ENT Flashcards

(141 cards)

1
Q

What is a cataract?

A

A cataract is the opacification of the lens due to the normal ageing process, infection, trauma, medications or congenital problems.

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2
Q

What are the RFs for cataracts?

A

Age >65, trauma, long term UV, smoking, long term corticosteroid use, DM, uveitis, FHx

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3
Q

What are the signs and symptoms of cataracts?

A

Blurred/cloudy vision, dec in colour intensity, glare, decrease in vision

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4
Q

What are the investigations for cataracts?

A

Fundal exam = normal optic disk/fundus
Anterior chamber slit lamp = visualisation of cataract
IOP = NORMAL unless concomitant glaucoma
Glare vision = cataract visualisation

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5
Q

What is a thyroglossal cyst?

A

A fibrous cyst that results from the persistence of a thyroglossal duct

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6
Q

What is the aetiology of a thyrocyst?

A

Congenital

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7
Q

What investigation should be undertaken with thyroglossal cysts?

A

TFTs -> possibly radioiodine/tech99 uptake scan
USS - see fibrous or liquid nature
FNA - removal of cells for biopsy

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8
Q

What is tonsillitis?

A

Acute inflammation of the parenchyma of the palatine tonsils.

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9
Q

What are the RFs for tonsillitis?

A

5-15yo

Contact with infected

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10
Q

What are the signs and symptoms?

A

Oydonophagia, Fever >38, SO, exudate, swelling, erythema, abdo pain, cervical lymphadenopathy, N+V, cough /runny nose

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11
Q

What are the main causative organisms or tonsillitis?

A

Most = viral - rhinovirus, coronavirus, adenovirus
EBV - if mono
Bacterial - group a B haemolytic/other streptococci

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12
Q

What are the investigations for tonsillitis?

A
Normally clinical.
Throat swab - culture 
Rapid strep antigen testing 
WBC count
Penile/vag culture if N gonorr RFs
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13
Q

What is BBPV?

A

A peripheral vestibular disorder characterised by sudden onset episodes of vertigo elicited by specific head movements.
Chronic/relapsing

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14
Q

What is the aetiology of BPPV?

A

Migration of free floating canalith particles floating in the endolymph

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15
Q

What are the RF for BPPV?

A

Age, trauma, vestibular neuritis, migraine, labyrinthitis, Menieres, inner ear surgery, otitis media

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16
Q

What are the signs and symptoms of BPPV?

A

Sudden onset, provoking head positions, brief duration, severe, nausea inducing, light headedness, normal otological exam, normal neuro exam, episodic vertigo, +ve dix hallpike, nystagmus absence is possible but rarer.

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17
Q

What are the investigations for BPPV?

A

Dix hallpike - +ve
Supine lateral head tilting - horizontal nystagmus
Audiogram - N in primary, abnormal in secondary
MRI - MS/Tumour can mimic bppv

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18
Q

What is Menieres disease?

A

An auditory disease characterised by SO vertigo, LOW freq hearing loss, LOW freq tinnitus, and a sensation of fullness in the affected ear

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19
Q

What are the signs and symptoms of menieres?

A

Sudden onset vertigo
Low freq hearing loss associated with episodes of vertigo
Low freq tinnitus (roaring)
Sensation of fullness in affected ear
+ve rombergs
+ve fukudas stepping test = marching on spot causes circular drifting

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20
Q

What is uveitis?

A

Inflammation of one or all parts of the uvea, or the vascular area between the retina and sclera.

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21
Q

What is the aetiology of anterior uveitis?

A

idiopathic causes
infectious - CMV, HIV, HSV, Syphilis, lymes, histoplasmosis, TB
Non-infectious - IBD, sarcoidosis, MS, trauma

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22
Q

What are the many signs and symptoms?

A

Dull orbital pain, photophobia, dec vision, floaters, flare, redness, dec IOP, synechaie, tearing, retinal haemorrhages, non-reactive pupil,

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23
Q

What are the investigations for uveitis?

A

Clinical ->history, eye signs, RF, symptoms

WCC may be up. Test rhf, esr, crp hlab27,serum ace sarcoidosis

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24
Q

What is glaucoma?

A

A neurodegenerative disorder primary due to outflow problems of the aqueous humor resulting in an increase in IOP and retinal damage

