductive hearing loss , can also be associated with complications associated with spread of the disease within the temporal bone and intracranially?
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What is meant by inactive chronic otitis media?
Squamous: Retraction pocket which may develop into cholesteatoma Mucosal: TM perforation without active infection or discharge
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SQUAMOUS COM
Active: Cholesteatoma Inactive: Retraction pocket which may develop into active disease (cholesteatoma) Active develops when keratinized squamous cells are introduced to the middle ear from a retraction pocket or perforation
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MUCOSAL COM
Active: Perforated TM with discharge Inactive: Perforated TM without discharge or infection Thought to develop from an episode of AOM where after TM rupture there is failure to heal
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Management of COM (chronic otitis media)
Depends on type - active squamous disease (cholesteatoma) requires surgery to clear No cholesteatoma (often not known if this is the case when there is active ear discharge, initially assume there is not and opt for medical treatment and then surgicl if fails ) medical treatment: topical abx drops and an aural toilet
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Surgical management of COM?
When there is known cholesteatoma or ?cholesteatoma (chronically discharging ear that is not responding to medical therapy): COMPLPETE clearence of cholesteatoma Often requires surgery to the mastoid bone (mastoidectomy) as the cholesteatoma will often grow from the middle ear into the mastoid bone. If no cholesteatoma is found during surgery (mucosal COM) repair of perforation and ensure good ventillation of the middle ear and mastoid bone (no need to remove every last trace of disease as in cholesteatoma)
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What are the potential complications of mastoid surgery?
Facial nerve palsy Altered taste from damage to chorda typani CSF leak Tinnitus Vertigo Compete loss of hearing in the operated ear
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Why might a patient complain of altered taste following mastoid surgery?
Accidental damage to the chorda typani
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Acute otitis medial - buldging red tympanic membrane
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What is this called and what is it?
A cholesteatoma (an abnormal collection of skin cells in the middle ear) They're rare but, if left untreated, they can damage the delicate structures inside the ear ear that are essential for hearing and balance.
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What is seen on normal otoscopy
“Pearly-grey”, translucent and slightly shiny. Can visualise the pars tensa, pars flacida, cone of light and lateral process of maleoulus
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Name the four key structures
Cone of light/light reflex Pars flacida Pars tensa Lateral process of malleolus
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Normal TM Pearly grey, translucent, slightly shiny Not budlging Light reflex present Able visualise the malleus through the membrane
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Cholesteatoma pathophysiology?
Squamous epithelial cells originate from the outer surface of the tympanic membrane Negative pressure in the middle ear, caused by Eustachian tube dysfunction, causes a pocket of the tympanic membrane to retract into the middle ear. Essentially, a small area of the tympanic membrane gets sucked inwards. The squamous epithelial cells of this pocket continue to proliferate and grow into the surrounding space, bones and tissues. It can damage the ossicles (the tiny bones of the middle ear involved in hearing), resulting in permanent hearing loss.
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Cholesteatoma complications?
Permenant conductive hearing loss secondary to damage of the ossicles Infection Pain Vertigo Facial nerve palsy Tinnitus
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How might neuroimaging be utitilsed in cholestetoma?
A CT head can be used to confirm the diagnosis and plan for surgery. MRI may help assess invasion and damage to local soft tissues.
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Is otitis media with effusion painful?
No but may lead to acute otitis media which is (up until TM perforates)
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Investigations and examinations in suspected OME + findings
Otoscopy: Tympanic membrane is retracted and usually has a yellowish hue. There may also be air bubbles or increased opacity of TM Posterior rhinoscopy (to visualize the post nasal space) - tumours in this area can cause ET dysfunction leading to OME - especially important in adults with unilateral OME Tympanogram: Flat (Type B) Tracing Pure tone audiogram: conductive hearing loss Rinne's: abnormal in affected ear Weber's: localizes to effected ear (if unilateral)
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What problems might occur in children with OME?
Associated speech delay Reports of problems at school
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Diagnosis and indicative findings?
Otitis media with effusion (GLUE EAR) Tympanic membrane is retracted and usually has a yellowish hue. Air bubbles Increased opacity of the tympanic membrane.
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When might you worry about an underlying tumor in a patient with OME, and how do you address this concern?
In adults, especially when otitis media with effusion is unilateral - tumours in the postnasal space, as unilateral adult serous effusion is considered a nasopharyngeal tumour until proven otherwise Posterior rhinoscopy
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How can OME lead to hearing loss?
OME is caused by the build-up of a viscous inflammatory fluid within the middle ear, resulting in a conductive hearing impairment.
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Typical presenting features of cholesteotoma?
Foul discharge from the ear Unilateral conductive hearing loss
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What does Rinnes negative mean?
Meaning abnormal test - bone conduction is better than air conduction (normal hearing should mean that air conduction is best) Suggests conductive hearing loss If the patient has negative or abnormal Rinne negative, air vibrations are not being transmitted across the external auditory canal, the tympanic membrane, the ossicular chain, or the oval window.
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Why might cholesteatoma cause vertigo?
Breach of the otic capsule bone causing dizziness on pressure change transmitted from the middle ear to the vestibular system
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What type of hearing loss does cholesteatoma cause and why?
Conductive Debris or erosion by cholestotoma of the ossicles
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What is the most likely diagnosis in patients presentencing with episodic room dizziness with nausea especially with certain head movements and lying down?
BPPV - benign paroxysmal positional vertigo
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Gold standard test to diagnose BPPV?
Dix Hallpike maneuver
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What is considered an abnormal Dix Hallpike maneuver test?
When affected ear is undermost, the following will be observed: Latency Torsional geotropic nystagmus Fatigue Habituation on repeating the test
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What manouevere is used to manage BPPV?
Epley manouvere
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How to perform Dix-Hallpike manouevere?
When performing the Dix-Hallpike test, make sure to warn the patient in advance of each step, so that they know what to expect: 1. Ask the patient to sit upright on the examination couch. 2. Adjust the patient’s position so that when supine, their head will hang over the edge of the bed, allowing for head extension below the horizontal plane. 3. Position yourself standing behind the patient. 4. Turn the patient’s head 45º to one side. 5. Whilst supporting the neck, move the patient from their sitting position to a supine position in one brisk smooth motion, ensuring their head hangs over the bed 30º below the horizontal plane. Ask the patient to keep their eyes open throughout this process. 6. Inspect the patient’s eyes carefully for evidence of nystagmus for at least 30 seconds. 7. If no nystagmus is observed, the test is then complete for that side and you should carefully help the patient sit back up. 8. After a short break, the test should be repeated on the other side, turning the patient’s head in the opposite direction during step 4.
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How to perform Epley manouevere?
1. The Epley manoeuvre typically follows on from a positive Dix-Hallpike test, so we will assume the patient is still positioned lying flat, with the head hanging over the end of the bed, turned 45º away from the midline. 2. Turn the patient’s head 90º to the contralateral side, approximately 45º past the midline, still maintaining neck extension over the bed. Keep the patient in this position for 30 seconds. 3. Whilst maintaining the position of the patient’s head, ask the patient to roll onto their shoulder (on the side their head is currently turned towards). 4. Once the patient is on their side, rotate the patient’s head so that they are looking directly towards the floor. Maintain this position for 30 seconds to a minute. 5. Sit the patient up sideways, whilst maintaining head rotation. 6. Once the patient is sitting upright, the head can be re-aligned to the midline and the neck can be flexed so that the patient is facing downwards (chin to chest). Maintain this position for 30 seconds. The entire procedure can be repeated 2-3 times if needed, however, this will depend on whether the patient is able to tolerate further manoeuvres (as they often precipitate vertigo).
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What should you ask a patient presenting with 'vertigo'?
Is the room spinning around the patient? When did it start? Eposodic? How long does it last How often does it happen Positional? - lying down, head turning Other specific triggers Associated hearing loss Associated tinnitus Loss of conciousness with episodes If it has happened before - resolution: spontaneous? treatment?
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Indications for the Dix-Hallpike test
The Dix-Hallpike manoeuvre is indicated for patients with paroxysmal vertigo in whom BPPV is considered in the differential diagnosis. These patients experience vertigo in brief episodes lasting less than one minute with changes of head position and return to normal between episodes. Light-headedness or a sensation of nausea might last longer than one minute, however, if the sensation of movement persists for more than one-minute alternative diagnoses should be considered. ¹
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Absolute contraindications - Dix-Hallpike and Epley manouveres
Fractured odontoid peg Recent cervical spine fracture Atlanto-axial subluxation Cervical disc prolapse Vertebrobasilar insufficiency Recent neck trauma
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Relative contraindications - Dix-Hallpike and Epley maneuvers
Carotid sinus syncope Severe neck or back pain Recent stroke Cardiac bypass surgery within the last 3 months Rheumatoid arthritis affecting the neck Recent neck surgery Cervical myelopathy Severe orthopnea
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What is otosclerosis?
Disease affecting the ossicles in the middle ear with both genetic and environmental components. Remoddling of small bones in ear Mature bone is gradually replaced with woven bone and symptoms begin as the stapes footplate becomes fixed to the oval window. Most patients develop bilateral disease and most are female (2:1)
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When otosclerosis is prevalent in families what is the inheritance thought to be?
Autosomal dominant tranmission
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Before what age does otosclerosis tend to present?
Before 40 years
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Pathophysiology of otosclerosis?
The auditory ossicles are the tiny bones in the middle ear that transmit sound vibrations from the tympanic membrane to the cochlea. They are the malleus, incus and stapes. The stapes is connected to the oval window (fenestra ovalis) of the cochlea, where it transmits vibrations into the cochlea, which converts them into sensory signals. In patients with otosclerosis, these tiny bones in the middle are affected by abnormal bone remodelling and formation. Mature bone is gradually replaced with woven bone. This mainly affects the base of the stapes, where it attaches to the oval window, causing stiffening and fixation and preventing it from transmitting sound effectively. It causes conductive hearing loss and symptoms begin as the stapes footplate becomes fixed to the oval window.
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Typical presentation of otosclerosis?
Progressive hearing loss (more so with lower pitched sounds - women are easier to hear, conductive type hearing loss) Tinnitus Patient may speak quietly (bone conduction of their voice makes the patient think they are speaking loudly) Patients in early disease may report improved hearing in noisy surroundings Family history of hearing loss Pts presenting before age of 40
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Hearing loss in otosclerosis?
Worse with lower pitch/frequency (male voices harder to hear) Better in noise enviornments (early disease) Conductive hearing loss with intact sensory hearing so patient experiences their voice being loud compared to the environment (due to bone conduction of their voice) - patients will talk quietly
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Examinations and investigations in otosclerosis?
Otoscopy: normal usually, ocassionally Schwatze's sign (pink hue to tympanic membrane) Tympanogram: Normal type A trace - reduced admittance of sound as TM is stiff and non compliant and doesn't absorb sound, reflecting most of it back Pure tone audiogram: conductive hearing loss, characteristic ''Carhart notch'' at 2kHz Weber's: Localises to worst affected ear but may be normal if even bilateral disease Rinne's: Negative - conductive hearing loss - sound easily heard when fork applied to mastoid process (bone conduction > air conduction) High resolution CT: Can detect bondy changes associated with otosclerosis although not always required
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At what frequency is the characteristic ''Carhart notch'' seen during pure tone audiogram in otosclerosis?
2kHz
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What is Schwartze's sign and when is it seen?
Rare sign in otosclerosis - pink hue to tympanic membrane
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Otosclerosis management?
Conservative - hearing aids Surgical (stapedectomy or stapedotomy) generally scuessful with potential to restore hearing to normal - involves lifting the tympanic membrane and some of the surrounding skin out of the way to access the middle ear through the canal
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What are the two types of surgery used to manage otosclerosis and what do they invovle?
STAPEDECTOMY - removal of the entire stapes bone, replacing it with a prosthesis which attacthed to the oval window and hooks around the incus (transmitting sound from incus to choclea the same way the stapes normally would) STAPEDOTOMY - removal of part of stapes bone and leaving the base (footplate) attatched to the oval window. A small hole is made in the base of the stapes for the prosthesis to enter, which is added to transmit sound from the incus to cochlea
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The inner ear resides in which part of which bone?
Petrous part of the temporal bone
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The inner ear consists of a labrynith and canals and can be divided functionally into which two parts?
1. The vestibule and semicircular canals. 2. The cochlea
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Inner ear anatomy: membranous labrynth - what does it contain, what is it surrounded by, what is it suspended in, and what is contained in?
Filled with endolymph Surrounded by bony labyrinth Suspended in perilymph Contained within the bony labyrinth
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How does the perilymphatic system (membranous labryinth, endolymph, bony labryinth) communicated with the subarachnoid space and CSF?
The perilymphatic system communicates with the subarachnoid space and CSF via the cochlear aqueduct Perilymph fluid resembles CSF, and endolymph fluid resembles intracellular fluid
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What does perilymph fluid in the perilymphatic system resemble?
CSF
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What does endolymph in the perilymphatic system resemble?
INtracellular fluid
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Features and functions of the cochlea?
Responsible for perception of hearing - Articulated with oval window causing movement of perilymph and pressure change compensated by the round window - Vibrations are transmitted through the tectorial membrane -Low frequency sounds detected at apex (of the cochlea) - High frequency sounds detected at base (of the cochlea) -Movement of the tectorial membrane causes movement of the hair cells and subsequent depolarization of neuronal fibers - allowing for perception of sound - Transmission of information occurs via the cochlear nerve - Has 2.5 turns around a bony core- the modiolus
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What can the vestibular system be divided into and how does each component detect movement?
Semicircular canals (x3 at 90 degrees to eachother, detect movement in a rotational fashion) Utricle (detects linear/horizontal movement) Saccule (detects vertical movement) (Utricle – Hair cells point Up – Detect linear/horizontal movement Saccule – Hair cells stick out to the Side – Detect vertical movement)
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Central causes of vertigo
Stroke Migraine Neoplasms Demyelination e.g. MS Drugs
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Peripheral causes of vertigo?