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25
What are the RFs for glaucoma?
IOP >23mmhg, age >50, FHx, black, HTN, DM
26
What are the signs/symptoms of open angle glaucoma?
``` Cup to disk <0.4 Scotomas, IOP up Decreased peripheral vision Notching of optic nerve cup Loss of nerve fibre layer ```
27
What investigations confirm open angle glaucoma
Tanometry - inc IOP Ophthalmoscopy - cup to disk >0.4 of asymmetry >0.2 Slit lamp - deep anterior chamber, open drainage angle Gonioscopy - no obstruction of anterior chamber
28
What happens in closed angle glaucoma?
Closure of anterior chamber angle - increase in ICP ACUTE - SUDDEN blockage Chronic = iris and trabecular mesh work come into contact gradually
29
What investigations separate open and closed angle?
With ophthalmoscopy the trabecular mesh work will not be visible in angle closure Large optic cup and splinter haemorrhages. Shallow anterior chamber Apart from that investigations = same
30
What are the signs of angle closure?
Halos | Achieving brow pain, headache, redness, fixed dilated pupil, dec acuity and blurring
31
Define vestibular schwannoma / acoustic neuroma
A benign cerebellopontine angle tumour that grows from the superior vestibular component of the vestibulocochlear nerve, usually presenting with unilateral sensorineural hearing loss. Vestibular schwannomas are also called acoustic neuromas, and the two terms may be used interchangeably. However, acoustic neuroma is a misnomer, because the tumour actually grows on the vestibular component and is pathologically a schwannoma. Tumours can enlarge significantly to cause cerebellar findings and obstructive hydrocephalus, and may become life threatening as a result. A benign slow-growing tumour, which, following detection, usually remains stable. Unilateral sensorineural hearing loss is the most common symptom, followed by intermittent dizziness and facial numbness. Larger tumours may cause headaches, coordination difficulties, and obstructive hydrocephalus, and, as a result, may be life threatening. Diagnosis is confirmed by gadolinium-enhanced magnetic resonance imaging scan. Management includes observation, focused radiation, or surgery. Treatment options and outcome vary depending on local expertise and patient preference.
32
Epidemiology of vestibular schwannoma / acoustic neuroma
The annual incidence is 0.2 to 1.7 out of 100,000 with a 3:2 female-to-male ratio. Vestibular schwannomas comprise 6% of all intracranial tumours and 70% to 80% of all cerebellopontine angle tumours. All races and ethnicities are affected equally. Vestibular schwannomas are occasionally associated with the genetic disorder neurofibromatosis type 2, with a reported incidence of 1.4 to 4 out of 100,000 in people with this disorder.
33
Aetiology of vestibular schwannoma / acoustic neuroma
Tumour suppressor gene abnormalities on chromosome p22 (merlin or schwannomin protein) are thought to cause tumour growth. Tumours occur at the junction of the central and peripheral Schwann cells or Obersteiner-Redlich zone. Most growths are sporadic without a known underlying cause. There is a familial autosomal dominant form in which patients have bilateral tumours in addition to other intracranial tumours (neurofibromatosis type 2)
34
RFs for vestibular schwannoma / acoustic neuroma
STRONG | NF2
35
Sx of vestibular schwannoma / acoustic neuroma
``` COMMON Asymmetrical hearing loss Facial numbness Progressive episodes of dizziness Tinnitis Difficult localising sound ``` ``` UNCOMMON (related to larger tumours) Headache Facial weakness Increased or decreased tears Diplopia on lateral gaze Nystagmus Loss of balance/coordination Slower blink Swallowing difficulties Gait Hydrocephalus Papilloedema Raised ICP ```
36
Ix for vestibular schwannoma / acoustic neuroma
Audiogram - sensorineural/retrocochlear hearing loss Gadolinium enhanced MRI CT head Auditory brainstem reflexes
37
Rx of vestibular schwannoma / acoustic neuroma
Tumour less than 1-1.5cm Observe Focused radiation or surgery With growth Focused radiation / surgery Tumour >3cm = surgery With or without tumour growth on serial scans, surgery is recommended due to the large size and potential damage to adjacent structures and resulting functional deficits.
38
Prognosis of vestibular schwannoma / acoustic neuroma
Between 40% and 60% of small tumours may not require treatment. Tumours treated with focused radiation have a control rate of >90% Following surgery, patients have a recurrence rate of <5% If baseline hearing is near normal, 60% to 80% of hearing is preserved with radiation and up to 80% of hearing is preserved with surgery, depending on anatomy, size of tumour, and surgical approach.
39
Complications of vestibular schwannoma / acoustic neuroma
SURGERY: Hearing loss Facial numbness CSF leak ``` RADIO: Secondary malignancy Hydrocephalus Hearing loss Facial nerve palsy ```
40
A 45-year-old man has a routine hearing test for work and a sensorineural hearing loss is detected. He has no signs or symptoms.
vestibular schwannoma / acoustic neuroma Large tumours can cause significant problems with increased intracranial pressure, gait disturbance, and coordination difficulties. Papilloedema may present in large tumours with increased intracranial pressures; these patients may also develop hydrocephalus. Cranial nerves other than the facial and vestibulocochlear nerves may be affected, such as the trigeminal (facial sensation) and lower cranial nerves (swallow).
41
Define Bell's palsy
Bell's palsy is an acute unilateral peripheral facial nerve palsy in patients for whom physical examination and history are otherwise unremarkable, consisting of deficits affecting all facial zones equally that fully evolve within 72 hours. To date, it remains a clinical diagnosis of exclusion. Complete recovery to normal facial function occurs in approximately 70% of untreated cases, with permanently impaired facial function occurring to a minor degree in 13% and to a major degree in 16% of cases. Onset of clinical recovery is nearly always demonstrated within 4 to 6 months of symptom onset; absence of any return of hemi-facial tone or movement by this time is highly suggestive of an alternative diagnosis. Facial palsy of an otherwise known aetiology (e.g., Lyme disease-associated facial palsy), or facial palsy that is progressive, waxing and waning, or affects facial zones in an uneven fashion, is not Bell's palsy. Acute unilateral facial palsy of probable viral aetiology. Clinical diagnosis of exclusion. High-dose corticosteroids should be administered in all patients in the absence of significant contraindications. Other treatment options include concomitant antiviral agents, physiotherapy, and, in severe cases, surgical decompression. Eye protection should always be considered. Failure to demonstrate any return of hemi-facial tone or movement within 4 to 6 months suggests an alternative diagnosis.
42
Epidemiology of Bell's palsy
Bell's palsy is the most common aetiology of unilateral facial palsy among those 2 years of age or older. It is most prevalent in people between 15 and 45 years of age. The reported incidence is 23 to 32 cases per 100,000 per year. M=F
43
Aetiology of Bell's palsy
Strong evidence points to reactivation of herpes simplex virus type 1 (HSV-1) within the geniculate ganglion as the underlying cause of Bell's palsy.
44
RFs for Bell's palsy
STRONG Intranasal flu vaccine Pregnancy ``` WEAK URTI Black/hispanic Arid/cold climate HTN FHx DM ```
45
Sx of Bell's palsy
``` COMMON Unilateral Absence of constitutional Sx Involvement in all branches Keratoconjunctivitis sick Pain Synkinesis ``` UNCOMMON Hyperacusis Dysgeusia
46
A 40-year-old woman awakens with left-sided facial fullness and a subjective feeling of facial and tongue 'numbness' without objective hypoaesthesia. She also notes left-sided dysgeusia. Later that day she develops left-sided otalgia, hyperacusis, post-auricular pain, and facial discomfort. Left-sided facial palsy ensues, with associated oral incompetence, facial weakness, and asymmetry progressing to complete flaccid paralysis by the next morning. On physical examination, the resting appearance of the left face demonstrates brow ptosis, a widened palpebral fissure, effacement of the left nasolabial fold, and inferior malposition of the left oral commissure. There is complete absence of brow movement, incomplete eye closure with full effort, and loss of smile, snarl, and lip pucker on the affected side. The remainder of the history and physical examination are unremarkable.
Bell's palsy Post-auricular pain commonly occurs concurrently or as a prodrome to facial palsy in Bell's palsy.[1] At least one study demonstrated that up to 8% of those diagnosed with Bell's palsy present with additional cranial neuropathies, most commonly of the trigeminal nerve.[5] Facial weakness in Bell's palsy may range from a mild palsy to complete flaccid paralysis with absence of volitional and evoked electromyography (EMG) activity. One author has defined four patterns of facial palsy onset in Bell's palsy in order of worsening prognosis: 1) sudden incomplete, without progression; 2) sudden incomplete, with progression, yet remaining incomplete; 3) sudden complete; and 4) sudden incomplete, with rapid progression to complete.[6] Degrees of otalgia, post-auricular pain, facial dysaesthesias, hypogeusia, and hyperacusis vary.