BPPV Menieres disease Vestibular neuronitis
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Pathophysiology of BPPV?
Crystals of calcium carbonate (otoconia) become displaced into the semicircular canals (most often posterior semicircular canal) due to a viral infection, head trauma, ageing or without clear cause Otoliths (crystals) disrupt the normal flow of endolymph through the canals, causing abnormal stimulation of hair cells giving the hallucination of movement - ie. triggering episodes of vertigo
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BPPV presenation?
Attacks of vertigo that settle after around 20-60 seconds Often episodes occur over several weeks and then resolve but can reoccur weeks or months later Triggers: lying down, turning head
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What exercises can patients perform at home to help BPPV and how do they do them?
BRANDT-DAROFF EXERCISES Brandt-Daroff exercises can be performed by the patient at home to improve the symptoms of BPPV. These involve sitting on the end of a bed and lying sideways, from one side to the other, while rotating the head slightly to face the ceiling. The exercises are repeated several times a day until symptoms improve.
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Peripheral causes of vertigo differentiating symptoms and their management
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What is an acoustic neuroma/vestibular schwannoma, how and why might they present?
An acoustic neuroma, also known as a vestibular schwannoma, is a tumour of the vestibulocochlear nerve (cranial nerve VIII). They are classically benign tumours that are slow-growing but may become symptomatic through local mass effect, and in some cases may be life-threatening if they extend into the cerebellopontine angle, where they behave as a space-occupying lesion and can lead to hydrocephalus. The most common presentation is unilateral sensorineural hearing loss, with other symptoms including tinnitus, dizziness and balance problems. With enlarging tumours, compression of local structures may lead to facial paraesthesia/sensory loss, ear pain, ataxia, and in severe cases there may be evidence of raised intracranial pressure (e.g. headache).
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How does noise relating hearing loss present
NIHL usually develops after long periods of noise exposure and is usually bilateral in nature. NIHL typically causes sensorineural hearing loss in both ears. The ability to perceive higher sound frequencies is lost first, later followed by impairment of lower frequency perception.
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Investigations and examinations in noise related hearing loss
Weber’s test does not lateralise if the level of sensorineural loss is equal bilaterally Rinnes test will confirm that air conduction is greater than bone conduction in both ears (in the absence of conductive hearing loss). Pure tone audiometry will highlight a bilateral sensorineural hearing loss (i.e. bone and air conduction thresholds in both ears will be above 25dB and within 10 dB of one another).
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Normal hearing can be definied as what
Normal hearing can be defined as the ability to detect noises between 0-25dB.
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When are abx recommended in AOM?
Antibiotics are generally recommended in patients with AOM If they are: <6 months of age 6 months to 2 years with bilateral AOM >2 years or older who appear toxic have persistent otalgia for > 48 hours have temperature > 39 C in the past 48 hours have bilateral AOM
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First line drops for otitis externa
Ofloxacin otic drops are used first-line in both bacterial cases of otitis externa when the tympanic membrane is intact
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Clinical features of Ménière’s disease?
Hearing loss (initally fluctuates, associated with vertigo attacks, gradually becomes oermenant, sensorineural, unilateral, low frequencies affected first) Vertigo Tinnitus (unilateral) Aural fullness Drop attacks (unexplained falls without LOC) Imbalance which can persist after episodesnresolve
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What is MénIères disease and what is the pathophysiology?
Long term inner ear disorder that causes recurrent attacks of vertigo, tinnitus hearing loss and aural fullness. Excessive build up of ENDOLYMPH in the LABYRINTH of the INNER EAR, causing a higher pressure than normal and disrupting the sensory signal. This increased pressure of the endolymph is called endolymphatic hydrops.
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Ménière’s Disease - disease course
Initially patients are well between attacks As disease progresses patients may start to develop reduced vestibular function on the side of the disease and a progressive sensioneural hearing loss. Episodes tend tom come in clusters over several weeks followed by prolonged periods (months) without symtpoms. Over time the disease often burns itself out so that the patient doesn’t suffer from acute vertigo but will have reduced hearing and maybe generally unbalanced. If the vestibular system of the other ear is working well this can compensate for the bad ear to improve the overall balance but this can take time especially in the elderly.
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How long does vertigo last in Ménière’s disease?
20 minutes to several hours
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BPPV vs Ménière’s - history
BPPV: hearing unaffected, vertigo lasts seconds, no associated symptoms except nausea, triggered by movement Ménèires: hearing loss and tinnitus, lasts up to several hours and no less than 20 mins, aural fullness, drop attacks and persistent imbalance, spontaneous nystagmus NO MOVEMENT OR POSTURAL TRIGGER
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Hearing in Ménière’s?
Hearing Initially fluctuates Hearing loss and tinnitus Associated with vertigo attacks Hearing loss and tinnitus gradually become permenant Sensioneural hearing loss Unilateral Affecting low frequencies first (male voices worse)
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Tinnitus in Ménière’s?
Initial
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What neurological sign might you observe during an acute Ménière’s attack?
Spontaneous nystagmus (unidirectional)
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Examination and investigations in Ménière’s disease?
Clinical diagnosis made by ENT specialist Audiology assessment required Rinnes positive (as sensioneural) Webers lateralises to unaffected ear Pure tone audiometry: sensioneural Electronystagmogram (ENG) to help guide cause of vertigo MRI/CT head can rule out other causes of vertigo - will not show changes in Ménière’s
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How is Ménière’s managed?
Acute attacks (no more than 3 days use): Prochlorperazine Antihistamines (cyclizine,cinnarizine and Promethazine) Prophylaxis of attacks: Betahistine Thiazide diuretics e.g. bendrofluazide Dietary – reduce salt, chocolate, alcohol, caffeine, chinese food Surgical o Grommet insertion o Dexamethasone middle ear injection o Endolymphatic sac decompression o Vestibular destruction using middle ear injection of gentamicin o Surgical labyrinthectomy – very rarely required
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Stages of Ménière’s disease and the implications
Stages 1, 2, 3 and 4 1 and 2 are considered early reversible disease susceptible to remission 3 and 4 are considered fixed or not reversible
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What age to patients with Ménière’s typically present?
40-50 years old
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Presentation of an acoustic neuroma?
The typical patient is aged 40-60 years presenting with a gradual onset of: Unilateral sensorineural hearing loss (often the first symptom) Unilateral tinnitus Dizziness or imbalance A sensation of fullness in the ear If tumour grows large enough may be a facial nerve palsy
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Acoustic neuromas are usually unilateral, when might they not be?
Bilateral acoustic neuromas almost certainly indicate neurofibromatosis type II.
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What are acoustic neuromas and where do they occur?
Acoustic neuromas (vestibular schwannomas) are benign tumours of the Schwann cells (PNS cells providing myelin sheath around neurones) surrounding the auditory nerve (vestibulocochlear nerve) that innervates the inner ear. They occur at the cerebellopontine angle and are sometimes referred to as cerebellopontine angle tumours.
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Investigations in acoustic neuroma?
Audiometry: sensioneural pattern of hearing loss Brain imagaing (MRI or CT): establish dgx and features of the tumour
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Management of acoustic neuroma?
ENT specialist management options include: Conservative management with monitoring may be used if there are no symptoms or treatment is inappropriate Surgery to remove the tumour (partial or total removal) Radiotherapy to reduce the growth
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Risks associated with treatment of a vestibular shwannoma/ acoustic neuroma?
Vestibulocochlear nerve injury, with permanent hearing loss or dizziness Facial nerve injury, with facial weakness
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What is vestibular neuronitis?
Vestibular neuronitis describes inflammation of the vestibular nerve. This is usually attributed to a viral infection.
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Presentation of vestibular neuronitis?
In this condition inflammation in the inner ear causes severe incapacitating vertigo lasting several days associated with nausea and vomiting. During an attack patients will have horizontal nystagmus but an otherwise normal neurological examination.
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Vestibular neuronitis main differentials?
Posterior circulation infarction (neurological signs present) Labrinythitis (hearing loss present) In VN no neurological signs (other than horizontal nystagmus) and no hearing loss
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Management of vestibular neuronitis?
IV fluids (Patients may need admission if they are becoming dehydrated due to severe nausea and vomiting For peripheral vertigo, short-term options for managing symptoms include: Prochlorperazine Antihistamines (e.g., cyclizine, cinnarizine and promethazine) (NICE advise that symptomatic treatment can be used for up to 3 days. More extended use may slow down the recovery) NICE also recommend referral if the symptoms do not improve after 1 week or resolve after 6 weeks, as they may require further investigation or vestibular rehabilitation therapy (VRT) - (Cawthorne-Cooksey exercises)
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Prognosis of vestibular neuronitis?
Symptoms are most severe for the first few days, after which they gradually resolve over the following 2-6 weeks. (There is often an associated long term vestibular deficit after the acute episode which can lead to a generalized unsteadiness after the acute episode for a number of weeks while the brain compensates for this) Benign paroxysmal positional vertigo (BPPV) may develop after vestibular neuronitis.
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Pathophysiology of vestibular neuronitits?
Vestibular neuronitis refers to inflammation of the vestibular nerve. A viral infection may trigger this inflammation. It distorts the signals travelling from the vestibular system to the brain, confusing the signal required to sense movements of the head. This results in episodes of vertigo, where the brain thinks the head is moving when it is not. Cochlea nerve is not affected and hence there is no hearing loss
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What are the semicircular canals responsible for detecting?
Rotation of the head
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What are the otolith organs (urticle and saccule) responsible for detecting?
Gravity and acceletation
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What test can be used to diagnose peripheral causes of vertigo (problems with vestibular system)?
Head impulse test
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How is the head impulse test performed?
The head impulse test involves the patient sitting upright and fixing their gaze on the examiner’s nose. The examiner holds the patient’s head and rapidly jerks it 10-20 degrees in one direction while the patient continues looking at the examiner’s nose. The head is slowly moved back to the centre before repeating in the opposite direction. Ensure they have no neck pain or pathology before performing the test.
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Implications of the results of the head impulse test?
Normal: eyes remain fixed on examiners nose - no problem with vestibular system - either no vertigo or central cause Abnormal: Eyes will saccade (rapidly move back and forth) and will eventually fix back on examiner - abnormally functioning vestibular system - ie. vestibular neuronititis, labrythitis
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What is labyrinthitis and why might it occur?
Labyrinthitis refers to inflammation of the bony labyrinth of the inner ear, including the semicircular canals, vestibule (middle section) and cochlea. The inflammation is usually attributed to a viral upper respiratory tract infection. Rarely labyrinthitis can be caused by a bacterial infection. This may be an inflammatory response to a nearby infection or the result of bacteria or bacterial toxins entering the labyrinth. It is usually secondary to otitis media or meningitis.
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Presentation of labyrinthitis?
(Vestibular neuronititis+hearing loss and tinnitus) Hearing loss Tinnitus Acute onset vertigo Possible nystagmus Patients may have symptoms associated with the causative virus, such as a cough, sore throat and blocked nose. May arise as a compliaction of AOM
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How is labyrinthitis diagnosed?
A clinical diagnosis is based on history and examination findings. It is important to exclude a central cause of the vertigo. The head impulse test can be used to diagnose peripheral causes of vertigo, resulting from problems with the vestibular system (e.g., vestibular neuronitis or labyrinthitis).
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Management of labyrinthitis?
Management is the same as with vestibular neuronitis, with supportive care and short-term use (up to 3 days) of medication to suppress the symptoms. Options for managing symptoms are: Prochlorperazine Antihistamines (e.g., cyclizine, cinnarizine and promethazine) Antibiotics are used to treat bacterial labyrinthitis. The underlying infection (e.g., otitis media or meningitis) needs appropriate treatment.
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Complications of labyrinthitis?
Patients rarely have lasting symptoms, including permanent hearing impairment. This is more common after bacterial labyrinthitis, particularly associated with meningitis (All patients with meningitis are offered audiology assessment as soon as they are recovered to assess for hearing impairment. )
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What is sudden sensorineural hearing loss?
Sudden sensorineural hearing loss (SSNHL) is defined as hearing loss over less than 72 hours, unexplained by other causes. This is considered an otological emergency and requires an immediate referral to the on-call ENT team. The diagnosis is made when someone rapidly loses their hearing, and no conductive cause can be found. With SSNHL, hearing loss is most often unilateral. It may be permanent or resolve over days to weeks.
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Causes of rapid onset CONDUCTIVE hearing loss?
Conductive causes of rapid-onset hearing loss (not classed as SSNHL) include: Ear wax (or something else blocking the canal) Infection (e.g., otitis media or otitis externa) Fluid in the middle ear (effusion) Eustachian tube dysfunction Perforated tympanic membrane
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Causes of SSNHL?
Most cases (90%) of SSNHL are idiopathic, meaning no specific cause is found. Other causes of SSNHL include: Infection (e.g., meningitis, HIV and mumps) Ménière’s disease Ototoxic medications Multiple sclerosis Migraine Stroke Acoustic neuroma Cogan’s syndrome (a rare autoimmune condition causing inflammation of the eyes and inner ear)
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How is SSNHL investigated?
Audiometry is required to establish the diagnosis. A diagnosis of SSNHL requires a loss of at least 30 decibels in three consecutive frequencies on an audiogram. MRI or CT head may be used if a stroke or acoustic neuroma are being considered.
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Criteria for sudden sensorineural hearing loss?
Sensorineural hearing loss over less than 72 hours at least 30 decibels in three consecutive frequeencies on audiogram
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Management of SSNHL?
The NICE clinical knowledge summaries (updated September 2019) recommend an immediate referral to ENT for assessment within 24 hours for patients presenting with sudden sensorineural hearing loss presenting within 30 days of onset. Where an underlying cause is found (e.g., infection), treatment can be directed at this (e.g. antivirals, antibiotics) Idiopathic SSNHL may be treated with steroids under the guidance of the ENT team. Steroids may be: Oral Intra-tympanic (via an injection of steroids through the tympanic membrane) Other treatments are used e.g. hyperbaric oxygen, carbogen but are not widely practice
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Prognosis of SSNHL?
1/3 recover to normal 1/3 some recovery 1/3 no recovery
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What is Presbycusis and it’s pathophysiology?
Age related hearing loss. Loss of hair cells in the cochlea, Loss of neurones in the cochlea Atrophy of the stria vascularis Endolymphatic potential
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Hearing loss in Presbycusis?
Sensorineural Symmetrical High pitched sounds lost first (female voices harder to head) Gradual and insidious Worse in noisey environments
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Presentation of Presbycusis
Sensorineural symmetrical hearing loss, gradual and insidious, loss of high pitched sounds first, harder to hear in noisy environments. History of ‘not paying attention’ or missing parts of conversations - may be concerns of dementia when the actual issue is hearing loss May be associated tinnitus
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What does use of a hearing aid in Presbycusis reduce the risk of?
Dementia
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Risk factors for presbycusis?
Age Male gender Family history Loud noise exposure Diabetes Hypertensive Loud noise exposure HTN Ototoxic medications Smoking
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Audiometry in presbycusis?
Sensorineural hearing loss pattern Normal or near normal hearing at lower frequencies Worsening hearing loss at higher frequencies
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Investigation of choice for presbycusis?
Audiometry
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Management of presbycusis?
The effects of presbycusis cannot be reversed. Management involves supporting the person to maintain normal functioning: Optimising the environment, for example, reducing the ambient noise during conversations Hearing aids Cochlear implants (in patients where hearing aids are not sufficient)
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What is cerumen?
Ear wax is also called cerumen. It is normally produced in small amounts in the external ear canal. It is created from a combination of secretions, dead skin cells and any substances that enter the ear. Ear wax has a protective effect, helping to prevent infection in the ear canal. In most people, ear wax does not cause any problems.
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What problems might impacted ear was cause?
Ear wax can build up and become impacted and stuck to the tympanic membrane. This can result in: Conductive hearing loss Discomfort in the ear A feeling of fullness Pain Tinnitus
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Impacted ear wax (cerumen)
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If earwax is causing problems, how can it be managed?
In most cases, ear wax does not require any interventions. The ears should naturally regulate the amount of wax in the ear canal without any issues. Inserting cotton buds into the ear should be avoided, as this can press the wax in further and cause impaction. There are three main methods for removing ear wax: Ear drops – usually olive oil or sodium bicarbonate 5% Ear irrigation – squirting water in the ears to clean away the wax Microsuction – using a tiny suction device to suck out the wax Ear drops may be enough to clear the ears. If not, ear irrigation can often be performed in primary care. Where there are contraindications to ear irrigation (e.g., perforated tympanic membrane or infection), microsuction can be performed by specialist ear, nose and throat services.
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Structures of ear from outside to in
The pinna is the external portion of the ear The external auditory canal is the tube into the ear The tympanic membrane is the eardrum The Eustachian tube connects the middle ear with the throat to equalise pressure The malleus, incus and stapes are the small bones in the middle ear that connect the tympanic membrane to the structures of the inner ear The semicircular canals are responsible for sensing head movement (the vestibular system) The cochlea is responsible for converting the sound vibration into a nervous signal The vestibulocochlear nerve transmits nerve signals from the semicircular canals and cochlea to the brain
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Causes of sensorineural hearing loss
Causes Of Sensorineural Hearing Loss The causes of adult-onset sensorineural hearing loss are: Sudden sensorineural hearing loss (over less than 72 hours) Presbycusis (age-related) Noise exposure Ménière’s disease Labyrinthitis Acoustic neuroma Neurological conditions (e.g., stroke, multiple sclerosis or brain tumours) Infections (e.g., meningitis) Medications
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What medications can cause sensorineural hearing loss?
Loop diuretics (e.g., furosemide) Aminoglycoside antibiotics (e.g., gentamicin) Chemotherapy drugs (e.g., cisplatin)
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Causes of conductive hearing loss
Ear wax (or something else blocking the canal) Infection (e.g., otitis media or otitis externa) Fluid in the middle ear (effusion) Eustachian tube dysfunction Perforated tympanic membrane Otosclerosis Cholesteatoma Exostoses Tumours
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What is tinnitus and why does it happen?
Tinnitus refers to a persistent addition sound that is heard but is not present in the surrounding environment. It may be described as a “ringing in the ears”, but it can also be a buzzing, hissing or humming noise. The additional noise experienced with tinnitus is thought to be the result of a background sensory signal produced by the cochlea that is not effectively filtered out by the central auditory system. In a quiet enough environment, almost everyone will experience some background noise (tinnitus). This becomes more prominent the more attention it is given.
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Causes of tinnitus?
Primary tinnitus has no identifiable cause and often occurs with sensorineural hearing loss. Secondary tinnitus refers to tinnitus with an identifiable cause. Causes include: Impacted ear wax Ear infection Ménière’s disease Noise exposure Medications (e.g., loop diuretics, gentamicin and chemotherapy drugs such as cisplatin) Acoustic neuroma Multiple sclerosis Trauma Depression Tinnitus may also be associated with systemic conditions: Anaemia Diabetes Hypothyroidism or hyperthyroidism Hyperlipidaemia Objective tinnitus refers to when the patient can objectively hear an extra sound within their head. This sound can also be observable on examination by auscultating with a stethoscope around the ear. Actual additional sounds may be caused by: Carotid artery stenosis (pulsatile carotid bruit) Aortic stenosis (radiating pulsatile murmur sounds) Arteriovenous malformations (pulsatile) Eustachian tube dysfunction (popping or clicking noises)
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Tinnitus: history and investigations
Ask about the pattern of symptoms: Unilateral or bilateral Frequency and duration Severity Pulsatile or non-pulsatile (pulsatile may indicate a cardiovascular cause, such as carotid artery stenosis with a bruit) A focused history and examination can be used to identify any underlying causes, including: Contributing factors, such as hearing loss or noise exposure Associated symptoms (e.g., hearing loss, vertigo, pain or discharge) Stress and anxiety Otoscopy to look for causes such as ear wax or infection Weber’s and Rinne’s tests for hearing loss
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How might you investigate tinnitus?
The NICE clinical knowledge summaries (updated March 2020) suggest considering blood tests for possible underlying causes: Full blood count (anaemia) Glucose (diabetes) TSH (thyroid disorders) Lipids (hyperlipidaemia) Audiology can be used to assess the hearing in detail and help establish the underlying cause. Imaging (e.g., CT or MRI) may be rarely required to investigate for underlying causes such as vascular malformations or acoustic neuromas.
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Red flags that could indicate a serious underlying cause and the need for specialist assessment in a patient presenting with tinnitus?
Unilateral tinnitus Pulsatile tinnitus Hyperacusis (hypersensitivity, pain or distress with environmental sounds) Associated unilateral hearing loss Associated sudden onset hearing loss Associated vertigo or dizziness Headaches or visual symptoms Associated neurological symptoms or signs (e.g., facial nerve palsy or signs of stroke) Suicidal ideation related to the tinnitus
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Management of tinnitus?
Tinnitus tends to improve or resolve over time without any interventions. Underlying causes of tinnitus can be treated, such as impacted ear wax or infection. Several measures can be used to help improve and manage symptoms: Hearing aids Sound therapy (adding background noise to mask the tinnitus) Cognitive behavioural therapy
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Causes of peripheral vertigo?
BPPV Meniere's disease Labyrinthitis Acute vestibular neuronitis Trauma to the vestibular nerve Vestibular nerve tumours (acoustic neuromas) Otosclerosis Hyperviscosity syndromes Varicella zoster infection (often with facial nerve weakness and vesicles around the ear – Ramsay Hunt syndrome)
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Causes of central vertigo?
Posterior circulation infarction (stroke) Tumour Multiple sclerosis Vestibular migraine
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Clues that vertigo has central etiology as opposed to peripheral?
All the central causes of vertigo will cause sustained, non-positional vertigo. Posterior circulation infarction will have a sudden onset and may be associated with other symptoms, such as ataxia, diplopia, cranial nerve defects or limb symptoms. Tumours in the cerebellum or brainstem will have a gradual onset with associated symptoms of cerebellar or brainstem dysfunction. Multiple sclerosis may cause relapsing and remitting symptoms, with other associated features of multiple sclerosis, such as optic neuritis or transverse myelitis. Vestibular migraine will cause symptoms lasting minutes to hours, often associated with visual aura and headache. Attacks may be triggered
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Potential triggers of vestibular migraine?
Vestibular migraine will cause symptoms lasting minutes to hours, often associated with visual aura and headache. Attacks may be triggered by: Stress Bright lights Strong smells Certain foods (e.g. chocolate, cheese and caffeine) Dehydration Menstruation Abnormal sleep patterns
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Peripheral vs. central vertigo: onset
Peripheral: Sudden onset Central: Gradual onset (except stroke)
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Peripheral vs. central vertigo: duration
Peripheral: Short (seconds or minutes) Central: Persistent
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Peripheral vs. central vertigo: hearing loss or tinnitus?
Peripheral: often present Central: Usually not
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Peripheral vs. central vertigo: coordination
Peripheral: intact Central: lost
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Peripheral vs. central vertigo: nausea?
Peripheral: severe Central: mild
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What should be examined when a patient presents with vertigo?
Ear examination to look for signs of infection or other pathology Neurological examination to assess for central causes of vertigo (e.g., stroke or multiple sclerosis) Cerebellar examination Cardiovascular examination to assess for cardiovascular causes of dizziness (e.g., arrhythmias or valve disease) Special tests: Romberg’s test (screens for problems with proprioception or vestibular function) Dix-Hallpike manoeuvre (to diagnose BPPV) HINTS examination (to distinguish between central and peripheral vertigo)
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What is the HINTs examination?
The HINTS examination can be used to distinguish between central and peripheral vertigo. It stands for: HI – Head Impulse N – Nystagmus TS – Test of Skew
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Nystagmus: central vs peripheral vertigo?
Unilateral horizontal nystagmus is more likely to be a peripheral cause. Bilateral or vertical nystagmus suggests a central cause.
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What is the role of the ET tube and what happens when it is dysfunctional?
Eustachian tube dysfunction is when the tube between the middle ear and throat is not functioning properly. The Eustachian tube is present mainly to equalise the air pressure in the middle ear and drain fluid from the middle ear. When the Eustachian tube is not functioning correctly or becomes blocked, the air pressure cannot equalise properly and fluid cannot drain freely from the middle ear. The air pressure between the middle ear and the environment can become unequal. The middle ear can fill with fluid. Eustachian tube dysfunction may be related to a viral upper respiratory tract infection (URTI), allergies (e.g., hayfever) or smoking.
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Presentation of ET tube dysfunction?
Reduced or altered hearing Popping noises/sensation within the ear A fullness sensation within the ear Pain or discomfort Exacerbation of symptoms when the external air pressure changes and the middle ear pressure cannot equalize to the outside pressure - for example when scuba diving, flying in an earoplane
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Why is ET tube dysfunction not routinely investigated unless there are persistent, problematic severe symptoms (to establish the diagnosis and cause)?
Often Eustachian tube dysfunction gives a typical set of symptoms and is associated with a clear cause, for example, a recent viral upper respiratory tract infection or hayfever. In this situation, investigations are not required as the symptoms will resolve with time or simple treatments.
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In Eustation Tube dysfunction is persistent, problematic or severe symptoms, investigations to help establish the diagnosis and cause include what?
Tympanometry Audiometry Nasopharyngoscopy (inspect the ET tube openings) CT scan (asses for structural pathology)
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What does tympanometry involve?
Measurement of compliance of TM, can be done at any age as minimal complience required from patient (small probe in ear only) A device is inserted into the external auditory canal, creating different ear pressures within the canal Sound is sent in the direction of the tympanic membrane The amount of sound reflected back off the tympanic membrane is measured A tympanogram of the sound absorbed (admittance) is plotted at different air pressures
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What is meant by 'admittance' in terms of tympanometry?
The amount of sound absorbed by the TM and middle ear (measured at various ear pressures)
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Tympanometry - normal
Normally, sound is absorbed best when the air pressure in the ear canal matches the ambient air pressure. The ambient air pressure is equal to the middle ear pressure in healthy ears.
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Tympanometry in ET tube dysfunction?
Peak admittance at negative ear canal pressures This is because the air pressure is lower in the middle ear than the ambient air pressure (new air cannot get through TM to equalise the pressures)
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Management of ET tube dysfunction?
None - wait for it to resolve spontaneously - e.g. recovering from URTI Valsalva maneuverer (holding nose and blowing into it to inflate the ET tube). Decongestant nasal sprays (short term only) Antihistamines and a steroid nasal spray (short term only) Antihistamines - steroid nasal spray for allergies or rhinitis Sugery may be required in severe or persistent cases Otovent - OTC device where the patient blows into a balloon which can help inflate the ET tube, clear blockages and equalize pressure
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Surgical management of ET tube dysfunction?
Treatment of other pathology that might cause symptoms, for example, adenoidectomy Grommets (tubes inserted into TM by ENT surgeon allowing air or fluid to drain through the ear canal, fall out typically within about 18 months) Under local Balloon dilation ET tuboplasty involves insetring a deflated balloon into the ET tube for a short period of time (a2 mins) to stretch the ET tube, then deflating and removing it, Under GA
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What are the potential complications of ET tube dysfunction
Recurrence Chronic otitis media, a middle ear infection Otitis media with effusion, or “glue ear,” a fluid buildup in the middle ear that can last for weeks and could damage hearing Eardrum retraction, when the eardrum is seemingly sucked farther into the ear canal
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Risk factors for ET tube dysfunction
Cleft pallette Nasal polyps Smoking (damage to cilia) Obesity (fatty deposits can form around the Eustachian tubes, leading to dysfunction) Allergies (frequent episodes of mucus production and congestion) Down syndrome Young children - 1 - 6 years (narrower ET tube)
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What does audiometry involve?