47
Ix for Bell's palsy
Clinical eEMG - >90% decrease in the amplitude Needle EMG - absence of voluntary motor unit potentials Serology for B burgdorferi
48
Rx of Bell's palsy
1. prednisolone: 60 mg orally once daily for 5 days, then 50 mg once daily for 1 day, then 40 mg once daily for 1 day, then 30 mg once daily for 1 day, then 20 mg once daily for 1 day, then 10 mg once daily for 1 day, then stop Keratoconjunctivitis sicca (dry eye) is common and may lead to exposure keratopathy. During the daytime, glasses may be worn and artificial tears used as needed. Overnight, ophthalmic lubricant should be applied and the eyelid taped closed. Eye patching should be avoided. SEVERE: valaciclovir: 500-1000 mg orally twice daily for 5 -7 days OR aciclovir: 400 mg orally five times daily for 10 days Surgical decompression
49
Prognosis of Bell's palsy
The extent of facial palsy following complete evolution of Bell's palsy (i.e., within 72 hours of onset) is the parameter most predictive of ultimate recovery outcome. Of those who present with incomplete paralysis on clinical examination, 94% will fully recover, as compared to 61% of those who present with complete paralysis Further evidence has demonstrated that spontaneous return of normal or near-normal facial function (i.e., HBS I or II) following Bell's palsy is reduced by 50% when electroneuronography (ENoG) reveals a >95% difference between sides within 14 days of symptom onset. Other poor prognostic factors include advanced age, diabetes mellitus, and taste disturbance on presentation
50
Complications of Bell's palsy
Keratoconjunctivitis sick Ectropion (sagging eyelid) Contracture + synkinesis (Synkinesis is a neurological symptom in which a voluntary muscle movement causes the simultaneous involuntary contraction of other muscles.) Gustatory hyperlacrimation
51
A 40-year-old woman awakens with left-sided facial fullness and a subjective feeling of facial and tongue 'numbness' without objective hypoaesthesia. She also notes left-sided dysgeusia. Later that day she develops left-sided otalgia, hyperacusis, post-auricular pain, and facial discomfort. Left-sided facial palsy ensues, with associated oral incompetence, facial weakness, and asymmetry progressing to complete flaccid paralysis by the next morning. On physical examination, the resting appearance of the left face demonstrates brow ptosis, a widened palpebral fissure, effacement of the left nasolabial fold, and inferior malposition of the left oral commissure. There is complete absence of brow movement, incomplete eye closure with full effort, and loss of smile, snarl, and lip pucker on the affected side. The remainder of the history and physical examination are unremarkable.
Bell's palsy Post-auricular pain commonly occurs concurrently or as a prodrome to facial palsy in Bell's palsy.[1] At least one study demonstrated that up to 8% of those diagnosed with Bell's palsy present with additional cranial neuropathies, most commonly of the trigeminal nerve.[5] Facial weakness in Bell's palsy may range from a mild palsy to complete flaccid paralysis with absence of volitional and evoked electromyography (EMG) activity. One author has defined four patterns of facial palsy onset in Bell's palsy in order of worsening prognosis: 1) sudden incomplete, without progression; 2) sudden incomplete, with progression, yet remaining incomplete; 3) sudden complete; and 4) sudden incomplete, with rapid progression to complete.[6] Degrees of otalgia, post-auricular pain, facial dysaesthesias, hypogeusia, and hyperacusis vary.
52
Define cholesteatoma
Cholesteatoma is defined as the presence of keratinising squamous epithelium within the middle ear, or in other pneumatised areas of the temporal bone. This keratinising epithelium exhibits independent growth, leading to expansion and to resorption of underlying bone. Focal erosion of external canal bone with accumulation of keratin is called external canal cholesteatoma. Accumulation of squamous epithelium and keratin debris that usually involves the middle ear and mastoid. Although benign, it may enlarge and invade adjacent bone. Often presents with a malodorous ear discharge with associated hearing loss. Diagnosis is clinical based on history and otoscopic findings. CT scan provides lesion definition and extent. Treatment is surgical removal. Adjunctive topical antimicrobial treatment may help reduce acute symptoms preoperatively. Complications include recurrence, meningitis, facial palsy, and a labyrinthine fistula.
53
Epidemiology of cholesteatoma
Scotland = an annual incidence of 13 per 100,000 Both males and females are affected, with a ratio of 3:2. Cholesteatoma in children has been found to affect the eustachian tube, anterior mesotympanum, retrolabyrinthine cells, and mastoid tip more than in adults. Clinical and histological evidence suggest that cholesteatoma in children tends to be more aggressive.
54
Aetiology of cholesteatoma
Stage I: retracted membrane Stage II: retraction onto the incus Stage III: middle ear atelectasis Stage IV: adhesive otitis media.
55
RFs for cholesteatoma
``` STRONG Middle ear disease Eustacian tube dysfunction Otological surgery Traumatic blast injury to ear Congenital abnormalities ``` WEAK FHx
56
Sx of cholesteatoma
``` COMMON Hearing loss Ear discharge resistant to Rx Attic crust in retraction pocket White mass behind intact tympanic membrane Tinnitus ``` ``` UNCOMMON Otalgia Altered taste Dizziness Facial nerve weakness ```
57
Ix for cholesteatoma
Pure tone audiogram - variable; may show a conductive hearing loss CT - opacification of the middle ear or mastoid; erosion of the scutum, ossicular chain, labyrinth, facial canal, tegmen, or bony capsule of the sigmoid sinus
58
Rx of cholesteatoma
Surgery: canal wall up mastoidectomy OR canal wall down mastoidectomy Pre-op ABx: ciprofloxacin/dexamethasone otic: (0.3%/0.1%) 4 drops into the affected ear(s) twice daily for 7-10 days OR ofloxacin otic: (0.3%) 10 drops into the affected ear(s) once daily for 7 days Second look surgery or MRI
59
Prognosis of cholesteatoma
Cholesteatoma has a tendency to recur despite treatment, and may recur long after the initial surgical excision. The risk of recurrence after surgery in children has been shown to be higher if the disease involves the posterior mesotympanum, and if the ossicular chain is interrupted after excision, or both. A relative lack of experience of the surgeon (and presumed incomplete excision of the disease) may also contribute to disease recurrence.
60
Complications of cholesteatoma
``` RECURRENCE Hearing loss Labyrinth FISTULA Facial palsy Meningitis Brain abscess Signoid sinus thrombosis Mastoiditis ```
61
A 37-year-old man presents with hearing loss and a painful intermittent purulent discharge from his right ear. He also reports intermittent dizziness, and tinnitus in the right ear. On otoscopy, he has an attic crust on his right tympanic membrane. Examination with an otomicroscope and micro-suctioning reveals keratin in an attic retraction pocket. An audiogram demonstrates a conductive hearing loss on the right side.
cholesteatoma Congenital cholesteatoma is often an incidental finding. The patient may have hearing loss, and is found to have a white mass behind the tympanic membrane, with a normal pars tensa and pars flaccida of the tympanic membrane, and no prior history of ear discharge, tympanic membrane perforation, or surgical procedures on the ear. Patients (more commonly adults) may also present with complications of a cholesteatoma such as meningitis, facial palsy, sensorineural hearing loss, or vertigo, due to destruction of the cochlea or vestibular anatomy.
62
A 12-year-old girl presents with a history of a recurrently discharging left ear for several months. She complains of an offensive discharge and hearing loss. She reports a previous history of grommet insertion. Otoscopy reveals a posterosuperior perforation of the tympanic membrane with a white keratin-like discharge. She has a conductive hearing loss on audiometry.
cholesteatoma Congenital cholesteatoma is often an incidental finding. The patient may have hearing loss, and is found to have a white mass behind the tympanic membrane, with a normal pars tensa and pars flaccida of the tympanic membrane, and no prior history of ear discharge, tympanic membrane perforation, or surgical procedures on the ear. Patients (more commonly adults) may also present with complications of a cholesteatoma such as meningitis, facial palsy, sensorineural hearing loss, or vertigo, due to destruction of the cochlea or vestibular anatomy.
63
Define epiglottitis