Testing a patients hearing by playing a variety of tones and volumes using headphones (air conduction) and an oscillator (conduction device) . Audiometry results are recorded on an audiogram. Audiograms can help identify and differentiate conductive and sensorineural hearing loss.
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Components of an audiogram
Chart documenting the volume at which patients can hear differnt tones x axis: frequency/Hz y axis: volume/decebils (quitest volume that can be heard at given frequency) (gets lower going upwards)
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Plotting in an audiogram?
X - left sided air conduction ] - left sided bone conduction O - right sided air conduction [ - right sided bone conduction
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Sensorineural hearing loss on audogram?
In patients with sensorineural hearing loss, both air and bone conduction readings will be more than 20 dB, plotted below the 20 dB line on the chart. This may affect only one side, one side more than the other or both sides equally.
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Conductive hearing loss on audiogram?
In patients with conductive hearing loss, bone conduction readings will be normal (between 0 and 20 dB). However, air conduction readings will be greater than 20 dB, plotted below the 20 dB line on the chart. In conductive hearing loss, sound can travel through bone but is not conducted through air due to pathology along the route into the ear.
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Normal hearing on audiogram
When a patient has normal hearing, all readings will be between 0 and 20 dB, at the top of the chart.
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Normal audiogram
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Conductive hearin loss
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Sensorineural hearing loss
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Mixed hearing loss - audiogram
Both air and bone conduction readings will be more than 20 dB in patients with mixed hearing loss. However, there will be a difference of more than 15 dB between the two (bone conduction > air conduction).
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Both air and bone conduction readings will be more than 20 dB in patients with mixed hearing loss. However, there will be a difference of more than 15 dB between the two (bone conduction > air conduction).
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Common causes of congenital hearing loss?
Maternal rubella or cytomegalovirus infection during pregnancy Genetic deafness can be autosomal recessive or autosomal dominant Associated syndromes, for example Down’s syndrome
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Perinatal causes of hearing loss?
Prematurity Hypoxia during or after birth
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Causes of childhood hearing loss that are neither perinatal nor congenital causes?
Jaundice Meningitis and encephalitis Otitis media or glue ear Chemotherapy
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How is hearing tested in neonates?
The UK newborn hearing screening programme (NHSP) tests hearing in all neonates. This involves special equipment that delivers sound to each eardrum individually and checks for a response. This can identify congenital hearing problems early.
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How might children with hearing loss present?
Children with hearing difficulties may present with parental concerns about hearing or with behavioural changes associated with not being able to hear: Ignoring calls or sounds Frustration or bad behaviour Poor speech and language development Poor school performance
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How is hearing loss assessed in children?
NHSP - neonates - special equiptment that delivers sound to each eardrum and checks for a response Looking for basic turning towards a sound - children under 3 Audiometry - headphones at specific tones and volumes
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Management of childhood hearing loss?
Establishing the diagnosis is the first step. After the diagnosis is established, input from the multidisciplinary team is required for support with hearing, speech, language and learning: Speech and language therapy Educational psychology ENT specialist Hearing aids for children who retain some hearing Sign language
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What is a compliance peak in a tympanogram?
The point at which pressure in the canal equals that of the middle ear
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Type A tympanogram trace?
Normal result Peak centred on 0 daPa on x axis
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Type A Tympanogram (normal, peak centred at 0daPa on x axis)
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Type B tympanogram
Flat tracing Suggests middle ear effusion or perforation
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How can you differentiate between effusion and perforation on tympanogram?
Both type b (flat line) Effusion: normal canal volume (around 1cm3 in adults) Perforation: Larger volume measure as both middle and external ear volume
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Type B tympanogram
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Type C tympanogram
Suggests ET tube dysfunction The peak of the tracing has negative pressure
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Triggers of nosebleeds
Nosebleeds are common in young children and older adults. They can be triggered by: Nose picking Colds Sinusitis Vigorous nose-blowing Trauma Changes in the weather Coagulation disorders (e.g., thrombocytopenia or Von Willebrand disease) Anticoagulant medication (e.g., aspirin, DOACs or warfarin) Snorting cocaine Tumours (e.g., squamous cell carcinoma) When a patient swallows blood during a nosebleed, they may present with vomiting blood. Bleeding is usually unilateral. Bleeding from both nostrils may indicate bleeding posteriorly in the nose. Posterior bleeding presents a higher risk of aspiration of blood.
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Management of nosebleed under 10-15 mins
Sit up and tilt the head forwards (tilting the head backwards is not advised as blood will flow towards the airway) Squeeze the soft part of the nostrils together for 10 – 15 minutes Spit out any blood in the mouth, rather than swallowing
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Management of nosebleed in cases of 10-15 mins, bilateral bleeds, hemodynamic instability?
Nasal packing using nasal tampons or inflatable packs Nasal cautery using silver nitrate sticks After treating an acute nosebleed, consider prescribing Naseptin nasal cream (chlorhexidine and neomycin) four times daily for 10 days to reduce any crusting, inflammation and infection. This is contraindicated in peanut or soya allergy.
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What should you consider in recurrent or severe nosebleeds?
Recurrent and significant nosebleeds might require further investigation to look for an underlying cause, such as thrombocytopenia or clotting disorders.
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What is sinusitis?
Sinusitis refers to inflammation of the paranasal sinuses in the face. This is usually accompanied by inflammation of the nasal cavity and can be referred to as rhinosinusitis. It is very common. Sinusitis can be: Acute (less than 12 weeks) Chronic (more than 12 weeks)
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What are the four sets of paranasal sinuses?
Frontal sinuses (above the eyebrows) Maxillary sinuses (either side of the nose below the eyes) Ethmoid sinuses (in the ethmoid bone in the middle of the nasal cavity) Sphenoid sinuses (in the sphenoid bone at the back of the nasal cavity)
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What are the paranasal sinuses and how can sinusitis occur?
The paranasal sinuses are hollow spaces within the bones of the face Arranged symmetrically around the nasal cavity Produce mucous and drain into the nasal cavities via ostia (holes) Blockage of the ostia prevents drainage of the sinuses, resulting in sinusitis
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Causes of sinusitis?
Inflammation of the sinuses can be caused by: Infection, particularly following viral upper respiratory tract infections Allergies, such as hayfever (with allergic rhinitis) Obstruction of drainage, for example, due to a foreign body, trauma or polyps Smoking Patients with asthma are more likely to suffer from sinusitis.
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Typical presentation of acute sinusitis?
The typical presentation of acute sinusitis is someone with a recent viral upper respiratory tract infection presenting with: Nasal congestion Nasal discharge Facial pain or headache Facial pressure Facial swelling over the affected areas Loss of smell
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What might chronic sinusitis be associated with?
Nasal polyps
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What might examination reveal in a patient with acute sinusitis?
Tenderness to palpation of the affected areas Inflammation and oedema of the nasal mucosa Discharge Fever Other signs of systemic infection (e.g., tachycardia)
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In sinusitis investigation is rarely necessary, what might you do if patients have persistent symptoms despite treatment?
Nasal endoscopy CT scan
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When patients with acute sinusitis symptoms persisting past 10 days, what options does nice reccomend?
High dose steroid nasal spray for 14 days (e.g., mometasone 200 mcg twice daily) A delayed antibiotic prescription, used if worsening or not improving within 7 days (phenoxymethylpenicillin first-line)
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Management of chronic sinusitis?
Options for chronic sinusitis are: Saline nasal irrigation Steroid nasal sprays or drops (e.g., mometasone or fluticasone) Functional endoscopic sinus surgery (FESS)
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How should patients be instructed to use steroid nasal spray?
Tilting the head slightly forward Using the left hand to spray into the right nostril, and vice versa (this directs the spray slightly away from the septum) NOT sniffing hard during the spray Very gently inhaling through the nose after the spray
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If a patient can 'taste the spray at the back of their throat' when using steroid nasal spray, what odes this suggest?
Spray has gone past the nasal mucosa It will be ineffective
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What is Functional Endoscopic Sinus Surgery?
Functional endoscopic sinus surgery (FESS) involves using a small endoscope inserted through the nostrils and sinuses. Instruments are used to remove or correct any obstructions to the sinues. Obstruction may be cause by swollen mucosa, bone, polyps or a deviated septum. Balloons may be inflated to dilate the opening of the sinuses. Patients need a CT scan before the procedure to confirm the diagnosis and assess the structures?
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What surgery is used to correct a deviated septum?
Septoplasty
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What are nasal polyps?
Nasal polyps are growth of the nasal mucosa that can occur in the nasal cavity or sinuses. They are often associated with inflammation (chronic rhinitis) They grow slowly and gradually obstruct the nasal passage Polyps are usually bilateral
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What makes unilateral nasal polyps concerning?
unilateral polyps are concerning for malignancy and require a specialist referral for assessment
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What conditions are associated with nasal polyps?
Chronic rhinitis or sinusitis Asthma Samter's triad (nasal polyps, asthma and aspirin intolerance/allergy) Cystic fibrosis Eosinophillic granulomatosis with polyangitis (Chrug-Strauss syndrome)
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How might nasal polyps present?
Chronic rhinosinusitis Difficulty breathing through the nose Snoring Nasal discharge Loss of sense of smell (anosmia)
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How can you examine nasal polyps?
Nasal speculum - hold the nostrils open Otoscope with large speculum Nasal endoscopy to visualize the cavity in detail to assess any polyps
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What do nasal polyps look like?
Nasal polyps appear as round pale grey/yellow growths on the mucosal wall.
385
Nasal polyp
386
Management of nasal polyps?
Unilateral polyps should be referred for specialist assessment to exclude malignancy. Medical management involves intranasal topical steroid drops or spray. Surgical management is used where medical treatment fails. This involves removing the polyps: Intranasal polypectomy is used where the polyps are visible close to the nostrils Endoscopic nasal polypectomy is used where the polyps are further in the nose or the sinuses
387
What is obstructive sleep apnoea?
Obstructive sleep apnoea is caused by collapse of the pharyngeal airway. It is characterised by episodes of apnoea during sleep, where the person stops breathing periodically for up to a few minutes. The partner usually reports this happening, and the patient is unaware of the episodes.
388
Risk factors for sleep apnoea?
Middle age Male Obesity Alcohol Smoking
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Feature of sleep apnea
Episodes of apnoea during sleep (reported by their partner) Snoring Morning headache Waking up unrefreshed from sleep Daytime sleepiness Concentration problems Reduced oxygen saturation during sleep Severe cases can cause hypertension, heart failure and can increase the risk of myocardial infarction and stroke.
390
What can be used to asses the symptoms of sleepiness associated with obstructive sleep apnoea?
Epworth sleepiness scale
391
Management of sleep apnoea?
Sleep studies under sleep clinic (measuring sats, HR, respiratory rate and breathing to establish any episodes of apnoea and the extent of pts snoring) Address risk patients (drinking alcohol, stop smoking and lose weight) CPAP to maintain patency of the airway using continous pressure Surgery - uvulopalatopharyngoplasty (UPPP) to reconstruct the soft palate and jaw, children –adenotonsillectomy Mandibular positioning devices in selected cases
392
Bones and cartillage of the nose and blood supply
Quadrangular cartillage Ethmoid Vomer Anterior ethmoidal, posterior ethmoidal, septal branches of the spheno-palatine, branch of greater palatine, Little's area , septal branch of superior labial
393
Local causes of epistaxis?
Local  Idiopathic – 85%  Traumatic  Iatrogenic  Foreign Body  Inflammatory – Rhinitis, Polyps  Neoplastic
394
Systemic causes of nosebleeds
 Hypertension  Coagulopathies  Vasculopathies  Hereditary Haemorrhagic Telangiectasia/Osler-Weber-Rendu disease
395
Which should be tried first in management of epistaxis- packing or cautery?
Cautery, then anterior packing, then posterior packing (if continues to bleed into the oropharynx
396
How should cautery be performed as per source of epistaxis?
Anterior bleed: anterior rhinoscopy Posterior bleed - rigid endoscope (Topical adrenaline may also help to control the bleed)
397
Potential complications of nasal bone fracture (often as a result of assult, sports, falls, RTC)
Septal hematoma CSF leak associated with skull base fracture (rare)
398
Management of nasal trauma
 ABC – epistaxis normally self-limiting  Examine for septal haematoma  No XR required  If deviated nose consider Manipulation under anaesthetic (LA/GA) within 2 weeks of injury
399
Paranasal sinus anatomy
Structures of importance: lamina papracea forming the medial wall of the orbit, anterior cranial fossa, internal catorid artery
400
The sites of drainage of the paranasal sinuses?
Sphenoid sinus: spheno-ethmoidal recess Posterior ethmoid cells: superior meatus Frontal, maxillary and anterior ethmoid cells: Middle meatus Nasolacrimal duct: inferior meatus
401
Potential complications related to the sinuses?
Surgery Damage to orbit (orbit lies lateral to the ethmoid sinus and superior to the maxillary sinus and its contents are at risk during sinus surgery and in severe cases can cause loss of sight. Anterior skull base - lies just above the sphenoid and ethmoid sinuses and can be breached during surgery which can cause as CSF leak and even brain damage Rhinosinusitis: Orbit - infective rhinosinusitis can spread to the orbit and cause periobrital sinusitis (can be sight threatneing) Intracranial infection - infective rhinosisitus particularly of the frontal sinuse can spread intracranially to cause menigitis and intracranial abcsess formation
402
DEFINITION of rhinosinusitis (ie. required criteria)?
Inflammation of the nose and the paranasal sinuses characterised by TWO or more symptoms, one of which should be: - Nasal blockage/obstruction/congestion or discharge - Anterior/posterior nasal drip - Facial pain/pressure - Reduction or loss of smell And either of: - Endoscopic signs of: polyps, mucopurulent discharge or oedema in the middle meatus - CT changes - mucosal changes within the osteomeatal complex or sinuses
403
After how long might you consider nasal steroids and oral antibiotics in acute rhinosinusitis?
5 days
404
Predisposing factors for rhinosinusitis?
Allergy: atopy can predispose and associated Infections: Bacterial such as Staph aureus and streptococcus pneumonia and fungal infections Cillary impairment such as CF due to inability of cilia to clear mucus. Nasal polyps are present in about 40% of patients with cystic fibrosis. An anatomical abnormality such as spetal deviation and abnormal uncinate process leads to narrow infundibulum and occlusion of osteomeatal complex Immunocompromised host Aspirin hypersentivity Atmostpheric irritants: smoking, dusts, fumes Hormonal: pregnancy and hypothroidism, nasal congestion is high due to oestrogen and progesterone effect on nasal mucosal vascularity Trauma: surgical (oroantral fistula), nasal sinus fracture Swimming and diving
405
How might you investigate CRS?
Skin prick test Radiology o CT Sinuses If surgery planned / Atypical features to history or examination ( Not good for diagnosis as large numbers of asymptomatic patients have changes in the sinuses on CT scanning )
406
What is ARIA in terms of sinusitis
Allergic rhinosinusitis impact on asthma (classification of allergic rhinosinusitis) Duration: intermittent (less than 4 days a week less than 4 weeks), persistent (more than 4 days a week for more than 4 weeks) Severity Mild: normal daily activities, and sleep. No troublesome symptoms Moderate to severe: Impairment of daily activities and sleep. Troublesomesymptoms.
407
Investigating allergic rhinosinusitis?
Skin prick tests (SPT) for specific allergens RAST blood tests if SPT not possible
408
How does allergic rhinosinusitis cause symptoms?
Type 1 hypersensitivity reaction Allergic reaction leads to synthesis and release of arachidonic acid metabolites (prostaglandin D& leukotrienes) and mast cell degranulation to release histamine. The effect is to increase capillary permeability which leads to congestion, oedema, rhinorrhoea, sneezing and irritation
409
Management of allergic rhinosinusitis?
Conservative o Allergen avoidance o Nasal douching Medical o Antihistamines o Topical nasal steroids Immunotherapy
410
Peri - orbital cellulitis and odema
This is a site-threatening emergency which is more common in children and often results from direct spread of pus from the ethmoid sinus, or from thrombophlebitis of mucosal vessels in any of the sinuses. Patients develop pain followed by oedema of the eyelids and with orbital collection, the eye will become proptosed and eye movements will be reduced. There is a risk of blindness as a result of tension and septic necrosis of the optic nerve. Colour blindness is an early sign. A CT scan will confirm the collection and extent of the disease. Treatment with intravenous antibiotics, nasal decongestants, and urgent surgical drainage of any abscess is indicate
411
How might a septal haematoma present?
Post traumatic Palpable buldging septum Can detect on anterior rhinoscopy
412
What causes 'saddle nose deformity' (obvious step in nose)
Nasal septal haematoma left untreated leading to erosion of the septal cartillage
413
What recreational drug s commonly implicated in nasal septal defects and what is its method of damage?
Cocaine Disruption of blood supply to the cartillage
414
What should be done if a patient with epistaxis controlled by packing starts to spit up blood/.
Use tounge depressor and torch to visualise the oropharynx wall, if fresh blood is running down it remove anterior pack and post nasal pack or inflate nasopharangeal balloon followed by further anterior nasal packign
415
How is a patient with epistaxis managed if packing and cautery of the bleeding vessels were to fail?
GA to cauterise bleeding point/pack more effectively/ ligate sphenopalaetine and possibly anterior ethmoidal artery
416
Identify labled structures of the neck
Trachea Eosophagous Carotid sheath Spine
417
Boundaries of the anterior triangle of the neck
Lateral - Anterior boarder of the SCM (sternocleidomastoid) Medial - midline of neck Superior - Lower border of the mandible
418
Boundaries of the posterior triangle of the neck?
Medial: posterior boarder of sternocleidomastoid Inferior: middle third of clavicle Lateral: anterior edge of the trapezius
419
Sub triangles of the neck?
Submental Supraclavicular Occipital Carotid Supramandibular (digastric) Omotracheal (muscular)
420
How is retropharyngeal abscess investigated?
CT neck
421
Associated mortality in retropharyngeal abscess
Airway problems Mediastinitis
422
What is the retropharyngeal space?
Potential space behind the pharynx and anterior to the prevertable fascia extending from the base of the skull to the mediastinum.
423
Retropharyngeal abscess
424
What's Ludwing's Angina?
Infection of the space between the FLOOR OF THE MOUTH and MYLOHYOID - associated with dental infection
425
Presentation of Ludwig's angina?
Swelling of the floor of the mouth Painful mouth Protuding tongue Airway compromise Drooling
426
How might you investigate Ludwig's angina?
CT neck OPG
427
Management of Ludwig's angina?
Secure airway IV abx Surgical drainage of any collections
428
What is the parapharyngeal space?
Potential space postero-lateral to the oropharynx and nasopharynx which is divided by the styloid process. Contains carotid sheath
429
What is a parapharyngeal abscess?
Abcess in parapharyngeal space (potential space postero-lateral to the oropharynx and nasopharynx which is divided by the styloid process) Presents ins a similar manner to quinsy (peritonsillar abscess)
430
How might a parapharyngeal abscess present?
Hx febrile illness Odynophagia Tismus Reduced neck movement Swelling in the neck around the upper part of the SCM
431
Management of parapharyngeal abscess
Secure airway if any concerns IV abx Surgical drainage
432
Management of epiglottitis
Do not examine patient as this may precipitate airway obstruction and keep them in a calm environment with their parents to avoid undue distress (ditto) If possible, child taken to theatre to be intubated by a pediatric anesthetist with an ENT surgeon on standby to do a surgical airway if intubation not possible, if transfer unsafe intubation in A&E IV abx, pts usually respond well and can be intubated after a couple of days
433
How should neck lumps be investigated?
Ultrasound guided fine needle aspiration (except for pulsitile masses)
434
What might cause a neck lump and where?
Parotid neoplasam - anterior to ear Jugulodiagastric - angle of mandible Submandibular gland - inferior border of madnible Carotid body tumor or aneurysm - at bifurcation of common carotid artery (usually C3-C5 level) Thryoglossal cysts - in midline between hyoid bone and thyroid gland Brachial cyst - anterior border of sternocleidomastoid Thyroid nodule - level of thryoid Virchow's node - supravicular fossa node (may represent mets)
435
Regions of the pharynx and oral cavity?
Oral cavity – Extends from the lips to the posterior soft palate. Nasopharynx – Superiorly bound by the base of the skull, and inferiorly by an imaginary line at the level of the soft palate o Contents include the adenoids and eustachian tube opening Oropharynx – Extends from the level of the soft palate to the superior border of the epiglottis o Contents include the palatine tonsils, anterior and posterior tonsillar pillars Hypopharynx – Extends down from the superior border of the epiglottis to the inferior border of the cricoid cartilage. It is posterior to the larynx.
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Muscle of the pharynx vs rest of the GI tract
Unlike the rest of the GI tract where the muscular layers are arranged in circular and longitudinal layers, the pharynx has only a circular layer which is formed in principle by four muscles; Superior, middle, and inferior constrictors, and cricopharyngeus
437
What is s Killian’s dehiscence?
Pharyngeal weak point formed between the horizontal fibers of the cricopharyngeus (CP) muscle and the oblique fibers of the inferior pharyngeal constrictors (IPCs) This is the site of pharyngeal pouch formation
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How does a pharyngeal pouch present?
Pharyngeal pouches typically present with dysphagia, delayed regurgitation of food and sometimes recurrent chest infections from aspirated food.
439
Where do pharyngeal pouches occur?
Killian's triangle (pharyngeal weak point formed between the horizontal fibers of the cricopharyngeus (CP) muscle and the oblique fibers of the inferior pharyngeal constrictors (IPCs)) - also known as Killian's dehiscence.
440
Muscles of the pharynx responsible for its elevation and depression?
stylopharyngeus, salpingopharyngeus, and palatopharyngeus.
441
What imagaing is this and what does it show?
Barium swallow Pharangeal pouch
442
What is the most common cause of sleep apnoea in children (VS obesity in adults)
adenotonsillar hypertrophy
443
What bloods might you perform when investigating sleep apnoea and why
TFTs - ?hypothyroidism
444
Why might ECG and CXR be warrented in possible sleep apnoea?
 CXR – ?Signs of obstructive lung disease  ECG – ?Signs of right ventricular failure
445
Bacterial causes of tonsilitis?
 Beta-haemolytic Streptococci  Staphylococci  Streptococcus pneumoniae  Haemophilus influenza  Escherischia coli
446
Viral causes of tonsilitis?
 Rhinovirus  Adenovirus  Enterovirus  Epstein-Barr virus (EBV)
447
Most common cause of bacterial tonisilitis?
group A streptococcus (Streptococcus pyogenes).
448
Clinical features of tonsilitis?
 Pyrexia > 38  Dysphagia  Lymphadenopathy (anterior cervical lymphadenopathy)  Odynophagia  Trismus  Swollen tonsils with or without exudate  Otalgia (Referred pain)
449
Lymphadenopathy in tonsilitis?
There may be anterior cervical lymphadenopathy, which refers to swollen, tender lymph nodes in the anterior triangle of the neck (anterior to the sternocleidomastoid muscle and below the mandible). The tonsillar lymph nodes are just behind the angle of the mandible (jawbone).
450
Why should amoxicillin be avoided in tonsilitis?
Treatment with amoxicillin should be avoided as this will cause a maculopapular rash in the presence of EBV (glandular fever). Furthermore, patients with EBV should be advised to avoid contact sports for 2-3 months as the virus commonly causes hepatosplenomegaly.
451
Waldeyer’s Tonsillar Ring
In the pharynx, at the back of the throat, there is a ring of lymphoid tissue. There are six areas of lymphoid tissue in Waldeyer’s ring, comprising of the adenoids, tubal tonsils, palatine tonsils and the lingual tonsil. The palatine tonsils are the ones typically infected and enlarged in tonsillitis. These are the tonsils on either side at the back of the throat.
452
What is the centor criteria?
The Centor criteria can be used to estimate the probability that tonsillitis is due to bacterial infection and will benefit from antibiotics. A score of 3 or more gives a 40 – 60 % probability of bacterial tonsillitis, and it is appropriate to offer antibiotics. A point is given if each of the following features are present: Fever over 38ºC Tonsillar exudates Absence of cough Tender anterior cervical lymph nodes (lymphadenopathy)
453
What is the FeverPAIN score?
The FeverPAIN score is an alternative to the Centor criteria. A score of 2 – 3 gives a 34 – 40% probability, and 4 – 5 gives a 62 – 65% probability of bacterial tonsillitis: Fever during previous 24 hours P – Purulence (pus on tonsils) A – Attended within 3 days of the onset of symptoms I – Inflamed tonsils (severely inflamed) N – No cough or coryza
454
Management of tonsilitis?
Consider admission if the patient is immunocompromised, systemically unwell, dehydrated, has stridor, respiratory distress or evidence of a peritonsillar abscess or cellulitis. When tonsillitis is the most likely diagnosis, calculate the Centor criteria or FeverPAIN score. Educate patients with likely viral tonsillitis and give safety net advice about when to seek medical advice. Advise simple analgesia with paracetamol and ibuprofen to control pain and fever. NICE clinical knowledge summaries suggest advising patients to return if the pain has not settled after 3 days or the fever rises above 38.3ºC. Starting antibiotics or an alternative diagnosis should be considered. Consider prescribing antibiotics if the Centor score is ≥ 3, or the FeverPAIN score is ≥ 4. Also, consider antibiotics if they are at risk of more severe infections, such as young infants, immunocompromised patients or those with significant co-morbidity, or a history of rheumatic fever. Delayed prescriptions can be considered. This involves educating patients or parents about the likely viral nature of the sore throat and providing a prescription to be collected only if the symptoms worsen or do not improve in the next 2 – 3 days. Draining of peritonsilar abcsess
455
What antibiotic is used to treat tonsilitis
Penicillin V (also called phenoxymethylpenicillin) for a 10-day course is typically first-line. It has a relatively narrow spectrum of activity and is effective against Streptococcus pyogenes. Clarithromycin is the usual first-line choice in true penicillin allergy.
456
Complications of tonsilitis?
Peritonsillar abscess, also known as quinsy Otitis media, if the infection spreads to the inner ear Scarlet fever Rheumatic fever Post-streptococcal glomerulonephritis Post-streptococcal reactive arthritis
457
Quinsy (peritonsilar abscess)
458
What is quinsy?
Peritonsilar abscess These normally present with a sore throat that is lateralised to one side and a “hot potato” voice. They may be amenable to drainage under local anaesthetic Peritonsillar abscess arises when there is a bacterial infection with trapped pus, forming an abscess in the region of the tonsils. Peritonsillar abscess is a complication of untreated or partially treated tonsillitis, although it can arise without tonsillitis. Quinsy can occur just as frequently in teenagers and adults as it does in children, unlike tonsillitis which is much more common in children.
459
Presentation of quinsy?
Patients present with similar symptoms to tonsillitis: Sore throat Painful swallowing Fever Neck pain Referred ear pain Swollen tender lymph nodes Additional symptoms that can indicate a peritonsillar abscess include: Trismus, which refers to when the patient is unable to open their mouth Change in voice due to the pharyngeal swelling, described in textbooks as a “hot potato voice” Swelling and erythema in the area beside the tonsils
460
Quinsy - causative microorganism
Quinsy is usually due to a bacterial infection. The most common organism is streptococcus pyogenes (group A strep), but it is also commonly caused by staphylococcus aureus and haemophilus influenzae.
461
Management of peritonsillar abscess?
Patients should be referred to the hospital under the ENT team’s care for needle aspiration or surgical incision and drainage to remove the pus from the abscess. Quinsy typically has an underlying bacterial cause. Therefore, antibiotics are appropriate before and after surgery. A broad-spectrum antibiotic such as co-amoxiclav would be an appropriate choice to cover the common causes, but local guidelines will guide antibiotic selection according to local bacterial resistance. Some ENT surgeons give steroids (i.e. dexamethasone) to settle inflammation and help recovery, although this is not universal.