Epiglottitis is a cellulitis of the supraglottis with the potential to cause airway compromise, and should be treated as a surgical emergency until the airway is examined and secured. Pertinent diagnostic criteria include the classic 'tripod' position of the patient, drooling, high fever, and a toxic appearance. A cellulitis of the supraglottis that may cause airway compromise. An airway emergency, especially in children, and precautionary measures must be taken. Epiglottitis is classically described in children aged 2 to 6 years of age; however, it may manifest at any age, including in newborns. It may now be more common in older children and adults due to the Haemophilus influenzae type B (Hib) vaccine. The most common signs are rapid onset of high fever, sore throat, inability to control secretions, classic tripod positioning, difficulty breathing, and irritability. Adults may have a more indolent presentation and may not require airway intervention (only about 20% of adults require intubation whereas most children do). Cooperation between the otolaryngologist, paediatrician, or emergency department physician and anaesthetist is crucial. No action should be taken that could stimulate a child with suspected epiglottitis, including examination of the oral cavity, starting intravenous lines, blood draws, or even separation from a parent. Similar caution is required in fulminant acute epiglottitis in adults. Diagnosis is made on clinical grounds, and laboratory or other interventions should not preclude or delay timely control of the airway in a suspected case of epiglottitis. Once the airway has been secured and antibiotics have been initiated, the condition usually resolves rapidly. Vaccination does not preclude the possibility of epiglottitis or even the possibility of epiglottitis from Haemophilus influenzae.
64
Epidemiology of epiglottitis
Epiglottitis is most common between the ages of 3 and 5 years, but it can occur at any age
65
Aetiology of epiglottitis
Infection of the supraglottis: classically with Haemophilus influenzae, but also from other potential pathogens, including Streptococcus pneumoniae, Staphylococcus aureus, and MRSA. Other rare bacterial pathogens such as Pasteurella multocida have been reported. Less commonly, viral pathogens such as parainfluenza have been implicated as aetiological agents. Another rare aetiology of epiglottitis is fungal infection. Several reports of candidial epiglottitis have been reported. Traumatic: a mechanical insult to the epiglottis can occur, most commonly from caustic ingestion or thermal injury, which may result in marked oedema and inflammation of the epiglottis.
66
RFs for epiglottitis
STRONG No HIB vaccine Immunocompromise Middle age
67
Sx of epiglottitis
``` COMMON Sore throat Dysphagia Drooling Toxic appearance Acute distress Fever Tripod Dyspnoea Decreased oral intake Muffled voice Stridor Irritability ```
68
Ix for epiglottitis
Laryngoscopy | Lateral neck radiograph - markedly enlarged epiglottis, referred to as a 'thumbprint sign'
69
Rx of epiglottitis
1. Secure airway + supplemental O2 IV ABx - cef drugs 2. Corticosteroids dexamethasone: children: 0.08 to 0.3 mg/kg/day orally given in divided doses every 6-12 hours; adults: 0.75 to 9 mg/day orally given in divided doses every 6-12 hours according to response 3. Inhaled adrenaline 4. Prolonged intubation may be necessary Oral ABx once tolerating orally
70
Prognosis of epiglottitis
Epiglottitis is an acute condition and, though very severe (especially so in children), if the patient is treated appropriately the prognosis is excellent for a quick and complete recovery. Other than in unvaccinated or immunocompromised individuals, there is no theoretical increased risk for future episodes of this disease. ____________________ There are numerous sequelae of not treating an infectious process that causes airway obstruction. These include: death, mediastinitis, neck space infection, necrotising fasciitis, pneumonia, aspiration, and asphyxiation.
71
Complications of epiglottitis
Mediastinitis Neck infection Pneumonia
72
A 4-year-old boy presents to the emergency department with complaints of dysphagia, fever, drooling, and muffled voice. Symptoms have progressively worsened over the course of the day. He is toxic-appearing, and leans forwards while sitting on his mother's lap. He is drooling, and speaks with a muffled 'hot potato' voice. The parents deny trauma or evidence of foreign-body ingestion. They have no recollection of the child receiving a Haemophilus influenzae type B (Hib) vaccine.
epiglottitis The presentation of a patient with epiglottitis, especially in the post-Hib vaccine era, can be varied.[3] Vaccination is not 100% effective, so it is possible that patients may present with only some of the typical symptoms. Adults may have a more indolent presentation than children.[4] A South Korean review documented a high incidence of epiglottic cysts in patients presenting with epiglottis (29%). In this series, these cysts predisposed patients to more severe airway obstruction and a higher risk of recurrence.[5]
73
Define otitis externa
Acute otitis externa (AOE) is defined as diffuse inflammation of the external ear canal, which may also involve the pinna or tympanic membrane. It is a form of cellulitis that involves the skin and subdermis of the external auditory canal, with acute inflammation and variable oedema. It is most commonly caused by bacterial infection. The diagnosis of AOE requires the presence of rapid onset (generally within 48 hours) of symptoms within the past 3 weeks, coupled with signs of ear canal inflammation. Most commonly caused by Pseudomonas aeruginosa and Staphylococcus species. Presents with rapid onset of ear pain, tenderness, itching, aural fullness, and hearing loss. The development of malignant or necrotising otitis externa is more common in diabetic and immunocompromised people. Treatment of the uncomplicated form is cleaning of the ear canal and application of topical anti-infective agents.
74
Epidemiology of otitis externa
AOE has a lifetime incidence of 10%. The condition is known to affect people of all age groups but was found to peak in the 7- to 12-year-old age group and to decline in incidence among subjects >50 years of age. 4 in 1000
75
Aetiology of otitis externa
It is often polymicrobial, but the most common pathogens are Pseudomonas aeruginosa (20%-60% prevalence) and Staphylococcus aureus (10%-70% prevalence). Other aetiologies are idiopathic, trauma (from scratching, aggressive cleaning), chemical irritants, allergy (most commonly to antibiotic ear drops such as neomycin), high-humidity conditions, swimming, or skin disease (allergic dermatitis, atopic dermatitis, psoriasis). Fungal aetiology is uncommon in primary AOE, but may be more common in chronic otitis externa or after treatment of AOE with antibiotics, particularly topical antibiotics. The most common pathogens are Aspergillus species (60%-90%) and Candida species (10%-40%).
76
RFs for otitis externa
``` STRONG External auditory canal obstruction High humidity Warmer environment temps Swimming Local trauma Allergy Skin disease - eg psoriasis + eczema DM Immunocompromised Prolonged use topical ABx ``` WEAK Chemical irritants
77
Sx of otitis externa
``` COMMON Ear pain Tragal tenderness Ear canal swelling and erythema Otorrhoea Aural fullness Itching Decreased hearing Erythematous tympanic membrane ``` UNCOMMON Granulation tissue in ear canal
78
Ix for otitis externa
Pneumatic otoscopy - normal Tympanometry - normal Possible to do ear culture but rarely needed / MC+S
79
Rx of otitis externa
Prior to the use of topical ear drops, the ear canal needs to be cleaned of any debris or wax. ABx ear drops Pain management Refractory to initial treatment, or diabetic or immunocompromised: Topical / systemic - cipro used Malignant or necrotising = hyperbaric O2 and specialist
80
Prognosis of otitis externa
Patients with uncomplicated diffuse otitis externa usually respond to treatment. Between 65% and 90% of patients have clinical resolution within 7 to 10 days, regardless of agent used A search for predisposing factors is helpful and sometimes necessary in patients with recurrent AOE. Patients should be educated to avoid the use of cotton-tipped applicators or other foreign objects. Patients who report ear pain and infections after swimming should use occlusive ear plugs. Underlying dermatitis or other skin disorders should be attended to and treated with topical corticosteroids whenever needed. A search for possible allergy to certain ear drops and/or hearing aid components should be considered.
81
Complications of otitis externa
Contact dermatitis CN palsy Osteomyelitis of skull base
82
A 35-year-old man presents with a 2-day history of rapid-onset severe ear pain and fullness. The patient complains of otorrhoea and mild decreased hearing. He reports that his symptoms started after swimming. No fever is reported. On physical examination the external ear canal is diffusely swollen and erythematous. He has tenderness of the tragus and pain with movement of the auricle. The tympanic membrane was partially visualised due to the swelling. The concha and the pinna look normal. Neck examination fails to reveal any lymphadenopathy.