462
Indications for tonsilectomy?
The SIGN guidelines (2010) give the indications for tonsillectomy. The number of episodes of acute sore throat they specify for a tonsillectomy are: 7 or more in 1 year 5 per year for 2 years 3 per year for 3 years Other indications are: Recurrent tonsillar abscesses (2 episodes) Enlarged tonsils causing difficulty breathing, swallowing or snoring
463
Tonsilectomy - potential complications
Sore throat where the tonsillar tissue has been removed (this can last 2 weeks) Damage to teeth Infection Post-tonsillectomy bleeding (can be significant and an emegrency, can occur as late as 2 weeks after tonsilectomy) Risks associated with a general anaesthetic
464
Post-tonsillectomy bleeding - management?
Call the ENT registrar and get them involved early Get IV access and send bloods including an FBC, clotting screen, group and save and crossmatch Keep the patient calm and give adequate analgesia Sit them up and encourage them to spit out the blood rather than swallowing Make the patient nil by mouth in case an anaesthetic and operation is required IV fluids for maintenance and resuscitation, if required If there is severe bleeding or airway compromise, call an anaesthetist. Intubation may be required. Before going back to theatre there are two options for stopping less severe bleeds: Hydrogen peroxide gargle Adrenalin soaked swab applied topically
465
How do head and neck cancers typically present?
Dysphonia (esp laryngeal malignancy which may cause hoarseness) Dysphagia/odynaphagia Dyspnoea –stridor from narrowing of airway, especially laryngeal tumours Neck Mass Pain from site of pathology or referred e.g. to ear Bleeding from nose or mouth depending on site of primary(rare presentation) Nasal blockage –normally unilateral progressive for nasal/nasopharyngeal pathology
466
Most common histopathological type of head and neck cancer?
The majority (90%) are squamous cell carcinomas.
467
TNM staging
T= Tumour size, 1 (small) – 4 (big) N= Nodal Metastasis, 0 (no nodes) - N3 (big/multiple nodes) M= Distant metastasis 0 (none) – 1 (present)
468
Head and neck cancers: risk factors?
Alcohol Chewing tobacco Beetle nut chewing for oral cavity malignancies Chinese ethnic origin for nasopharyngeal malignancy HPV strain 16 EBV infection Smoking
469
Beetle nut chewing increases the risk of which type of cancer?
Oral cavity mallignancies
470
Investigation of primary tumour - head and neck cancers
Examination under anaesthetic o Also called Panendoscopy or laryngopharyngo-oesophagoscopy in H&N o Purpose – Biopsy for histological diagnosis, assess size of tumour, look for second primary  CT Neck o Purpose – assess size of tumour and neck node metastasis
471
Investigating neck lumps - head and neck cancer
If a patient has a biopsy proven primary squamous cell carcinoma in the head and neck it can be assumed that any palpable cervical lymphadenopathy is secondary to this primary and the CT scan of the neck to assess the primary will give all the information required for staging. If this is not the case any palpable neck masses should be investigated with an ultrasound guided fine needle aspiration (FNA). While blind (i.e. no US) FNA can be done the ultrasound will increase the accuracy of the specimen taken and will give extra information on the mass being sampled.
472
Sometimes patients with head and neck squamous cell carcinoma may present with neck metastases with no obviously primary even after examination under anaesthetic and imaging - how should these be diagnosed?
These should be diagnosed with a FNA of the neck mass
473
Role of biopsy in suspicious neck lumps
Biopsy can lead to seeding and poor prognosis, however FNA is not so good for other causes of cervical lymphadenopathy other than SCC, such as tuberculosis and lymphoma which often require an open biopsy so in these cases an FNA should be carried out to exclude SCC before an open biopsy is done
474
Head and neck cancers - investigation of distant mets
CT chest are routinely done to check for metastasis in the chest, the commonest site of distant metastasis. Other investigations are not routinely done unless there is suspicion of other distant metastesis
475
Management of head and neck cancers?
Treatment needs to be aimed at the primary site and also any neck metastases. In some head and neck cancers there is a high rate of metastasis to the neck so even if no neck metastasis are detected treatment will still be given to the neck (if curative aim) Radiotherapy – to the primary site +/- to the neck, +/- chemotherapy - curative or palliative Endoscopic surgery - e.g. laser resection Open surgery  To primary site – e.g. laryngectomy  To neck – i.e. neck dissection
476
Descriptions to note the location of a neck lump?
Anterior triangle Posterior triangle Midline (vertically along the centre of the neck)
477
Neck lump differentials - adult
Normal anatomy - ie bony prominence Skin abcess Lymphadenopathy Tumour (SCC, sarcoma) Lipoma Goitre Salivary gland stone or infection Carotid body tumour/anyerysm Haematoma Thyroglossal cyst Brachial cyst
478
Neck lump differentials more specific to children?
Cystic hygromas Dermoid cyst Haemangioma Venous malformation
479
What should be looked for when examining a neck lump to distinguish its features?
Location (anterior/posterior triangle or midline) Size Shape (oval, round, irregular) Consistency (hard, soft, rubbery) Mobile or tethered to underlying tissue or skin Warmth Tenderness (?infection) Pulsatile (think carotid body anyeurysm) Movement with swallowing (thyroid) or tounge protusion (thyroglossal cyst) Transillunination with light (cystic hygroma)
480
What should be looked for when examining a patient with a neck lump to help establish the cause (other than the actual lumps features)
Weight loss (malignancy, hyperthyroid) ENT infection Skin pallor and bruising - leukaemia Focal chest sounds (lung ca) Clubbing (lung cancer) Hepatosplenomegaly (leukaemia)
481
For which patients with a neck lump is a 2 week wait referral warranted?
Unexplained neck lump in over 45s A persistent neck lump at any age
482
How urgent is an ultrasound in a patient with a neck lump that is growing in size?
Within 2 weeks if under 25 Within 48hrs if 25+ If suggestive of soft tissue sarcoma requires a 2WW
483
What bloods might be undertaken in a patient with a neck lump?
Dependent on the suspected cause FBC and blood film for leukaemia and infection HIV test Monospot test or EBV antibodies for infectious mononucleosis Thyroid function tests for goitre or thyroid nodules Antinuclear antibodies for systemic lupus erythematosus Lactate dehydrogenase (LDH) is a very non-specific tumour marker for Hodgkin’s lymphoma
484
Investigating a neck lump?
Bloods (FBC, blood film, TFTs, HIV, monospot/EBV ab, ANA, LDH) Imaging (USS first line, CT or MRI, nuclear medicine scan - toxic thyroid nodules, PET scan for metastatic cancer) Biopsy (FNA, core, incision, removal of lump)
485
Causes of lymphadenopathy?
REACTIVE: URTI, dental infection, tonsillitis INFECTED: HIV, TB, EBV INFLAMMATORY CONDITIONS: SLE, sarcoidosis MALIGNANCY: lymphoma, leukaemia, metastasis
486
Which of the cervical lymph nodes, if enlarged, are the most concerning for malignancy?
Supraclavicular lymph nodes (malignancy of chest of abdomen)
487
Red flags - lymphadenopathy?
Unexplained - not associated with infection Persistently enlarged > 3cm diameter Abnormally shaped (ie oval with length more than double width) Hard or rubbery Thethered or fixed to skin or underlying tissues Associated constitutional symptoms
488
Lymphadenopathy- infectious mononucleosis
Infectious mononucleosis is a cause of lymphadenopathy. It is caused by infection with the Epstein Barr virus (EBV) and most often affects teenagers and young adults. It is found in the saliva of infected individuals and may be spread by kissing or sharing cups, toothbrushes and other equipment that transmits saliva. It presents with Fever Sore throat Fatigue Lymphadenopathy Mononucleosis can present with an intensely itchy maculopapular rash in response to amoxicillin or cefalosporins. The first-line investigation is the Monospot test. It is also possible to test for IgM (acute infection) and IgG (immunity) to the Epstein Barr virus. Management is supportive. Patients should avoid alcohol (risk of liver impairment) and contact sports (risk of splenic rupture).
489
Key finding in lymph node biopsy in patients with Hodgkin’s lymphoma?
Reed Sternberg cells
490
What are B symptoms in lymphoma?
Systemic symptoms, including: Fever Weight loss Night sweats
491
What are lymphomas?
Lymphomas are a group of cancers that affect the lymphocytes inside the lymphatic system. These cancerous cells proliferate within the lymph nodes and cause the lymph nodes to become abnormally large (lymphadenopathy). There are two categories of lymphoma: Hodgkin’s lymphoma and non-Hodgkin’s lymphoma. Hodgkin’s lymphoma is a specific disease and non-Hodgkins lymphoma encompasses all the other lymphomas.
492
What cells proliferate in lymphoma?
Lymphocytes
493
What age of patient typically presents with lymphoma
Binomial age distribution Peak around 20 and 75 years
494
Lymphadenopathy - lymphoma
Lymphadenopathy is the key presenting symptom. The enlarged lymph node or nodes might be in the neck, axilla (armpit) or inguinal (groin) region. They are characteristically non-tender and feel “rubbery”. Some patients will experience pain in the lymph nodes when they drink alcohol.
495
What staging system is used for lymphoma?
Ann Arbor staging system
496
Lymphadenopathy- leukaemia
Leukaemia is the name for cancer of a particular line of the stem cells in the bone marrow. This causes the unregulated production of certain types of blood cells. They can be classified depending on how rapidly they progress (chronic is slow and acute is fast) and the cell line that is affected (myeloid or lymphoid) to make four main types: Acute myeloid leukaemia Acute lymphoblastic leukaemia Chronic myeloid leukaemia Chronic lymphocytic leukaemia The presentation of leukaemia is quite non-specific. If leukaemia appears on your list of differentials then get an urgent full blood count. Some typical features are: Fatigue Fever Pallor due to anaemia Petechiae and abnormal bruising due to thrombocytopenia Abnormal bleeding Lymphadenopathy Hepatosplenomegaly
497
What is a goitre?
Generalised swelling of the thyroid gland
498
Causes of goitre?
Graves disease (hyperhtyroidism) Toxic multinodular goitre (hyperthyroidsm) Hashimoto's thyroiditis (hypothyroidism) Iodine deficiency Lithium
499
What are the three salivary gland locations?
Parotid glands Submandibular glands Sublingal glands
500
Why might individual lumps in the thyroid occur?
Benign hyperplastic nodules Thyroid cysts Thyroid adenomas (benign tumours that can release excessive thyroid hormone) Thyroid cancer (papillary or follicular) Parathyroid tumour
501
What are the main reasons salivary glands may be enlarged?
Sialolithasis - stones blocking the drainage of the glands Infection Tumours (benign or mallignant)
502
What cells does the carotid body contain and what is their role?
Glomus cells - chemoreceptors that detect the bloods oxygen, CO2 and pH. Paraganglia - group of glomus cells
503
What is a paragangliomas? Where do they present and what are there features?
Tumour of the glomus cells of the carotid body. Usually benign and slow growing. Painless, pulsatile lump which is mobile laterally (not vertically) with associated bruit found in the anterior triangle of the neck (near the angle of the mandible)
504
When might a carotid body tumour/paraganglioma cause symptoms?
Compression of the glospharygeal (IX) nerve, vagus nerve (X), acessory nerve (XI) or hypoglosssal (XII) nerve
505
What might compression of the vagus nerve (e.g. carotid body tumour) result in?
Horners syndrome: Ptosis, miosis, anhidrosis
506
Compression of which nerve can cause Horner's syndrome?
Vagus nerve
507
Triad of symptoms in Horner's syndrome?
Ptosis Miosis Anhidrosis
508
Characteristic findings on imagine of a paraganglioma (carotid body tumour)
A characteristic finding on imaging investigations is splaying (separating) of the internal and external carotid arteries (lyre sign).
509
How are paragangliomas (carotid body tumours) mostly treated?
Surgical removal
510
What are lipomas and how do they appear on examination? How are they managed?
Benign tumours of adipose tissue Soft Painless Mobile Absence of skin changes They are typically treated conservatively with reassurance (after excluding other pathology). Alternatively, they can be surgically removed.
511
Thyroglossal cyst O/E
Midline of neck Mobile Non tender Soft Fluctuant Move up and down with movement of the tongue (due to connection between thyroglossal duct and tounge) Can use USS or CT to confirm diagnosis
512
How are thyroglossal cysts managed and why?
Surgical removal: To confirm diagnosis on histology To prevent infection of the cyst (causing a hot, tender and painful lump) May recurr after surgical removal
513
What kind of neck lump moves on toungue protusion?
Thyroglossal cyst
514
What is a key differential for a thyroglossal cyst (since it occurs at a similar location)
Ectopic thyroid tissue
515
Why does a thyroglossal cyst occurs?
Thyroid gland starts developing in the fetus at the base of the toungue It graduall travels down the neck to final position in front the the trachea and beaneath the larynx It leaves a track behind called the thyroglossal duct which usually regresses but can persist and give rise to a fluid-filled cyst
516
Why do brachial cysts arise?
Congenital abnormality Failure of complete second brachial cleft formation This leaves space surrounded by epitherial tissue in the LATERAL aspect of the neck which can fill with fluid
517
How do brachial cysts present?
Soft Round Cystic swelling Between angle of the jaw and sternocleidomastoid muscle in the anterior triangle of the neck Usually after 10 years of age once the cyst becomes noticible or infected
518
How do brachial cysts present?
Soft Round Cystic swelling Between angle of the jaw and sternocleidomastoid muscle in the anterior triangle of the neck Usually after 10 years of age once the cyst becomes noticible or infected
519
How are brachial cysts managed?
Conservative, without any active intervention, where it is not causing problems Surgical excision where recurrent infections are occurring, there is diagnostic doubt, or it is causing other problems
520
Round soft non-tender lump just anterior to the SCM presenting in a teenager?