otitis externa Malignant or necrotising otitis externa is a form of otitis externa that is more common in older patients with uncontrolled diabetes or in patients with immunodeficiency.[1][4] In malignant otitis externa, the infection and the inflammatory process involve not only the skin and soft tissue of the external auditory canal but the bone tissue of the temporal bone as well.[5] If left untreated, osteomyelitis of the petrous bone and/or skull base could result.[5][6] It is most commonly caused by Pseudomonas species.[1][5] Patients usually present with severe ear pain, otorrhoea, and fullness, and are not responding to the conventional treatment of AOE. Depending on the stage of presentation and the extent of invasion, patients may have facial weakness and other cranial nerve abnormalities.[1] On physical examination the external auditory canal is swollen, with evidence of granulation tissue in the floor of the canal.[1] The diagnosis is usually made by computed tomography or magnetic resonance imaging scans, which show presence of soft tissue and bone destruction.[5] Technetium-99 or gallium scans will show increased radioisotope uptake in the temporal bone and/or skull base. Otomycosis is fungal otitis externa. Acute fungal otitis externa is less common than acute bacterial otitis externa.[1] It is most commonly caused by Aspergillus species.[3] It presents in a similar way with ear pain, itching, aural fullness, and otorrhoea. Physical examination reveals swollen ear canal skin and discharge. The presence of black spores indicates Aspergillus niger as the causative organism.[1][3] White filamentous hyphae can often be seen. The definitive diagnosis of otomycosis can be helped by microscopic examination and ear cultures. Otomycosis should be suspected in patients who fail treatment with antibacterial agents.[3] Secondary fungal infection of the external auditory canal is well known after prolonged treatment with topical antibacterial agents.
83
Define otitis media
Acute otitis media (AOM) is an infection involving the middle ear space and is a common complication of viral respiratory illnesses. May present with otalgia, irritability, decreased hearing, anorexia, vomiting, or fever, usually in the presence of an ongoing viral respiratory infection. Physical examination will reveal a bulging, opacified tympanic membrane with decreased mobility. The membrane may be white, yellow, pink, or red. Diagnosis is generally made with conventional otoscopy. Additional tests might include pneumatic otoscopy or tympanometry to confirm the presence of an effusion. Treatment includes pain control with analgesics and might include antibiotics. Complications include perforation of the tympanic membrane and, rarely, mastoiditis, seventh cranial nerve palsy, or sigmoid sinus thrombosis. NB glue ear is fluid in middle ear WO infection
84
Epidemiology of otitis media
More than 80% of children experience at least one episode of AOM before the age of 2 years with a peak incidence between 6 and 18 months. Children with anatomical anomalies (e.g., cleft palate, cleft uvula) or immunological deficiencies encounter more AOM than their peers. Environmental risk factors include childcare attendance, exposure to older siblings, exposure to tobacco smoke, absence of breastfeeding, bottle feeding in a supine position, and dummy use. A higher incidence among boys, children with a family history of AOM, and certain ethnic groups (Native Americans and Native Alaskans) suggests a genetic susceptibility.
85
Aetiology of otitis media
Respiratory viruses account for most cases of otitis media and are self-limiting. Co-infections of the middle ear with a virus and a bacterium demonstrate the role that both play in the development of acute, suppurative otitis media or pus drum. The most common bacteria responsible for AOM are Streptococcus pneumoniae (approximately 40%), non-typable Haemophilus influenzae (25% to 30%), and Moraxella catarrhalis (10% to 15%). Unfortunately, an aetiological diagnosis in a clinic setting is not readily feasible. Under normal conditions the mucociliary action and ventilatory function of the eustachian tube clear the nasopharyngeal flora that enter the middle ear. However, upper respiratory viruses can infect the nasal passages, eustachian tube, and middle ear, causing inflammation and impairing these processes. This may then contribute to the development of AOM. A middle ear effusion develops, and nasopharyngeal bacteria contaminate the effusion.
86
RFs for otitis media
``` STRONG Day care Older siblings Young FHx Native American or alaskan Absence of breast feeding Bottle propping Lower socio E Craniofacial anomaly Immunological deficiency ``` WEAK Male Dummy use Environmental tobacco smoke
87
Sx of otitis media
``` COMMON Otalgia URTI Hx Bulging tympanic membrane Myringitis Irritability Sleep disturbance Fever ``` UNCOMMON Reduced appetite
88
Ix for otitis media
CLINICAL
89
Rx of otitis media
Suspected AOM Oral analgesia P+I Delayed ABx: Amox or Co-Amox A recommended approach is to provide analgesia and observe for 2 to 3 days. If the patient remains symptomatic after the observation period ends, the antibiotic is started. This approach may reduce the number of unnecessary antibiotic courses, decrease the occurrence of adverse antibiotic reactions, improve the benefit provided by antibiotics, and reduce healthcare expenditures. Azithromycin is a suitable option in patients allergic to beta-lactam antibiotics.
90
Prognosis of otitis media
Patients treated for AOM have an excellent prognosis. Once analgesia and/or antibiotics are initiated, most patients improve quickly over the course of 2 to 3 days. An overwhelming majority become asymptomatic within 1 week of clinical diagnosis irrespective of the choice of treatment options. Few patients experience a resistant or recurrent infection
91
Complications of otitis media
``` Bullous myringitis Perforated tymp Mastoiditis Otitis media with effusion Chrom perf tymp ```
92
An 18-month-old toddler presents with 1 week of rhinorrhoea, cough, and congestion. Her parents report she is irritable, sleeping restlessly, and not eating well. Overnight she developed a fever. She attends day care and both parents smoke. On examination signs are found consistent with a viral respiratory infection including rhinorrhoea and congestion. The toddler appears irritable and apprehensive and has a fever. Otoscopy reveals a bulging, erythematous tympanic membrane and absent landmarks.
otitis media In older (verbal) children and adults the history should include otalgia. Some patients may report decreased hearing or popping sensations on the affected side, nausea, poor appetite, and restless sleep. As in infants, the examination often reveals signs consistent with a viral respiratory infection including rhinorrhoea and congestion. Conventional otoscopy reveals a bulging tympanic membrane, a requirement for the diagnosis. Occasionally a patient will present with purulent otorrhoea, which indicates that the tympanic membrane has ruptured as a result of positive pressure within the middle ear space. Once the membrane is perforated, many of these patients will cease complaining of otalgia and other symptoms of discomfort. The presence of copious amounts of purulent otorrhoea may interfere with the examiner's ability to visualise the ear drum. When visible the tympanic membrane will appear dull and shagrinated (cobblestoning).
93
Define acute rhinosinusitis
Acute sinusitis (also commonly known as acute rhinosinusitis) is a symptomatic inflammation of the mucosal lining of the nasal cavity and paranasal sinuses, where clinical symptoms have been present for 4 weeks or less. It can be caused by either a viral or a bacterial infection. Majority of cases in adults and children are of viral aetiology. Duration of symptoms more than 10 days often indicates bacterial cause. Imaging is not required for diagnosis unless complications are suspected. Condition is usually self-limiting; however, symptomatic therapy is recommended. Antibiotics are only recommended in select patient groups (e.g., immunocompromised or with severe disease).
94
Epidemiology of acute rhinosinusitis
16% of the adult population Approximately 0.5% to 13% of viral upper respiratory tract infections progress to acute bacterial sinusitis. It is estimated that 6% to 13% of children will have had one case of acute sinusitis by the age of 3 years. School-age children on average contract 6 to 8 upper respiratory tract infections per year, and of these, 5% to 10% will be complicated by sinusitis F>M
95
Aetiology of acute rhinosinusitis
The most common cause of acute sinusitis is a viral infection. Following an episode of viral sinusitis, 0.5% to 2% of cases of acute viral sinusitis will progress to acute bacterial sinusitis The three most common bacteria are Streptococcus pneumoniae (20% to 43% of cases), Haemophilus influenzae (22% to 35% of cases), and Moraxella catarrhalis (2% to 10% of cases). M catarrhalis is less common in the adult population. PATH With increased oedema and mucus production, the sinus ostium is obstructed, blocking normal ventilation and drainage of the sinus. With decreased mucociliary clearance, stasis of secretions occurs and a secondary bacterial infection can take place. From an inflammatory standpoint, high levels of tumour necrosis factor-beta and interferon-gamma are associated with release of various pro-inflammatory cytokines.
96
RFs for acute rhinosinusitis
STRONG URTI Allergic rhinitis WEAK GORD
97
Sx of acute rhinosinusitis
``` COMMON Sx <10 days = viral Sx >10 days = bacterial Sx worsen after initial improvement - bacterial Purulent nasal discharge Nasal blockage Facial pain/pressure Dental pain Cough Myalgia Sore thoat Hyposmia Oedematous turbinate ``` UNCOMMON Fever
98
Ix for acute rhinosinusitis
Clinical Possible to culture
99
Rx of acute rhinosinusitis
1. Supportive Viral sinusitis is suspected when symptoms are stable and present for less than 10 days. Generally a self-limiting disease, and treatment is primarily symptomatic. Adequate rest and hydration, warm facial packs, and steam inhalation may be useful. Treatments should be tried for 5 to 10 days before re-assessing the patient. 2. Analgesic/pyretic 3. Nasal decongestant +/- intranasal corticosteroid +/- Ipatropium nasal +/- intranasal saline +/- mucolytic ``` SUSPECTED BACTERIAL ABx - co-amox ENT referral 2. Analgesic/pyretic 3. Nasal decongestant +/- intranasal corticosteroid +/- Ipatropium nasal +/- intranasal saline +/- mucolytic ``` Fungal = ENT referral
100
Prognosis of acute rhinosinusitis
In general, acute sinusitis is a self-limiting disease and generally resolves within 1 month. However, the use of antibiotics in appropriately selected patients may limit the length and severity of symptoms. Recurrence Patients with structural anatomical variants (e.g., concha bullosa, deviated septum, infra-orbital ethmoid cell) are more prone to develop recurrent acute sinusitis and even persistent sinusitis. Recurrence is also dependent on exposure to an exacerbating condition such as a viral upper respiratory tract infection. Complications Complications are more commonly seen in the paediatric population, and occur due to direct extension of the infection into neighbouring structures. Orbital spread of infection with orbital cellulitis or orbital abscess represent the most common complications. Intracranial spread of infection resulting in meningitis or abscess is much less common.
101
Complications of acute rhinosinusitis
``` Chronic sinusitis Bacterial meningitis Subdurral abscess Peri/orbital cellulitis Periosteal abscess/cellulitls Cavernous sinus thrombosis ```
102
A 19-year-old woman presents with a 12-day history of purulent nasal drainage and nasal congestion, and reports a history of fever, myalgia, and facial pressure. She is otherwise healthy and works as a teacher. After 5 days of illness, the patient's symptoms started to improve; however, they have worsened in the last few days, despite the use of over-the-counter medications. Physical examination shows oedematous mucosa of the inferior turbinate. There is also thick mucus in the nasal cavity. Nasal endoscopy demonstrates purulent drainage and a small polyp in the ostiomeatal complex. The adenoids are small and erythematous.
acute rhinosinusitis Other symptoms may include sore throat or clear nasal discharge, which usually indicates a viral cause.[4] Patients may also present with a cough secondary to post-nasal drainage or exacerbation of asthma.
103
A 33-year-old man with a medical history of paediatric-onset asthma, atopic dermatitis, and allergic rhinitis presents with a 7-day history of facial pressure, dental pain, nasal blockage, and hyposmia. The patient developed these symptoms after recently mowing his lawn. The symptoms have not improved despite use of an intranasal corticosteroid, an antihistamine, and intranasal saline washes. Physical examination shows a septum deviated to the left side, and a large concha bullosa on the right side. There are no polyps, but there are swollen turbinates and thin, clear mucus present.
acute rhinosinusitis Other symptoms may include sore throat or clear nasal discharge, which usually indicates a viral cause.[4] Patients may also present with a cough secondary to post-nasal drainage or exacerbation of asthma.
104
Define labyrinthitis
An inflammatory condition caused by bacteria or viruses that affects the inner ear, which consists of the cochlea and vestibular system. Typically, it presents with sensorineural hearing loss, vertigo, and disequilibrium (problems with balance) and may affect one or both ears. It may be further classified as suppurative or serous. Suppurative (bacterial) labyrinthitis follows direct microbial invasion of the inner ear and usually presents with severe to profound hearing loss and vertigo. Serous (viral) labyrinthitis results from inflammation of the labyrinth only and usually presents with less severe hearing loss and vertigo than suppurative labyrinthitis, and the hearing loss often recovers. Inflammatory condition affecting the labyrinth in the cochlea and vestibular system of the inner ear. Viral infections are the most common cause of labyrinthitis. Bacterial labyrinthitis is a complication of otitis media or meningitis. Typical presentation includes vertigo, imbalance, and hearing loss. Diagnosis is supported by history, physical examination, and audiometry. Treatment is typically symptomatic and primarily involves the use of vestibular suppressants and anti-emetics.
105
Epidemiology of labyrinthitis
The actual incidence and prevalence of labyrinthitis are unknown. Viral infections are the most common cause of labyrinthitis. They typically occur in adults, whereas purulent bacterial labyrinthitis is more common in children who are otitis-prone. Bacterial labyrinthitis is a rare complication of otitis media
106
Aetiology of labyrinthitis
Viral labyrinthitis is typically associated with a preceding upper respiratory tract infection. Aetiological viral agents include varicella zoster virus, cytomegalovirus, mumps, measles, rubella, and HIV. Potential bacterial causes include Treponema pallidum, Haemophilus influenzae, Streptococcus species, Staphylococcus species, and Neisseria meningitidis
107
RFs for labyrinthitis
``` STRONG Viral infections Chronic suppurative otitis media AOM Cholesteatoma Meningitis Inner ear malformations ``` WEAK AI ear diseases Syphilis
108
Sx of labyrinthitis
``` COMMON Vertigo Dizziness N+V Hearing loss Otorrhoea Nystagmus Tinnitus Vertigo related quick head/body movements ``` Viral labyrinthitis may occur during an influenza-like illness or during illnesses such as measles or mumps. Therefore, fever, sore throat, and influenza-like symptoms may be present. UNCOMMON Otalgia
109
Ix for labyrinthitis
Webers + Rinnes test - some sensorineural deafness | Audiogram
110
Rx of labyrinthitis
VIRAL Vestibular suppressants: diazepam: children: consult specialist for guidance on dose; adults: 2-10 mg orally/intravenously every 4-8 hours when required Anti-emetics: metoclopramide: adults: 5-10 mg orally/intravenously every 8 hours when required for a maximum of 5 days, maximum 30 mg/day Steroids: For patients with sudden sensorineural hearing loss, corticosteroids are considered the standard of care. prednisolone: children: 1 mg/kg/day orally; adults: 60 mg/day orally Bacterial = SAME BUT topical/oral ABxs Ongoing: Vestibular rehabilitation programme
111
Complications of labyrinthitis
``` Mastoiditis Cholesteatoma Cochlear ossifications Hearing loss Bilateral vestibular hypofunction ```
112
Prognosis of labyrinthitis
If the patient has no serious neurological sequelae, the prognosis for acute labyrinthitis is generally good. Patients with other neurological complications from bacterial meningitis such as hydrocephalus or stroke may require additional therapy such as a ventriculoperitoneal shunt or physiotherapy and occupational therapy. Patients with cerebral infarcts in critical areas are often left with significant disabilities.
113
A 46-year-old man presents with a 1-year history of imbalance, deafness, and tinnitus. His symptoms began after being discharged from a prolonged admission to hospital secondary to pneumococcal meningitis.
labyrinthitis Patients with bacterial meningitis are often critically ill and may present after resolution of the acute illness with profound hearing loss and imbalance without a history of acute vertigo.[2] Patients with syphilitic labyrinthitis can present with progressive hearing loss and pressure- or sound-induced vertigo (Hennebert and Tullio signs).[4] Syphilitic labyrinthitis may follow tertiary neurosyphilis that occurs many years after the primary infection, and is not seen with acute primary or secondary syphilis.[4] Labyrinthitis may also be associated with autoimmune inner ear disease (e.g., Cogan's syndrome or Behcet's disease).
114