Likely brachial cyst (most commonly originating from the second brachial cleft)
521
Potential areas of head and neck cancers
Nasal cavity Paranasal sinuses Mouth Salivary gland Pharynx (throat) Larynx (epiglottis, supraglottic, vocal cords, glottis and sub glottis)
522
The HPV vaccine protects against strains 6, 11, 16 and 18. Which of these is most commonly involved in head and neck cancer?
16
523
Head and neck cancer management?
Management will be guided by the multidisciplinary team (MDT). It will be dependent on the location, stage and individual patient factors. Staging usually involves the TNM staging system, grading the tumour, node involvement and metastases. Treatment may involve any combination of: Chemotherapy Radiotherapy Surgery Targeted cancer drugs (i.e., monoclonal antibodies) Palliative care Cetuximab is an example of a monoclonal antibody used in treating squamous cell carcinomas of the head and neck. It may also be used to treat bowel cancer. It targets epidermal growth factor receptor, blocking the activation of this receptor and inhibiting the growth and metastasis of the tumour.
524
What is cetuximab and how can it treat SCC?
Cetuximab is an example of a monoclonal antibody used in treating squamous cell carcinomas of the head and neck. It may also be used to treat bowel cancer. It targets epidermal growth factor receptor, blocking the activation of this receptor and inhibiting the growth and metastasis of the tumour.
525
What is glossitis?
Glossitis refers to an inflamed tongue. The tongue becomes red, sore and swollen. The papillae of the tongue atrophy (shrink), giving the tongue a smooth appearance. It is sometimes described as “beefy”.
526
Causes of glossitis?
Iron deficiency anaemia B12 deficiency Folate deficiency Coeliac disease Injury or irritant exposure
527
What is angioedema and what are the top three causes?
Angioedema refers to fluid accumulating in the tissues, resulting in swelling. It can affect a number of areas, such as the limbs, face and lips. It can affect the tongue, causing the tongue to swell. The three top causes of angioedema to remember for exams are: Allergic reactions ACE inhibitors C1 esterase inhibitor deficiency (hereditary angioedema)
528
Angioodema
529
Glossitis
530
What is oral candisasis?
Oral candidiasis is also called oral thrush. It refers to an overgrowth of candida albicans, a type of fungus, in the mouth. This results in white spots or patches that coat the surface of the tongue and palate.
531
Causes of oral candidiasis?
Inhaled corticosteroids (particularly with poor technique, not using a spacer and not rinsing with water afterwards) Antibiotics (disrupt the normal bacterial flora giving candida a chance to thrive) Diabetes Immunodeficiency (consider HIV) Smoking
532
Management of oral candidiasis?
Miconazole gel Nystatin suspension Fluconazole tablets (in severe or recurrent cases)
533
What is geographic tongue?
Inflammatory condition where patches of epithelium and papillae of the tongue are lost. Patches are irregular shaped (resembelling a map) The condition tends to relapse and remit, with episodes of the abnormal tongue appearance that can last days to weeks before resolving or changing. The cause of these changes is not known. Geographic tongue is a benign condition and does not cause any harmful effects. It does not usually require any treatment. Symptoms such as discomfort or burning are sometimes treated with topical steroids or antihistamines.
534
Geographic tongue
535
What might geographic tongue be associated with?
Geographic tongue often occurs without any associations. However, it can be related to: Stress and mental illness Psoriasis Atopy (asthma, hayfever and eczema) Diabetes
535
What might geographic tongue be associated with?
Geographic tongue often occurs without any associations. However, it can be related to: Stress and mental illness Psoriasis Atopy (asthma, hayfever and eczema) Diabetes
536
What is a strawberry tongue and what are the key causes?
A strawberry tongue appearance occurs when the tongue becomes swollen and red, and the papillae become enlarged, white and prominent. The two key causes of a strawberry tongue to remember are: Scarlet fever Kawasaki disease
537
Strawberry tongue
538
What causes black hairy tongue and how is it managed?
Black hairy tongue results from decreased shedding (exfoliation) of keratin from the tongue’s surface. The papillae elongate and take on the appearance of hairs. Bacteria and food cause the dark pigmentation. This gives the appearance of black hair on the tongue. Patients may also report sticky saliva and a metallic taste. Black hairy tongue may be due to dehydration, a dry mouth, poor oral hygiene and smoking. Management involves ensuring adequate hydration, gentle brushing of the tongue and stopping smoking.
539
Black hairy tongue results from decreased shedding (exfoliation) of keratin from the tongue’s surface. The papillae elongate and take on the appearance of hairs. Bacteria and food cause the dark pigmentation. This gives the appearance of black hair on the tongue. Patients may also report sticky saliva and a metallic taste.
540
What is Leukoplakia
White patches on mouth (tongue/buccal mucosa)
541
Why might leukoplakia require a biopsy?
It is a precancerous condition, meaning it increases the risk of squamous cell carcinoma of the mouth. They may require a biopsy to exclude abnormal cells (dysplasia) or cancer.
542
How is leukoplakia managed?
Management involves stopping smoking, reducing alcohol intake, close monitoring and potentially laser removal or surgical excision.
543
Leukoplakia
544
What is erythroplakia/eythroleukoplakia and why does it require management?
Erythroplakia is similar to leukoplakia (white patches on tongue/bucal mucosa), except the lesions are red. Erythroleukoplakia refers to lesions that are a mixture of red and white. Both erythroplakia and erythroleukoplakia are associated with a high risk of squamous cell carcinoma and should be referred urgently to exclude cancer.
545
Erythroplakia/erythroplasia
546
What is lichen planus and what patterns does it appear in?
Lichen planus is an autoimmune condition that causes localised chronic inflammation of the skin. The skin has shiny, purplish, flat-topped raised areas with white lines across the surface called Wickham’s striae. It usually occurs in patients over 45 and is more common in women. Lichen planus can also affect the mucosal membranes, including the mouth. Often it only affects the mouth. In the mouth, it can take three patterns: Reticular Erosive Plaque
547
Lichen planus
548
Lichen planus - reticular pattern
A reticular pattern involves a net-like web of white lines called Wickham’s striae.
549
Lichen plannus reticular pattern (Wickham's striae)
550
Lichen planus - erosive lesions
Erosive lesions are where the surface layer of the mucosa is eroded, leaving bright red and sore areas of mucosa.
551
Erosive lichen planus
552
Lichen planus - plaque pattern
Plaques are larger continuous areas of white mucosa.
553
Oral lichen planus plaque pattern
554
Management of oral lichen planus
Smoking cessation Good oral hygiene Topical steroids
555
What is gingivitis and how does it present?
Gum inflammation Swollen gums Bleeding after burshing Halitosis (bad breath)
556
What might gingivitis lead to?
Periodontitis refers to severe and chronic inflammation of the gums and the tissues that support the teeth. This often leads to loss of teeth. Acute necrotising ulcerative gingivitis is a rapid onset of more severe inflammation in the gums. It presents similarly to gingivitis, however, it is painful. Anaerobic bacteria usually cause this.
557
Risk factors for gingivitis?
Palque build up - inadequete brushing Smoking Diabetes Malnutrition Stress
558
What is plaque?
Bacteria live in plaque, damaging the teeth and gums. Hardened plaque is called tartar.
559
Gingivitis management?
Good oral hygiene Stopping smoking Dental hygienist treatment to remove plaque and tartar Chlorhexidine mouth wash Antibiotics for acute necrotising ulcerative gingivitis (e.g., metronidazole) Dental surgery if required
560
What is gingivits and what causes it?
Gingival hyperplasia refers to abnormal growth of the gums. The gums are notably enlarged around the teeth. Possible causes of gingival hyperplasia include: Gingivitis Pregnancy Vitamin C deficiency (scurvy) Acute myeloid leukaemia Medications, particularly calcium channel blockers, phenytoin and ciclosporin
561
Relations of the submandibular gland
Two parts, superficial and deep to the posterior boarder of the mylohiod in a U shaped pattern. Superficial part: in the digastric triangle, partially deep to the maindible, covered superficially by the plasmyta and the skin Deep part: between myohyoid and the hypoglossus Duct runs from deep part and is crossed by the lingual nerve Hypoglossal nerve runs deep to the gland Cervical branch of the facial nerve runs superfically to the gland
562
Removal of which gland might result in damage to the cervical branch of the facial nerve?
Submandibular (cervical branch runs superfically to gland)
563
What nerve damage might occur during removal of the submandibular gland?
Lingual Hypoglossal Cervical branch of CN7
564
Muscular contents of the posterior triangle
Inferior belly of omohyoid muscle crosses SCM to anterior triangle A number of vertebral muscles (covered by prevertebral fascia) form the floor of the posterior triangle: Splenius capitis Levator scapulae Anterior, middle and posterior scalenes
565
Vascular contents of the posterior triangle
External jugular vein (superficially) after crossing SCM Within the posterior triangle, the external jugular vein pierces the investing layer of fascia and empties into the subclavian vein.
566
Anatomical clinical relevance of external juglar vein
The external jugular vein has a relatively superficial course down the neck, leaving it vulnerable to damage. If it is severed, in an injury such as a knife slash, its lumen is held open – this is due to the thick layer of investing fascia Air will be drawn into the vein, producing cyanosis, and can stop blood flow through the right atrium. This is a medical emergency, managed by the application of pressure to the wound – stopping the bleeding, and the entry of air. The transverse cervical and suprascapular veins also lie in the posterior triangle The subclavian, transverse cervical and suprascapular veins are accompanied by their respective arteries in the posterior triangle.
567
Nerve contents of the posterior triangle
Accessory nerve (XI) crosses the posterior triangle in an oblique, inferoposterior direction, within the investing layer of fascia. It lies relatively superficial in the posterior triangle, leaving it vulnerable to injury. The cervical plexus forms within the muscles of the floor of the posterior triangle. A major branch of this plexus is the phrenic nerve, which arises from the anterior divisions of spinal nerves C3-C5. It descends down the neck, within the prevertebral fascia, to innervate the diaphragm. Other branches of the cervical plexus innervate the vertebral muscles, and provide cutaneous innervation to parts of the neck and scalp. The trunks of the brachial plexus also cross the floor of the posterior triangle.
568
Nerve point of the neck
For anaesthesia of the neck area, a cervical plexus block can be used. Local anaesthetic is injected along the posterior border of sternocleidomastoid at the junction of its superior and middle thirds. This junction is where the cutaneous branches of the cervical plexus emerge, known as the nerve point of the neck.
569
Subdivisions of the posterior triangle
The omohyoid muscle splits the posterior triangle of the neck into two: The larger, superior part is termed the occipital triangle. The inferior triangle is known as the subclavian triangle and contains the distal portion of the subclavian artery. It is also known as the omoclavicular or supraclavicular triangle.
570
Where would a parotid gland tumour cause a lump?
Neck mass anterior to the ear
571
How might a parotid gland cancer present?
Lump anterior to ear Palpable lymph nodes in neck Facial nerve palsy (drooling, face droop, etc)
572
What would an acessory nerve plasy cause?
Shoulder drop
573
Freys syndrome
Freys syndrome is a rare neurological disorder resulting from damage to or near the parotid glands responsible for making saliva, and from damage to the auriculotemporal nerve often from surgery.
574
Risks of thryoid surgery on a hyperthryoid patient
High risk of bleeding Thyrotoxic storm
575
Risk of thyroid surgery on a euthyroid patient?
Hypothyroidism Damage to parathyroid glands - hypoparathyroidism and hypocalcemia RLN damage Bleeding infection
576
Course of the recurrent laryngeal nerve
The nerves branch off the vagus nerves in the neck Left side loops under the aortic arch The right loops under the right subclavian artery Both then pass upawrds to supply the larygeal muscles passing deep to the cricothyroid joint
577
What are aphthous ulcers?
Aphthous ulcers are very common, small, painful ulcers of the mucosa in the mouth. They have a well-circumscribed, punched-out, white appearance.
578
Apthous ulcers
579
Why might apthous ulcers occur?
Aphthous ulcers commonly occur in otherwise healthy people, with no underlying cause. They may be triggered by emotional or physical stress, trauma to the mucosa or particular foods. They may also be an indication of underlying conditions, notably: Inflammatory bowel disease (Crohn’s disease and ulcerative colitis) Coeliac disease Behçet disease Vitamin deficiency (e.g., iron, B12, folate and vitamin D) HIV
580
Management of aphthous ulcers?
Aphthous ulcers usually heal within 2 weeks. Manageable ulcers do not require any intervention. Topical treatments can be used to treat symptoms, including: Choline salicylate (e.g., Bonjela) Benzydamine (e.g., Difflam spray) Lidocaine Topical corticosteroids can be used in more severe ulcers. These may reduce the duration and severity of symptoms. Options include: Hydrocortisone buccal tablets applied to the lesion Betamethasone soluble tablets applied to the lesion Beclomethasone inhaler sprayed directly onto the lesion The NICE guidelines on suspected cancer (updated January 2021) recommend a two week wait referral in patients with “unexplained ulceration” lasting over 3 weeks.
581
Facial nerve pathway
The facial nerve exits the brainstem at the cerebellopontine angle. On its journey to the face, it passes through the temporal bone and parotid gland. It then divides into five branches that supply different areas of the face: Temporal Zygomatic Buccal Marginal mandibular Cervical
582
Motor function of the facial nerve?
Muscles of facial expression Stapedius Posterior digastric, stylohyoid and platysma muscles in the neck
583
Sensory function of the facial nerve?
Anterior 2/3 of the tongue
584
Parasympathetic function of the facial nerve
Submandibular and salivary glands Lacrimal glands
585
Significance of distinguishing between and upper and lower motor neuron facial nerve palsy?
It is essential to make this distinction because, in a patient with a new-onset upper motor neurone facial nerve palsy, you should be referring immediately with a suspected stroke. In contrast, patients with a lower motor neurone facial nerve palsy can be managed with less urgency.
586
How to differntiate between an upper and lower motor neuron palsy of the facial nerve
Each side of the forehead has upper motor neurone innervation by both sides of the brain. However, each side of the forehead only has lower motor neurone innervation from one side of the brain. In an upper motor neurone lesion, the forehead will be spared, and the patient can move their forehead on the affected side. In a lower motor neurone lesion, the forehead will NOT be spared, and the patient cannot move their forehead on the affected side. You can differentiate between an upper and lower motor neurone lesion by asking the patient to raise their eyebrows. If they can raise both eyebrows and wrinkle both sides of the forehead, the patient has an upper motor neurone lesion. If the eyebrow on the affected side cannot be raised and the forehead remains smooth, the patient has a lower motor neurone lesion.
587
Facial nerve palsy - UMN causes
Unilateral upper motor neurone lesions occur in: Cerebrovascular accidents (strokes) Tumours Bilateral upper motor neurone lesions are rare. They may occur in: Pseudobulbar palsies Motor neurone disease
588
Facial nerve plasy - LMN causes
Bells plasy Ramsy hunt syndrome Infection Trauma Tumour Systemic disease
589
What is Bell's Palsy and how is it managed?
Bell’s palsy is a relatively common condition. It is idiopathic, meaning there is no apparent cause. It presents as a unilateral lower motor neurone facial nerve palsy. The majority of patients fully recover over several weeks, but recovery may take up to 12 months. A third are left with some residual weakness. If patients present within 72 hours of developing symptoms, NICE clinical knowledge summaries (updated 2019) recommend considering prednisolone as treatment, either: 50mg for 10 days 60mg for 5 days followed by a 5-day reducing regime of 10mg a day Patients also require lubricating eye drops to prevent the eye on the affected side from drying out and being damaged. If they develop pain in the eye, they need an ophthalmology review for exposure keratopathy. The eye can be taped closed at night.
590
What is Ramsay Hunt syndrome, how does it present and how is it managed?
Ramsay-Hunt syndrome is caused by the varicella zoster virus (VZV). It presents as a unilateral lower motor neurone facial nerve palsy. Patients stereotypically have a painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side. This rash can extend to the anterior two-thirds of the tongue and hard palate. Treatment should ideally be initiated within 72 hours. Treatment is with: Prednisolone Aciclovir Patients also require lubricating eye drops.
591
Systemic diseases that might cause a lower motor neurone facial nerve palsy
Diabetes Sarcoidosis Leukaemia MS Gulliane Barre syndrome
592
Infections that might cause a lower motor neurone facial nerve palsy
Otitis media Mallignant otits externa HIV Lyme disease VZV
593
Tumours that might cause a lower motor neurone facial nerve palsy?
Acoustic neuroma Parotid tumour Cholesteoma
594
Trauma that might cause a lower motor neurone facial nerve palsy
Direct trauma Damage during surgery Base of skull fracture
595
Within what timeframe of presentation, do NICE recommend considering prednisolone as treatment for Bells Palsy?
72 hours
596
What is the thyroid gland?
The thyroid gland is located at the base of the neck. It is a highly vascular structure responsible for controlling the basal metabolic rate of the body through the production of thyroxine and triiodothyronine hormones.
597
Vasculature of the thyroid
The arterial supply to the thyroid is from the superior and inferior thyroid arteries. Venous drainage of the thyroid is via the superior, middle, and inferior thyroid veins
598
What nerve is of greatest significance during thyroid surgery and why?
The recurrent laryngeal nerves are intimately associated with the thyroid gland running in the tracheo-oesophageal groove and are at risk during surgery. They supply the muscles of the larynx (except cricothyroid) and sensation below the vocal cords. Injury causes vocal cord palsy with associated hoarseness and can also give problems with airway obstruction if the nerves on both sides are injured.
599
When might the parathyroid glands be at risk during ENT surgery
The parathyroid glands are also closely related to the thyroid gland. They are involved in calcium haemostasis and can be accidentally removed or damaged during surgery leading to hypocalcaemia. This is normally only a problem when both sides of the thyroid have been operated on. i.e. total or completion thyroidectomy
600
Most important investigations in a patient presenting with a thyroid lump?
TFTs FNA If there is any diagnostic doubt a hemithyroidectomy should be carried out to give definitive histology. Lumpectomies are not done on the thyroid because if it is a malignant nodule this will not give adequate margins on the mass and it would also make further surgery very difficult due to scarring and put the recurrent laryngeal nerve at an unacceptably high risk
601
How are follicular adenoma and follicular carcinoma of the thyroid managed and why are they managed the same way?
Both managed with total hemithyroidectomy as CANNOT differentiate between the two on FNA, sent for definitive histology
602
Non-neoplastic thyroid nodules?
Single nodule – colloid, cystic Multinodular goitre These are common and if they show typical features on ultrasound do not necessary require fine needle aspiration. Any dominant nodule should have an FNA.
603
Benign thyroid neoplasams
Adenoma - mainly follicular
604
Malignant thyroid neoplasms
o Papillary adenocarcinoma – 70% - Often seen in younger patients, or where there is a history of irradiation of the neck. o Follicular carcinoma – 20% - It has a preponderance to metastasis to the bones and lungs. o Medullary carcinoma – 5% - This is a neoplasm of the calcitonin regulating C-cells. It is typically seen in multiple endocrine neoplasia, and therefore screening of other organs involved in MEN syndromes is required. There is a genetic component. o Anaplastic carcinoma - ~5% - Typically seen in older patients. This has a poor prognosis and by the time of diagnosis the prognosis if often a matter of weeks to months.
605
Management of non neoplastic thyroid nodules
Conservative –these can be managed conservatively unless there is diagnostic uncertainty Surgery o For compressive symptoms, cosmesis or patient preference. o Should aim to restrict surgery to hemithyroidectomy due to the increased morbidity from a total thyroidectomy and the need for lifelong thyroxine replacement.
606
Management of neoplastic thyroid nodules?
Adenomas – require no further treatment after diagnostic hemithyroidectomy Carcinoma o Surgery Total Thyroidectomy for papillary, follicular and medullary carcinoma Anaplastic disease is normally too far advanced for curative surgery o Radio-iodine therapy For papillary and follicular carcinoma after surgery
607
General complications of thyroid surgery?
Post-operative haemorrhage Airway obstruction o Secondary to haemorrhage o Secondary to bilateral vocal cord palsy Vocal cord palsy Hypocalcaemia
608
Anatomy of the parotid gland?
The parotid gland is a serious salivary gland located anterior to the pinna and lateral to the ramus of the mandible. The gland is split into deep and superficial lobes by the facial nerve which passes through the gland. The majority of the gland lies superficial to the facial nerve. Facial palsy is one of the most serious risks from parotid surgery and can also be caused by a parotid malignancy
609
Parotid gland neoplasams
 80% of salivary gland neoplasms occur in the parotid gland.  80% of parotid neoplasms are benign in nature.  80% of benign parotid neoplasms are pleomorphic adenomas.
610
In which salivary gland are tumours most common?
Parotid gland
611
In which salivary gland is infection most common?
Submandibular gland
612
Submandibular gland anatomy
The submandibular gland is located inferior to the body of the mandible and superior to the digastric muscle. It’s duct opens into the mouth close to the frenulum of the tongue. The hypoglossal and lingual nerves run medial to the gland and are at risk during submandibular gland surgery. Unlike the parotid gland, the submandibular gland has mixed mucous and serous secretions.
613
The sublingual glands are entirely mucous and are located where?
In the floor of the mouth
614
What proporiton of neoplasms arising from the submandibular gland are malignant?
50% of neoplasms occurring in the submandibular gland are malignant
615
WHen might an abscess in the submandibular gland typically arise?
Submandibular abscesses may develop following sialolithiasis or sialadenitis
616
In which salivary gland are most neoplasms mallignant?
Sublingual (80%)
617
What is sialadenitis caused by?
Acute sialadenitis may be viral or bacterial. Bacterial disease is typically due to staphylococcal infection and is typically seen in dehydrated or immunocompromised individuals. Viral disease is caused by a range of viruses including: 1. Paramyxovirus – Mumps 2. Coxsackievirus 3. Echovirus 4. HIV Chronic sialadenitis is rare, and sometimes seen in TB, sarcoidosis, HIV, and syphilis.
618
What is sialadenitis?
Sialadenitis is the inflammation and enlargement of one or several major salivary glands.
619
In which salivary gland are stones most common?
Submandibular
620
How might you investigate sialolithiasis?
 Ultrasound  or sialogram
621
When is sialolithasis most painful?
During meals
622
Management of sialolithiasis?
Conservative o most will settle conservatively o analgesia o hydration o sialogogues Endoscopy Radiological removal Surgery o Intraoral removal of palpable stones o Removal of salivary gland
623
Potential complications of sialolithasis?
 Sialadenitis  Abscess formation
624
Sjögren’s Syndrome
This is an autoimmune disease causing lymphocytic infiltration into the ductal tissue of secretary glands. It classically presents with dry eyes and dry mouth and patients may have enlarged salivary glands. Patients are at increased risk of developing lymphoma. The disease may be primary: Xerostomia and xerophthalmia without connective tissue abnormality. Or secondary: As primary disease, with connective tissue disease, most commonly rheumatoid arthritis. Diagnosis is made from the history, examination, some specific autoantibodies and a biopsy of minor salivary glands on the inner lip
625
Thyroid lump 2ww referrals red flags
Cervical lymphadenopathy slow-onset and persistent pain, voice changes, family history, or rapidly enlarging masses.
626
Bilateral sensioneural hearing loss causes
Causes of bilateral sensorineural hearing loss include genetic diseases such as Charcot-Marie-Tooth disease, congenital rubella syndrome, presbycusis and ototoxicity at varying frequency range
627
What is Schwartze sign and what might it suggest
Patients with a positive Schwartze sign may be more likely to have sensorineural (cochlear) otosclerosis. [5] [6] The finding of a reddish discoloration in a patient with hearing loss may suggest otosclerosis, especially of the sensorineural (cochlear) area
628
The identification of an indurated ulcer involving the lateral tongue in a patient with a long-term smoking history should be considered what until proven otherwise
SCC
629
Examination in patient presenting with facial nerve palsy
Movement of the facial muscles Otoscopy Palpation of the parotid gland and neck detailed examination of the external auditory canal and tympanic membrane
630
Facial nerve and parotid gland
The facial nerve demarcates superficial and deep lobes
631
From, where does the facial nerve arise
The facial nerve arises from the skull base via the stylomastoid foramen.
632
What is Xerostomia and when might it occur
Xerostomia (dry mouth) represents a common sequelae following radiotherapy for parotid, oral cavity and oropharyngeal cancers. It is also a recognised side effect from medications including, but not limited to, diuretics, beta blockers, tricyclic antidepressants, antihistamines, anticonvulsants and antipsychotics.
633
Structures passing through the parenchyma of the parotid gland
External carotid artery Retromandibular vein Facial nerve
634
How is the severity of OSAH or OSAS graded?
The apnoea hypopnoea index (AHI) is the number of apnoeas (stopping breathing) or hypopnoeas (reduced airflow during breathing) recorded during the sleep study per hour of sleep. It is generally expressed as the number of events per hour. Based on the AHI, the severity of OSA is classified as follows: None/Minimal: AHI < 5 per hour Mild: AHI ≥ 5, but < 15 per hour Moderate: AHI ≥ 15, but < 30 per hour Severe: AHI ≥ 30 per hour
635
What conditions does OSA increase the risk o f
Hypertension Depression Ischaemic heart disease Accidents Diabetes
636
Management of broken nose
Book the patient for an ENT clinic appointment within 7-10 days
637
Managing primary haemorrhage following thyroid surgery
Apply high flow oxygen via face-mask and remove surgical clips/sutures
638
Wwat cancer accounts for up to 99% of cancers arising from the upper aerodigestive tract.
SCC
639
What type of laryngeal carcinoma has the best prognosis
Glottic tumours have the best prognosis
640
Associations with recurrent laryngeal nerve palsy
Thyroid surgery Aortic aneurysm repair Carcinoma of the oesophagus Carcinoma of the bronchus Polio
641
Ludwig’s angina
Ludwig’s angina is a form of severe, diffuse cellulitis with bilateral involvement of the submandibular space. Signs may include diffuse, bilateral submandibular and sublingual swelling. Oropharyngeal examination typically reveals elevation of the floor of mouth and posterior displacement of the tongue, creating the potential for a airway compromise. Ludwig’s angina therefore, represents a medical emergency. Temporising measures may include a nasopharyngeal airway. Oropharyngeal intubation is often extremely challenging due to retrograde tongue displacement. In extremis and in the presence of imminent, life-threatening airway obstruction, an emergency tracheostomy is indicated.
642
What structure is MOST at risk when performing external cervical incision and drainage of the submandibular space?
Marginal mandibular nerve- a branch of the facial nerve
643
Tonsilar SCC is associated with what infection
Tonsilar SCC is associated with HPV infection
644
Which part of the TM should be visualised to r/o cholesteotoma
In patients with chronic or recurrent ear discharge, ensure the attic is visualised to exclude cholesteatoma
645
What type of nystagmus is indicative of a positive Dix-Hallpike manoeuvre
Rotatory nystagmus is indicative of a positive Dix-Hallpike manoeuvre
646
What distinguishes vestibular neuronitis from labyrinthitis
Unaffected hearing distinguishes vestibular neuronitis from labyrinthitis
647
What is seen in the fluid of a brachial cyst
A biopsy is performed and reveals cholesterol crystals in the fluid extracted.
648
What is the main side-effect of using topical decongestants for prolonged periods?
After using topical decongestants for prolonged periods increasing doses are needed to provide the same effect, a phenomenon known as tachyphylaxis.
649
What cranial nerves are affected in vestibular schwannomas?
Cranial nerves V, VII and VIII are affected in vestibular schwannomas
650
Pure tone audiogram in NIHL
Pure tone audiogram shows that bone and air conduction in both ears are poor at lower volumes (below 25dB) and within 10 dB of one another
651
Can prochlorperazine be used to treat vestibular neuronitis?
Prochlorperazine may be useful in the acute phase of vestibular neuronitis, but should be stopped after a few days as it delays recovery by interfering with central compensatory mechanisms