A 65-year-old woman presents with a chief complaint of dizziness. She describes it as a sudden and severe spinning sensation precipitated by rolling over in bed onto her right side. Symptoms typically last <30 seconds. They have occurred nightly over the last month and occasionally during the day when she tilts her head back to look upwards. She describes no precipitating event prior to onset and no associated hearing loss, tinnitus, or other neurological symptoms. Otological and neurological examinations are normal except for the Dix-Hallpike manoeuvre, which is negative on the left but strongly positive on the right side.
BPPV BPPV can occur as a result of a closed-head injury or vestibular neuronitis, and it can also be associated with Meniere's disease or migraine. Most patients give the classic description of a short-lived vertigo sensation following rolling over in bed. However, many patients may not sense an actual turning sensation and may use other dizziness descriptors to describe their sensation. Because of the frightening intensity of the sensations, patients often report that the spells last for 5 or 10 minutes when in reality they typically last for no more than 20 seconds.
115
Rx of BPPV
The initial step in managing BPPV is patient education and reassurance. This is done by explaining its non-life-threatening nature and favourable prognosis, with spontaneous remission in one third of patients at 3 weeks 3-position particle repositioning manoeuvre Semont repositioning manoeuvre Vestibular suppressants Vestibular rehabilitation exercises eg Brandt-Daroff The surgical treatment of BPPV is reserved for unrelenting, incapacitating cases where repeated attempts with repositioning manoeuvres and vestibular rehabilitation exercises have failed. Surgical treatment may also be considered for patients who respond to particle repositioning manoeuvres (PRMs) but have unremitting recurrences soon afterwards, to the extent that they are keen on a definitive solution rather than repeated PRMs. Less than 1% of BPPV patients will ever require surgery
116
Prognosis of BPPV
One third of patients remit at 3 weeks and the majority of patients at 6 months from onset Recurrence of BPPV is a frequent problem. Meniere's disease (endolymphatic hydrops), central nervous system diseases, migraine headaches, and post-traumatic BPPV have all been associated with a greater risk of recurrence.
117
Complications of BPPV
``` Road traffic accidents Accidents at work/leisure Conversion of BPPV to lateral oe anterior canal variant Nausea Falls in elderly Hearing loss ```
118
A 65-year-old woman presents with a chief complaint of dizziness. She describes it as a sudden and severe spinning sensation precipitated by rolling over in bed onto her right side. Symptoms typically last <30 seconds. They have occurred nightly over the last month and occasionally during the day when she tilts her head back to look upwards. She describes no precipitating event prior to onset and no associated hearing loss, tinnitus, or other neurological symptoms. Otological and neurological examinations are normal except for the Dix-Hallpike manoeuvre, which is negative on the left but strongly positive on the right side.
BPPV BPPV can occur as a result of a closed-head injury or vestibular neuronitis, and it can also be associated with Meniere's disease or migraine. Most patients give the classic description of a short-lived vertigo sensation following rolling over in bed. However, many patients may not sense an actual turning sensation and may use other dizziness descriptors to describe their sensation. Because of the frightening intensity of the sensations, patients often report that the spells last for 5 or 10 minutes when in reality they typically last for no more than 20 seconds.
119
Aetiology of Meniere's disease
Endolymphatic hydrops is thought to be due to over-production or impaired absorption of endolymph. This may occur as a result of one or a combination of the proposed aetiological agents. Some histopathological studies of the temporal bones suggest that, although endolymphatic hydrops is a histological marker for MD, it is not directly responsible for its symptoms. During the acute attack the excessive endolymphatic fluid pressure causes distension and rupture of Reissner's membrane. This results in the release of potassium-rich endolymph into the perilymphatic space and causes injury to the sensory and neural elements of the inner ear, which manifests clinically as sudden hearing loss, tinnitus, and vertigo. Between attacks, Reissner's membrane may reattach itself, the chemical balance is restored, and symptoms remit. However, some researchers are questioning this theory because membrane ruptures were found post mortem in temporal bones with no history of vertigo. Immune-mediated mechanisms have long been implicated in the pathophysiology of MD. This has been supported by the presence of increased levels of immune complexes and the presence of auto-antibodies to structures of the inner ear in patients with MD. Lymphocytes and immunoglobulins have also been found in the endolymphatic sac.
120
Rx of Meniere's disease
Low salt-diet or thiazide (unproven but may be of benefit) +/- vestibular suppressants, anti-emetics, or corticosteroids Intratympanic infections with dex The Meniett device is a handheld device that delivers intermittent pressure pulses through the ear canal and is self-administered 3 times per day. Hearing loss = audiological counselling +/- hearing aid Endolymphatic sac surgery Its role in MD is controversial, with studies that show 90% resolution of vertigo,[4] and others that demonstrate that it is no more effective than placebo Vestibular nerve section In this procedure, the vestibular portion of the eighth cranial nerve (CN VIII) is selectively cut and its cochlear portion is left intact; thus, this is potentially a hearing conservation approach. This prevents the vestibular afferent stimuli from reaching the brain. This does not alter the pathophysiology of MD, but provides relief from vertigo, its most disturbing symptom. It should be avoided in bilateral MD, otherwise oscillopsia (perception of bouncing of the visual field with walking) and permanent imbalance may occur. Potential complications are uncommon and include hearing loss, facial nerve paralysis, cerebrospinal fluid leak, and headache.
121
Prognosis of Meniere's disease
Most patients start with hearing loss and tinnitus. Patients may or may not then develop the complete clinical profile of MD
122
Complications of Meniere's disease
Falls | Profound hearing loss
123
A 40-year-old woman presents with a 1-year history of recurrent episodes of vertigo. The vertigo spells are described as a sensation of the room spinning that lasts from 20 minutes to a few hours and may be associated with nausea and vomiting. The spells are incapacitating and are accompanied by dizziness, vertigo, and disequilibrium, which may last for days. No loss of consciousness is reported. The patient also reports aural fullness, tinnitus, and hearing loss in the right ear that is more pronounced around the time of her vertigo spells. Physical examination of the head and neck is normal. A horizontal nystagmus is noted. She is unable to maintain her position during Romberg's testing or the Fukuda stepping test. She turns towards the right side and she is unable to walk tandem. Her cerebellar function tests are normal.
Meniere's disease Patients may present with any combination of hearing loss, tinnitus, vertigo, or aural fullness.
124
Rx of tonsillitis
Viral = NSAIDs or paracetamol only Due to Group A Strep (beta haemolytic): phenoxymethylpenicillin: children ≤27 kg: 250 mg orally two to three times daily for 10 days; children >27 kg and adults: 500 mg orally two to three times daily for 10 days OR benzathine benzylpenicillin: children ≤27 kg: 600,000 units intramuscularly as a single dose; children >27 kg and adults: 1.2 million units intramuscularly as a single dose In patients with severe symptoms and signs, such as significant oropharyngeal swelling and upper airway limitation, a single dose of intramuscular or intravenous dexamethasone reduces symptoms earlier than placebo. RECURRENT Tonsillectomy may be considered for patients who have recurrent symptoms of tonsillitis that do not become less common with time and for whom there is no other explanation for the recurrent symptoms
125
What is the Centor criteria
The Centor criteria give an indication of the likelihood of a sore throat being due to bacterial infection. The criteria are: ``` Tonsillar exudate Tender anterior cervical adenopathy Fever over 38°C (100.5°F) by history Absence of cough. If 3 or 4 of Centor criteria are met, the positive predictive value is 40% to 60%. The absence of 3 or 4 of the Centor criteria has a fairly high negative predictive value of 80%. ```
126
Prognosis of tonsillitis
Acute tonsillitis is an acute, self-limiting infective condition that normally resolves completely within 1 week with no sequelae. In vulnerable people (e.g., infants, very old people, immunosuppressed or immunocompromised patients), tonsillitis may run a more severe course. Antibiotics and/or admission to hospital for a limited period of time may be advisable. Very rarely (but more commonly in developing countries) acute tonsillitis may be associated with significant suppurative complications, such as neck abscess, and non-suppurative complications, such as rheumatic fever or acute glomerulonephritis.
127
Complications of tonsillitis
``` Scarlet fever Acute sinusitis AOM Peritonsillar abscess Acute rheumatic fever Acute post-strep glomerulonephritis Streptococcal toxic shock syndrome ```
128
A 6-year-old previously healthy boy presents with acute onset of fever of 39°C (102°F), severe throat pain that is exacerbated by swallowing, headache, and malaise. On examination his tonsils are symmetrically enlarged and red, with purulent exudate. He has multiple enlarged, painful anterior neck lymph nodes, but no other lymphadenopathy and no splenomegaly. He has no runny nose or cough, and no difficulty breathing.
Tonsillitis Tonsillitis may occur in isolation or as part of a generalised pharyngitis. The clinical distinction between tonsillitis and pharyngitis is unclear in the literature, and the condition is often referred to simply as "acute sore throat". Its severity may vary from a mild sore throat that responds well to simple analgesics to a severe sore throat that is associated with significant malaise and reduced oral intake, necessitating admission to hospital.
129
Sx of thyroglossal cyst
Palpable asymptomatic midline neck mass usually below [65% of the time] the level of the hyoid bone Moves during swallowing or on protrusion of the tongue The persistent duct or sinus can promote oral secretions, which may cause cysts to become infected Differential diagnosis are ectopic thyroid, enlarged lymph nodes, dermoid cysts and goiter. There may be difficulty breathing, dysphagia (difficulty swallowing), or dyspepsia (discomfort in the upper abdomen), especially if the cyst becomes large.
130
Rx of Thyroglossal cyst
Although generally benign, the cyst must be removed if the patient exhibits difficulty in breathing or swallowing, or if the cyst is infected.
131
Complications of Thyroglossal cyst
Infection Thyroglossal fistula Thyroglossal Duct cyst carcinoma
132
Define oropharyngeal cancer
Oropharyngeal cancer is predominantly (90%) a squamous cell carcinoma arising from the subsites of the oropharynx: the base of the tongue, soft palate, palatine tonsillar fossa and pillars, and lateral and posterior pharyngeal wall. Non-epithelial tumours, such as minor salivary gland carcinomas and sarcoma, are uncommon. Tobacco and alcohol abuse are the strongest predictors of developing oropharyngeal carcinoma. Human papillomavirus infection is strongly implicated in people not exposed to smoking or alcohol. Betel nut chewing in developing countries is also a risk factor. Signs include sore throat, referred oral pain, dysphagia, and trismus. Weight loss and neck mass can be the first signs of otherwise asymptomatic oropharyngeal cancer. Patients should be referred to an ear, nose, and throat surgeon for histological diagnosis. Staging is through computed tomography (CT) scan or magnetic resonance imaging of the head and neck with contrast and ultrasound-guided fine needle aspiration cytology. This is traditionally followed by triple endoscopy under general anaesthesia. However, positron emission tomography (PET) scan either alone or combined with CT scan has become an acceptable method for detecting primary disease if there is a solitary neck node or there are distant metastases. Treatment regimens vary depending on the stage of the cancer and involve surgery, chemotherapy, radiotherapy, and monoclonal antibodies (in combination with radiotherapy). Patients should be managed by a multidisciplinary team in specialised head and neck centres to optimise outcome.
133
Epidemiology of oropharyngeal cancer
Most patients present with advanced stages (stage II to IV) at diagnosis (70%). There is a wide consensus that HPV infection is a causative agent, as the number of HPV-16-positive tumours has increased, and affects younger patients (aged 40 to 60 years). HPV-associated oropharyngeal tumours affect mainly the tonsillar region and, to a lesser extent, the base of the tongue. Patients with more sexual partners are at risk of HPV-induced oropharyngeal carcinoma
134
Aetiology of oropharyngeal cancer
``` Tobacco and alcohol abuse are the strongest predictors of developing oropharyngeal carcinoma. Heavy consumers of both alcohol and tobacco are at higher risk than non-exposed people. Human papillomavirus (HPV) infection is strongly implicated in people not exposed to smoking or alcohol. ``` Human papillomavirus-induced carcinogenesis is not clearly elucidated, and is believed to be secondary to viral inactivation of p53, a tumour suppressor gene. Alcohol-induced carcinogenesis is mediated through acetaldehyde. Anatomical sites that are directly exposed to alcohol, such as the oral cavity, oropharynx, and hypopharynx, are at risk of cancerisation. People who smoke and drink are at risk of secondary malignancies in their upper aerodigestive tract because of field cancerisation. Cigarette smoke contains about 50 carcinogens and pro-carcinogens. The most prominent pro-carcinogens are polycyclic aromatic hydrocarbons and aromatic amines
135
RFs for oropharyngeal cancer
``` STRONG Smoking Alcohol HPV-16 Tobacco and betel nut chewing ```
136
Sx of oropharyngeal cancer
``` Oral pain WL Sore throat Neck lump Indurated / ulcerated mass Dysphagia Neck lymphadenopathy Otalgia Trismus = lockjaw White leukoplakia + red plaques [erythroplakia] ```
137
Ix for oropharyngeal cancer
Biopsy of primary site PET-CT of head and neck FNA of neck nodes Excision biopsy of neck nodes Baseline tests
138
Rx of oropharyngeal cancer
STAGE 1/2 Radio or surgery STAGE 3/4A Surgery + post op radio OR Chemoradiotherapy Rx with cetuximab possible 2nd line - Head and neck cancers have a high expression of epidermal growth factor receptor (EGFR), a key receptor involved in signal transductions that are mitogenic, antiapoptotic, angiogenic, and pro-invasion. Cetuximab is a monoclonal antibody directed to the extracellular moiety of EGFR. For recurrent disease after previous local therapy without any evidence of distant metastases, salvage with surgery, radiotherapy, or chemoradiotherapy may be considered on an individual basis because of treatment toxicity
139
Prognosis of oropharyngeal cancer
Survival after definitive treatment for oropharyngeal carcinoma depends principally on the stage of disease and ability to undergo standard treatment. Patients who are positive for human papillomavirus (HPV)-16 may have a better survival. The presence of oncoprotein E6 may confer a survival advantage for HPV-16-induced oropharyngeal cancer because of the enhanced rate of apoptosis observed with radiation. Increased expression of epidermal growth factor receptor (EGFR) in the tumour specimen may confer a poor prognosis, highlighting the importance of biomarkers in future prospective trials. Future prospective trials will probably include HPV as a stratification factor. Young age (<50 years) is also associated with a better cancer-specific survival compared with older age (>50 years) for tonsillar carcinoma.
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Complications of oropharyngeal cancer
Oral mucositis - Oral mucositis secondary to cancer therapy is an acute inflammation of the oral mucosa in response to systemic chemotherapy and/or radiotherapy to fields involving the oral cavity. The clinical presentation ranges from a general erythaematous stomatitis to erosive lesions and overt ulceration. Lesions are often very painful, may compromise nutrition and oral hygiene, and increase the risk of local and systemic infection. Furthermore, severe oral mucositis may warrant an undesirable chemotherapy dose-reduction and/or a break in radiotherapy. ``` Osteoradionecrosis after radio Speech alteration after surgery Dysphagia + aspiration after Rx Xerostomia - dry mouth Hearing loss Hypothyroidism after neck radio ```
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A 62-year-old man presents with a sore throat and 6 kg unintentional weight loss. He has smoked 1 pack of cigarettes daily for the past 45 years and drank 1 bottle of whiskey daily for the past 5 years. On examination, there is a large left tonsillar mass extending to the soft palate, with no cervical adenopathy.
oropharyngeal cancer Oropharyngeal carcinoma can present with a neck mass, without any other symptoms. Head and neck examination may reveal no obvious primary, as the tumour may be submucosal and not visible on physical examination. Additional diagnostic studies such as positron emission tomography (PET) scan alone, or combined with computed tomography (CT) scan, can orient the surgeon to biopsy the primary site (base of tongue, tonsil) if the neck mass biopsy shows squamous cell carcinoma. If these studies are negative, an examination under general anaesthesia should follow, combined with directed biopsy.